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Gene Information
Gene symbol: CD36
Gene name: CD36 molecule (thrombospondin receptor)
HGNC ID: 1663
Synonyms: SCARB3, GPIV, FAT, GP4, GP3B
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 1559774 | Bovine collagen type I or human placental copolymerized collagen type I/III was used to create the lattices. |
| 2 | 1559774 | Growth factors included epidermal growth factor (EGF), basic fibroblastic growth factor (FGF), insulin-like growth factor (IGF-I), and platelet-derived growth factor homodimer beta beta (PDGF). |
| 3 | 1559774 | Dose-response experiments (0.01-100 ng/ml) demonstrated that PDGF at 10 ng/ml (P less than 0.005) and EGF at 1 and 10 ng/ml (P less than 0.0001) were the most effective in promoting gel contraction, compared to IGF-I and FGF. |
| 4 | 1559774 | Cells from insulin-dependent diabetics and cells from a donor with macular dystrophy contracted lattices more rapidly than cells from normal neonates (P less than 0.0001). |
| 5 | 1559774 | Lattices of copolymerized human collagen type III/I demonstrated significantly reduced contraction rates (P less than 0.0001) and increased optical transmittance, compared to bovine collagen type I lattices. |
| 6 | 1559774 | Bovine collagen type I or human placental copolymerized collagen type I/III was used to create the lattices. |
| 7 | 1559774 | Growth factors included epidermal growth factor (EGF), basic fibroblastic growth factor (FGF), insulin-like growth factor (IGF-I), and platelet-derived growth factor homodimer beta beta (PDGF). |
| 8 | 1559774 | Dose-response experiments (0.01-100 ng/ml) demonstrated that PDGF at 10 ng/ml (P less than 0.005) and EGF at 1 and 10 ng/ml (P less than 0.0001) were the most effective in promoting gel contraction, compared to IGF-I and FGF. |
| 9 | 1559774 | Cells from insulin-dependent diabetics and cells from a donor with macular dystrophy contracted lattices more rapidly than cells from normal neonates (P less than 0.0001). |
| 10 | 1559774 | Lattices of copolymerized human collagen type III/I demonstrated significantly reduced contraction rates (P less than 0.0001) and increased optical transmittance, compared to bovine collagen type I lattices. |
| 11 | 1898043 | Incubation of corneal collagen type I with glucose in the presence of transition metal ions (copper, iron) results in the formation of collagen aggregates insoluble in 6 M urea, and in 2% sodium dodecyl sulfate + 5% beta-mercaptoethanol. |
| 12 | 2108050 | Increases in collagen type IV and laminin in galactose-induced retinal capillary basement membrane thickening--prevention by an aldose reductase inhibitor. |
| 13 | 2108050 | Thinner fibrils reacted strongly with collagen type III antibody, whereas thicker fibrils reacted weakly with collagen type I antibody. |
| 14 | 2108050 | Our results indicate that there is an increase in labeling densities of collagen type IV and laminin in thickened basement membranes of retinal capillaries of galactosemic rats along with the expression of interstitial collagens like collagen type III and an abnormal collagen that weakly cross-reacts with antibody to collagen type I, and these effects of galactosemia on the basement membranes are preventable by an aldose reductase inhibitor. |
| 15 | 2108050 | Increases in collagen type IV and laminin in galactose-induced retinal capillary basement membrane thickening--prevention by an aldose reductase inhibitor. |
| 16 | 2108050 | Thinner fibrils reacted strongly with collagen type III antibody, whereas thicker fibrils reacted weakly with collagen type I antibody. |
| 17 | 2108050 | Our results indicate that there is an increase in labeling densities of collagen type IV and laminin in thickened basement membranes of retinal capillaries of galactosemic rats along with the expression of interstitial collagens like collagen type III and an abnormal collagen that weakly cross-reacts with antibody to collagen type I, and these effects of galactosemia on the basement membranes are preventable by an aldose reductase inhibitor. |
| 18 | 7544802 | Since capillary endothelial cell CD36 expression appeared to correlate with parenchymal cell fatty acid utilization and since CD26 has been identified recently as a long-chain fatty acid-binding protein, we examined heart tissue CD36 expression in murine models of insulin-dependent (nonobese diabetic, NOD) and non-insulin-dependent diabetes mellitus (KKAY). |
| 19 | 7553074 | This has been shown for skin by other methods previously and is well known to occur in bone, another tissue whose matrix as well as dermis consists mainly of collagen type I. |
| 20 | 7553074 | This newly developed method might be useful in clinical studies on endocrine disorders affecting skin (and bone) metabolism and the regulation of collagen type I metabolism in general. |
| 21 | 7553074 | This has been shown for skin by other methods previously and is well known to occur in bone, another tissue whose matrix as well as dermis consists mainly of collagen type I. |
| 22 | 7553074 | This newly developed method might be useful in clinical studies on endocrine disorders affecting skin (and bone) metabolism and the regulation of collagen type I metabolism in general. |
| 23 | 8174847 | No glomerular staining was seen for collagen type I. |
| 24 | 8886750 | Growth hormone substitution in growth hormone-deficient adults: effects on collagen type I synthesis and skin thickness. |
| 25 | 8886750 | Growth hormone stimulates collagen type I synthesis. |
| 26 | 8886750 | The aim of our study was to prove whether a stimulation of collagen type I synthesis might be accompanied by a deposition of collagen type I in the skin (cutis). |
| 27 | 8886750 | PICP, the indicator of collagen type I synthesis, was increased after six months of therapy when compared to placebo. |
| 28 | 8886750 | Our data indicate that the stimulation of collagen type I synthesis by growth hormone substitution is followed by a deposition of collagen type I in the skin. |
| 29 | 8886750 | Growth hormone substitution in growth hormone-deficient adults: effects on collagen type I synthesis and skin thickness. |
| 30 | 8886750 | Growth hormone stimulates collagen type I synthesis. |
| 31 | 8886750 | The aim of our study was to prove whether a stimulation of collagen type I synthesis might be accompanied by a deposition of collagen type I in the skin (cutis). |
| 32 | 8886750 | PICP, the indicator of collagen type I synthesis, was increased after six months of therapy when compared to placebo. |
| 33 | 8886750 | Our data indicate that the stimulation of collagen type I synthesis by growth hormone substitution is followed by a deposition of collagen type I in the skin. |
| 34 | 8886750 | Growth hormone substitution in growth hormone-deficient adults: effects on collagen type I synthesis and skin thickness. |
| 35 | 8886750 | Growth hormone stimulates collagen type I synthesis. |
| 36 | 8886750 | The aim of our study was to prove whether a stimulation of collagen type I synthesis might be accompanied by a deposition of collagen type I in the skin (cutis). |
| 37 | 8886750 | PICP, the indicator of collagen type I synthesis, was increased after six months of therapy when compared to placebo. |
| 38 | 8886750 | Our data indicate that the stimulation of collagen type I synthesis by growth hormone substitution is followed by a deposition of collagen type I in the skin. |
| 39 | 8886750 | Growth hormone substitution in growth hormone-deficient adults: effects on collagen type I synthesis and skin thickness. |
| 40 | 8886750 | Growth hormone stimulates collagen type I synthesis. |
| 41 | 8886750 | The aim of our study was to prove whether a stimulation of collagen type I synthesis might be accompanied by a deposition of collagen type I in the skin (cutis). |
| 42 | 8886750 | PICP, the indicator of collagen type I synthesis, was increased after six months of therapy when compared to placebo. |
| 43 | 8886750 | Our data indicate that the stimulation of collagen type I synthesis by growth hormone substitution is followed by a deposition of collagen type I in the skin. |
| 44 | 8886750 | Growth hormone substitution in growth hormone-deficient adults: effects on collagen type I synthesis and skin thickness. |
| 45 | 8886750 | Growth hormone stimulates collagen type I synthesis. |
| 46 | 8886750 | The aim of our study was to prove whether a stimulation of collagen type I synthesis might be accompanied by a deposition of collagen type I in the skin (cutis). |
| 47 | 8886750 | PICP, the indicator of collagen type I synthesis, was increased after six months of therapy when compared to placebo. |
| 48 | 8886750 | Our data indicate that the stimulation of collagen type I synthesis by growth hormone substitution is followed by a deposition of collagen type I in the skin. |
| 49 | 9079720 | Adipocyte mRNA levels of three putative transporters, mitochondrial aspartate aminotransferase, fatty acid translocase, and fatty acid transporting protein (FATP) were also determined; mitochondrial aspartate aminotransferase and FATP mRNAs correlated strongly with fatty acid uptake. |
| 50 | 9115153 | Osteopenia has been described as a complication of insulin-dependent diabetes mellitus (IDDM). |
| 51 | 9115153 | Height, height standard deviation scores, glycated haemoglobin (HbA1C), basal c-peptide concentrations, insulin dose, serum concentrations of procollagen type I C-terminal propeptide (PICP), and collagen type I C-terminal telopeptide (ICTP) were measured at onset of IDDM and at 3, 6 and 12 months. |
| 52 | 9115153 | ICTP was in the normal range at onset of IDDM and decreased during the follow-up to reach a significant difference compared to controls after 3, 6 and 12 months of insulin treatment (P < 0.04). |
| 53 | 9115153 | Bone formation at onset of IDDM is not impaired; the introduction of insulin therapy, together with the achievement of a good metabolic control, determines an increase of bone matrix formation coupled with a decrease of bone resorption, that determines a positive balance of bone modeling. |
| 54 | 9137941 | Markers of bone turnover (alkaline phosphatase, osteocalcin, procollagen type I C-terminal propeptide, collagen type I C-terminal telopeptide, tartrate-resistant acid phosphatase) were measured at baseline. |
| 55 | 9250603 | Much biochemical evidence has implicated rat adipocyte CD36 (FAT) in membrane binding and transport of long-chain fatty acids (FA). |
| 56 | 9686920 | The following antibodies were used for this immunohistochemical study: monoclonal antibodies against the heparan sulphate side chain (JM403) and core protein (JM72) of the glomerular heparan sulphate proteoglycan; polyclonal antibodies against the core protein (B31); polyclonal antibodies against collagen types I, III, and IV, fibronectin, and laminin; and monoclonal antibodies against the noncollagenous domain of alpha1(collagen IV) and alpha3(collagen IV), against transforming growth factor beta(2G7), and against advanced glycosylation end products (4G9). |
| 57 | 9686920 | Increased intensity of staining was found for collagen type I and advanced glycosylation end products in patients with diabetic nephropathy. |
| 58 | 9916795 | Identification of Cd36 (Fat) as an insulin-resistance gene causing defective fatty acid and glucose metabolism in hypertensive rats. |
| 59 | 9916795 | We conclude that Cd36 deficiency underlies insulin resistance, defective fatty acid metabolism and hypertriglyceridaemia in SHR and may be important in the pathogenesis of human insulin-resistance syndromes. |
| 60 | 9916795 | Identification of Cd36 (Fat) as an insulin-resistance gene causing defective fatty acid and glucose metabolism in hypertensive rats. |
| 61 | 9916795 | We conclude that Cd36 deficiency underlies insulin resistance, defective fatty acid metabolism and hypertriglyceridaemia in SHR and may be important in the pathogenesis of human insulin-resistance syndromes. |
| 62 | 10339462 | The alpha2 gene coding sequence T807/A873 of the platelet collagen receptor integrin alpha2beta1 might be a genetic risk factor for the development of stroke in younger patients. |
| 63 | 10339462 | The GPIa T807/A873 allele causes a higher receptor expression, enhancing platelet binding to collagen. |
| 64 | 10339462 | Large epidemiological studies should prove whether the platelet collagen receptor GPIa-IIa T807 allele is an independent risk factor for the development of stroke in younger patients. |
| 65 | 10339462 | The alpha2 gene coding sequence T807/A873 of the platelet collagen receptor integrin alpha2beta1 might be a genetic risk factor for the development of stroke in younger patients. |
| 66 | 10339462 | The GPIa T807/A873 allele causes a higher receptor expression, enhancing platelet binding to collagen. |
| 67 | 10339462 | Large epidemiological studies should prove whether the platelet collagen receptor GPIa-IIa T807 allele is an independent risk factor for the development of stroke in younger patients. |
| 68 | 10458104 | Histopathological and immunohistochemical analysis of the endocrine and exocrine pancreas in twelve cattle with insulin-dependent diabetes mellitus (IDDM). |
| 69 | 10458104 | Histological and immunohistochemical studies were carried out on the pancreas of twelve cattle of insulin-dependent diabetes mellitus (IDDM). |
| 70 | 10458104 | Immunohistochemical examination revealed that the atrophied islet cells did not react to anti-insulin antibody, but occasionally reacted to anti-glucagon or somatostatin antibodies. |
| 71 | 10458104 | Islet fibrosis was due to the proliferation of collagen fibers reactive to both anti-collagen type I and type III antibodies. |
| 72 | 10616837 | Connective tissue growth factor (CTGF) is a peptide secreted by cultured endothelial cells and fibroblasts when stimulated by transforming growth factor-beta (TGF-beta), and is overexpressed during fibrotic processes in coronary arteries and in skin. |
| 73 | 10616837 | Exposure of MC to recombinant human CTGF significantly increased fibronectin and collagen type I production. |
| 74 | 10616837 | Exposure of MC to TGF-beta, increased glucose concentrations, or cyclic mechanical strain, all causal factors in diabetic glomerulosclerosis, markedly induced the expression of CTGF transcripts, while recombinant human CTGF was able to autoinduce its own expression. |
| 75 | 10616837 | The induction of CTGF protein by a high glucose concentration was mediated by TGF-beta, since a TGF-beta-neutralizing antibody blocked this stimulation. |
| 76 | 10616837 | These results suggest that CTGF upregulation is an important factor in the pathogenesis of mesangial matrix accumulation and progressive glomerulosclerosis, acting downstream of TGF-beta. |
| 77 | 10652025 | Expression of decorin, biglycan, and collagen type I in human renal fibrosing disease. |
| 78 | 10666797 | Plasmodium falciparum infestation of erythrocytes induces knob formation at the cell surface and the P. falciparum protein binding to CD36, ICAM-1 and thrombospondin present on the endothelium, and facilitates the parasite dissemination. |
| 79 | 10688808 | Wide interindividual variations in the density of a platelet collagen receptor (alpha2beta1 integrin or glycoprotein Ia/IIa) are reportedly associated with polymorphism(s) in the gene encoding the alpha subunit of the receptor, including a Bgl II polymorphism in intron 7. |
| 80 | 10724355 | Troglitazone (Tro), a new anti-diabetic drug, is a thiazolidinedione (TZD) which promotes adipocyte differentiation by activating peroxisome proliferator activated receptor gamma (PPARgamma). |
| 81 | 10724355 | As bone resorption markers, urinary free and total deoxypyridinoline as well as urinary collagen type I C-terminal telopeptide were measured; as bone formation markers, serum bone type and total alkaline phosphatase (BALP and ALP) levels along with osteocalcin (OC) were used. |
| 82 | 10791882 | LW, CD36, CD58, and CD147 have been shown in other tissues to mediate cell-cell interaction. |
| 83 | 10791882 | Other receptors, such as CD44, VLA-4, and B-CAM/LU, can mediate adhesion to components of extracellular matrix. |
| 84 | 10822074 | It has been shown recently that the variable expression of the platelet collagen receptor integrin alpha2beta1 predisposes to thrombotic risk on the one hand and hemorrhagic risk on the other hand. |
| 85 | 10822074 | The expression level of this platelet collagen receptor may play a central role in the rapidly evolving coronary artery lesions that lead to malignant arrhythmia and sudden cardiac death. |
| 86 | 10822074 | It has been shown recently that the variable expression of the platelet collagen receptor integrin alpha2beta1 predisposes to thrombotic risk on the one hand and hemorrhagic risk on the other hand. |
| 87 | 10822074 | The expression level of this platelet collagen receptor may play a central role in the rapidly evolving coronary artery lesions that lead to malignant arrhythmia and sudden cardiac death. |
| 88 | 10868951 | Induction of fatty acid translocase/CD36, peroxisome proliferator-activated receptor-gamma2, leptin, uncoupling proteins 2 and 3, and tumor necrosis factor-alpha gene expression in human subcutaneous fat by lipid infusion. |
| 89 | 10868951 | Using reverse transcriptase-polymerase chain reaction analysis, the mRNA expression of fatty acid translocase (FAT)/CD36, PPAR-gamma2, leptin, uncoupling protein (UCP)-2 and UCP-3, and tumor necrosis factor (TNF)-alpha was investigated in gluteal subcutaneous fat biopsies before and after 5 h infusions of saline or Intralipid (Pharmacia and Upjohn, Milan, Italy) plus heparin, which does not modify insulinemia. |
| 90 | 10868951 | Marked increases in FAT/CD36 (724+/-18%; P < 0.05), PPAR-gamma2 (200+/-8%; P < 0.05), leptin (110+/-13%; P < 0.05), UCP-2 (120+/-7%; P < 0.05), UCP-3 (80+/-5%; P < 0.05), and TNF-alpha mRNA (130+/-12%; P < 0.05) were observed in comparison with pretreatment levels, whereas there was no change after saline infusion. |
| 91 | 10868951 | These data suggest that the in vivo gene expression of FAT/CD36, PPAR-gamma2, leptin, UCP-2, UCP-3, and TNF-alpha in subcutaneous adipose tissue is regulated by circulating lipids independent of insulin and that prolonged hyperlipidemia may therefore contribute to increased fat metabolism and storage as a result of the increased expression of these proteins. |
| 92 | 10868951 | Induction of fatty acid translocase/CD36, peroxisome proliferator-activated receptor-gamma2, leptin, uncoupling proteins 2 and 3, and tumor necrosis factor-alpha gene expression in human subcutaneous fat by lipid infusion. |
| 93 | 10868951 | Using reverse transcriptase-polymerase chain reaction analysis, the mRNA expression of fatty acid translocase (FAT)/CD36, PPAR-gamma2, leptin, uncoupling protein (UCP)-2 and UCP-3, and tumor necrosis factor (TNF)-alpha was investigated in gluteal subcutaneous fat biopsies before and after 5 h infusions of saline or Intralipid (Pharmacia and Upjohn, Milan, Italy) plus heparin, which does not modify insulinemia. |
| 94 | 10868951 | Marked increases in FAT/CD36 (724+/-18%; P < 0.05), PPAR-gamma2 (200+/-8%; P < 0.05), leptin (110+/-13%; P < 0.05), UCP-2 (120+/-7%; P < 0.05), UCP-3 (80+/-5%; P < 0.05), and TNF-alpha mRNA (130+/-12%; P < 0.05) were observed in comparison with pretreatment levels, whereas there was no change after saline infusion. |
| 95 | 10868951 | These data suggest that the in vivo gene expression of FAT/CD36, PPAR-gamma2, leptin, UCP-2, UCP-3, and TNF-alpha in subcutaneous adipose tissue is regulated by circulating lipids independent of insulin and that prolonged hyperlipidemia may therefore contribute to increased fat metabolism and storage as a result of the increased expression of these proteins. |
| 96 | 10868951 | Induction of fatty acid translocase/CD36, peroxisome proliferator-activated receptor-gamma2, leptin, uncoupling proteins 2 and 3, and tumor necrosis factor-alpha gene expression in human subcutaneous fat by lipid infusion. |
| 97 | 10868951 | Using reverse transcriptase-polymerase chain reaction analysis, the mRNA expression of fatty acid translocase (FAT)/CD36, PPAR-gamma2, leptin, uncoupling protein (UCP)-2 and UCP-3, and tumor necrosis factor (TNF)-alpha was investigated in gluteal subcutaneous fat biopsies before and after 5 h infusions of saline or Intralipid (Pharmacia and Upjohn, Milan, Italy) plus heparin, which does not modify insulinemia. |
| 98 | 10868951 | Marked increases in FAT/CD36 (724+/-18%; P < 0.05), PPAR-gamma2 (200+/-8%; P < 0.05), leptin (110+/-13%; P < 0.05), UCP-2 (120+/-7%; P < 0.05), UCP-3 (80+/-5%; P < 0.05), and TNF-alpha mRNA (130+/-12%; P < 0.05) were observed in comparison with pretreatment levels, whereas there was no change after saline infusion. |
| 99 | 10868951 | These data suggest that the in vivo gene expression of FAT/CD36, PPAR-gamma2, leptin, UCP-2, UCP-3, and TNF-alpha in subcutaneous adipose tissue is regulated by circulating lipids independent of insulin and that prolonged hyperlipidemia may therefore contribute to increased fat metabolism and storage as a result of the increased expression of these proteins. |
| 100 | 10868951 | Induction of fatty acid translocase/CD36, peroxisome proliferator-activated receptor-gamma2, leptin, uncoupling proteins 2 and 3, and tumor necrosis factor-alpha gene expression in human subcutaneous fat by lipid infusion. |
| 101 | 10868951 | Using reverse transcriptase-polymerase chain reaction analysis, the mRNA expression of fatty acid translocase (FAT)/CD36, PPAR-gamma2, leptin, uncoupling protein (UCP)-2 and UCP-3, and tumor necrosis factor (TNF)-alpha was investigated in gluteal subcutaneous fat biopsies before and after 5 h infusions of saline or Intralipid (Pharmacia and Upjohn, Milan, Italy) plus heparin, which does not modify insulinemia. |
| 102 | 10868951 | Marked increases in FAT/CD36 (724+/-18%; P < 0.05), PPAR-gamma2 (200+/-8%; P < 0.05), leptin (110+/-13%; P < 0.05), UCP-2 (120+/-7%; P < 0.05), UCP-3 (80+/-5%; P < 0.05), and TNF-alpha mRNA (130+/-12%; P < 0.05) were observed in comparison with pretreatment levels, whereas there was no change after saline infusion. |
| 103 | 10868951 | These data suggest that the in vivo gene expression of FAT/CD36, PPAR-gamma2, leptin, UCP-2, UCP-3, and TNF-alpha in subcutaneous adipose tissue is regulated by circulating lipids independent of insulin and that prolonged hyperlipidemia may therefore contribute to increased fat metabolism and storage as a result of the increased expression of these proteins. |
| 104 | 10953027 | Peroxisome proliferator-activated receptor gamma ligands inhibit development of atherosclerosis in LDL receptor-deficient mice. |
| 105 | 10953027 | The peroxisome proliferator-activated receptor gamma (PPARgamma) is a nuclear receptor that regulates fat-cell development and glucose homeostasis and is the molecular target of a class of insulin-sensitizing agents used for the management of type 2 diabetes mellitus. |
| 106 | 10953027 | We report here that the PPARgamma-specific agonists rosiglitazone and GW7845 strongly inhibited the development of atherosclerosis in LDL receptor-deficient male mice, despite increased expression of the CD36 scavenger receptor in the arterial wall. |
| 107 | 10953027 | The antiatherogenic effect in male mice was correlated with improved insulin sensitivity and decreased tissue expression of TNF-alpha and gelatinase B, indicating both systemic and local actions of PPARgamma. |
| 108 | 11032732 | Both RT-PCR procedure and Northern blot analysis revealed that AGEs induced not only the gene expression of two major OxLDL receptors, macrophage scavenger receptor (MSR) class A and CD36, but also MSR-B I and lectin-like oxidized low-density lipoprotein receptor 1. |
| 109 | 11032732 | Also, as a result of gel shift assay, AGEs increased transcriptional activities of AP-1, NF-kappaB, and peroxisome proliferator-activated receptor gamma. |
| 110 | 11089532 | Up-regulation of peroxisome proliferator-activated receptors (PPAR-alpha) and PPAR-gamma messenger ribonucleic acid expression in the liver in murine obesity: troglitazone induces expression of PPAR-gamma-responsive adipose tissue-specific genes in the liver of obese diabetic mice. |
| 111 | 11089532 | Peroxisome proliferator-activated receptors (PPARs) are transcription factors that play an important role in the regulation of genes involved in lipid utilization and storage, lipoprotein metabolism, adipocyte differentiation, and insulin action. |
| 112 | 11089532 | PPAR-alpha is predominantly present in the liver, and PPAR-gamma in adipose tissue, whereas PPAR-delta is ubiquitously expressed. |
| 113 | 11089532 | We have now examined the mRNA levels of PPAR-alpha, -delta, and -gamma in three murine models of obesity, namely, ob/ob (leptin-deficient), db/db (leptin-receptor deficient), and serotonin 5-HT2c receptor (5-HT2cR) mutant mice. 5-HT2cR mutant mice develop a late-onset obesity that is associated with higher plasma leptin levels. |
| 114 | 11089532 | Our results show that PPAR-alpha mRNA levels in the liver are increased by 2- to 3-fold in all three obese models, whereas hepatic PPAR-gamma mRNA levels are increased by 7- to 9-fold in ob/ob and db/db mice and by 2-fold in obese 5-HT2cR mutant mice. |
| 115 | 11089532 | The treatment of lean control mice with troglitazone significantly increased the expression of adipocyte fatty acid-binding protein (aP2) and fatty acid translocase (FAT/CD36) in the liver. |
| 116 | 11089532 | This troglitazone-induced increase in the expression of aP2 and FAT/CD36 was markedly enhanced in the liver in ob/ob mice. |
| 117 | 11089532 | In contrast to the liver, troglitazone did not increase the expression of aP2, FAT/CD36, and uncoupling protein-2 in adipose tissue in lean or ob/ob mice. |
| 118 | 11089532 | Up-regulation of peroxisome proliferator-activated receptors (PPAR-alpha) and PPAR-gamma messenger ribonucleic acid expression in the liver in murine obesity: troglitazone induces expression of PPAR-gamma-responsive adipose tissue-specific genes in the liver of obese diabetic mice. |
| 119 | 11089532 | Peroxisome proliferator-activated receptors (PPARs) are transcription factors that play an important role in the regulation of genes involved in lipid utilization and storage, lipoprotein metabolism, adipocyte differentiation, and insulin action. |
| 120 | 11089532 | PPAR-alpha is predominantly present in the liver, and PPAR-gamma in adipose tissue, whereas PPAR-delta is ubiquitously expressed. |
| 121 | 11089532 | We have now examined the mRNA levels of PPAR-alpha, -delta, and -gamma in three murine models of obesity, namely, ob/ob (leptin-deficient), db/db (leptin-receptor deficient), and serotonin 5-HT2c receptor (5-HT2cR) mutant mice. 5-HT2cR mutant mice develop a late-onset obesity that is associated with higher plasma leptin levels. |
| 122 | 11089532 | Our results show that PPAR-alpha mRNA levels in the liver are increased by 2- to 3-fold in all three obese models, whereas hepatic PPAR-gamma mRNA levels are increased by 7- to 9-fold in ob/ob and db/db mice and by 2-fold in obese 5-HT2cR mutant mice. |
| 123 | 11089532 | The treatment of lean control mice with troglitazone significantly increased the expression of adipocyte fatty acid-binding protein (aP2) and fatty acid translocase (FAT/CD36) in the liver. |
| 124 | 11089532 | This troglitazone-induced increase in the expression of aP2 and FAT/CD36 was markedly enhanced in the liver in ob/ob mice. |
| 125 | 11089532 | In contrast to the liver, troglitazone did not increase the expression of aP2, FAT/CD36, and uncoupling protein-2 in adipose tissue in lean or ob/ob mice. |
| 126 | 11089532 | Up-regulation of peroxisome proliferator-activated receptors (PPAR-alpha) and PPAR-gamma messenger ribonucleic acid expression in the liver in murine obesity: troglitazone induces expression of PPAR-gamma-responsive adipose tissue-specific genes in the liver of obese diabetic mice. |
| 127 | 11089532 | Peroxisome proliferator-activated receptors (PPARs) are transcription factors that play an important role in the regulation of genes involved in lipid utilization and storage, lipoprotein metabolism, adipocyte differentiation, and insulin action. |
| 128 | 11089532 | PPAR-alpha is predominantly present in the liver, and PPAR-gamma in adipose tissue, whereas PPAR-delta is ubiquitously expressed. |
| 129 | 11089532 | We have now examined the mRNA levels of PPAR-alpha, -delta, and -gamma in three murine models of obesity, namely, ob/ob (leptin-deficient), db/db (leptin-receptor deficient), and serotonin 5-HT2c receptor (5-HT2cR) mutant mice. 5-HT2cR mutant mice develop a late-onset obesity that is associated with higher plasma leptin levels. |
| 130 | 11089532 | Our results show that PPAR-alpha mRNA levels in the liver are increased by 2- to 3-fold in all three obese models, whereas hepatic PPAR-gamma mRNA levels are increased by 7- to 9-fold in ob/ob and db/db mice and by 2-fold in obese 5-HT2cR mutant mice. |
| 131 | 11089532 | The treatment of lean control mice with troglitazone significantly increased the expression of adipocyte fatty acid-binding protein (aP2) and fatty acid translocase (FAT/CD36) in the liver. |
| 132 | 11089532 | This troglitazone-induced increase in the expression of aP2 and FAT/CD36 was markedly enhanced in the liver in ob/ob mice. |
| 133 | 11089532 | In contrast to the liver, troglitazone did not increase the expression of aP2, FAT/CD36, and uncoupling protein-2 in adipose tissue in lean or ob/ob mice. |
| 134 | 11231915 | In contrast to these putative antiatherogenic activities, PPARgamma has been shown in vitro to upregulate the CD36 scavenger receptor, which could promote foam cell formation. |
| 135 | 11231915 | We report herein that the PPARgamma ligand, troglitazone, inhibited lesion formation in male low density lipoprotein receptor-deficient mice fed either a high-fat diet, which also induces type 2 diabetes, or a high-fructose diet. |
| 136 | 11231916 | Troglitazone inhibits atherosclerosis in apolipoprotein E-knockout mice: pleiotropic effects on CD36 expression and HDL. |
| 137 | 11231916 | Thiazolidinediones (TZDs), which are insulin-sensitizing antidiabetic agents, can modulate the development of atherosclerosis not only by changing the systemic metabolic conditions associated with insulin resistance but also by exerting direct effects on vascular wall cells that express peroxisome proliferator-activated receptor-gamma (PPAR-gamma), a nuclear receptor for TZDs. |
| 138 | 11246880 | Using reverse transcriptase-polymerase chain reaction and Northern blotting analyses, the mRNA expression of fatty acid translocase (FAT)/CD36, GLUT4, tumor necrosis factor (TNF)-alpha, peroxisome proliferator-activated receptor (PPAR)-gamma, leptin, uncoupling protein (UCP)-2, and UCP-3 was investigated in different fat depots and skeletal muscles before and after the study infusions. |
| 139 | 11246880 | Furthermore, there were marked increases in FAT/CD36, TNF-alpha, PPAR-gamma, leptin, UCP2, and UCP3 mRNA levels in the visceral fat and muscle of the treated animals in comparison with those measured in the saline-treated animals. |
| 140 | 11246880 | These data suggest that the in vivo gene expression of FAT/CD36, GLUT4, TNF-alpha, PPAR-gamma, leptin, UCP2, and UCP3 in visceral fat and red fiber-type muscle are differently regulated by circulating lipids and that selective insulin resistance seems to favor, at least in part, a prevention of fat accumulation in tissues not primarily destined for fat storage, thus contributing to increased adiposity and the development of a prediabetic syndrome. |
| 141 | 11246880 | Using reverse transcriptase-polymerase chain reaction and Northern blotting analyses, the mRNA expression of fatty acid translocase (FAT)/CD36, GLUT4, tumor necrosis factor (TNF)-alpha, peroxisome proliferator-activated receptor (PPAR)-gamma, leptin, uncoupling protein (UCP)-2, and UCP-3 was investigated in different fat depots and skeletal muscles before and after the study infusions. |
| 142 | 11246880 | Furthermore, there were marked increases in FAT/CD36, TNF-alpha, PPAR-gamma, leptin, UCP2, and UCP3 mRNA levels in the visceral fat and muscle of the treated animals in comparison with those measured in the saline-treated animals. |
| 143 | 11246880 | These data suggest that the in vivo gene expression of FAT/CD36, GLUT4, TNF-alpha, PPAR-gamma, leptin, UCP2, and UCP3 in visceral fat and red fiber-type muscle are differently regulated by circulating lipids and that selective insulin resistance seems to favor, at least in part, a prevention of fat accumulation in tissues not primarily destined for fat storage, thus contributing to increased adiposity and the development of a prediabetic syndrome. |
| 144 | 11246880 | Using reverse transcriptase-polymerase chain reaction and Northern blotting analyses, the mRNA expression of fatty acid translocase (FAT)/CD36, GLUT4, tumor necrosis factor (TNF)-alpha, peroxisome proliferator-activated receptor (PPAR)-gamma, leptin, uncoupling protein (UCP)-2, and UCP-3 was investigated in different fat depots and skeletal muscles before and after the study infusions. |
| 145 | 11246880 | Furthermore, there were marked increases in FAT/CD36, TNF-alpha, PPAR-gamma, leptin, UCP2, and UCP3 mRNA levels in the visceral fat and muscle of the treated animals in comparison with those measured in the saline-treated animals. |
| 146 | 11246880 | These data suggest that the in vivo gene expression of FAT/CD36, GLUT4, TNF-alpha, PPAR-gamma, leptin, UCP2, and UCP3 in visceral fat and red fiber-type muscle are differently regulated by circulating lipids and that selective insulin resistance seems to favor, at least in part, a prevention of fat accumulation in tissues not primarily destined for fat storage, thus contributing to increased adiposity and the development of a prediabetic syndrome. |
| 147 | 11259621 | Both retinoid X receptor (RXR)-selective agonists (rexinoids) and thiazolidinediones (TZDs), PPAR (peroxisome proliferator-activated receptor)-gamma-specific ligands, produce insulin sensitization in diabetic rodents. |
| 148 | 11259621 | In adipose tissue, rosiglitazone decreased tumor necrosis factor-alpha (TNF-alpha) mRNA and induced glucose transporter 4 (GLUT4), muscle carnitine palmitoyl-transferase (MCPT), stearoyl CoA desaturase (SCD1), and fatty acid translocase (CD36). |
| 149 | 11259621 | In contrast, LG100268 increased TNF-alpha and had no effect or suppressed the expression of GLUT4, MCPT, SCD1, and CD36. |
| 150 | 11259621 | In liver, the rexinoid increased MCPT, SCD1, and CD36 mRNAs, whereas rosiglitazone induced only a small increase in CD36. |
| 151 | 11259621 | In skeletal muscle, rosiglitazone and LG100268 have similar effects; both increased SCD1 and CD36 mRNAs. |
| 152 | 11259621 | Both retinoid X receptor (RXR)-selective agonists (rexinoids) and thiazolidinediones (TZDs), PPAR (peroxisome proliferator-activated receptor)-gamma-specific ligands, produce insulin sensitization in diabetic rodents. |
| 153 | 11259621 | In adipose tissue, rosiglitazone decreased tumor necrosis factor-alpha (TNF-alpha) mRNA and induced glucose transporter 4 (GLUT4), muscle carnitine palmitoyl-transferase (MCPT), stearoyl CoA desaturase (SCD1), and fatty acid translocase (CD36). |
| 154 | 11259621 | In contrast, LG100268 increased TNF-alpha and had no effect or suppressed the expression of GLUT4, MCPT, SCD1, and CD36. |
| 155 | 11259621 | In liver, the rexinoid increased MCPT, SCD1, and CD36 mRNAs, whereas rosiglitazone induced only a small increase in CD36. |
| 156 | 11259621 | In skeletal muscle, rosiglitazone and LG100268 have similar effects; both increased SCD1 and CD36 mRNAs. |
| 157 | 11259621 | Both retinoid X receptor (RXR)-selective agonists (rexinoids) and thiazolidinediones (TZDs), PPAR (peroxisome proliferator-activated receptor)-gamma-specific ligands, produce insulin sensitization in diabetic rodents. |
| 158 | 11259621 | In adipose tissue, rosiglitazone decreased tumor necrosis factor-alpha (TNF-alpha) mRNA and induced glucose transporter 4 (GLUT4), muscle carnitine palmitoyl-transferase (MCPT), stearoyl CoA desaturase (SCD1), and fatty acid translocase (CD36). |
| 159 | 11259621 | In contrast, LG100268 increased TNF-alpha and had no effect or suppressed the expression of GLUT4, MCPT, SCD1, and CD36. |
| 160 | 11259621 | In liver, the rexinoid increased MCPT, SCD1, and CD36 mRNAs, whereas rosiglitazone induced only a small increase in CD36. |
| 161 | 11259621 | In skeletal muscle, rosiglitazone and LG100268 have similar effects; both increased SCD1 and CD36 mRNAs. |
| 162 | 11259621 | Both retinoid X receptor (RXR)-selective agonists (rexinoids) and thiazolidinediones (TZDs), PPAR (peroxisome proliferator-activated receptor)-gamma-specific ligands, produce insulin sensitization in diabetic rodents. |
| 163 | 11259621 | In adipose tissue, rosiglitazone decreased tumor necrosis factor-alpha (TNF-alpha) mRNA and induced glucose transporter 4 (GLUT4), muscle carnitine palmitoyl-transferase (MCPT), stearoyl CoA desaturase (SCD1), and fatty acid translocase (CD36). |
| 164 | 11259621 | In contrast, LG100268 increased TNF-alpha and had no effect or suppressed the expression of GLUT4, MCPT, SCD1, and CD36. |
| 165 | 11259621 | In liver, the rexinoid increased MCPT, SCD1, and CD36 mRNAs, whereas rosiglitazone induced only a small increase in CD36. |
| 166 | 11259621 | In skeletal muscle, rosiglitazone and LG100268 have similar effects; both increased SCD1 and CD36 mRNAs. |
| 167 | 11473052 | The molecular mechanisms by which peroxisome proliferator-activated receptor (PPAR) activation by fibrates reduces fat deposition and improves insulin sensitivity are not completely understood. |
| 168 | 11473052 | These changes were accompanied by an increase in the transcript levels of the uncoupling protein-2 (UCP-2; 1.5-fold induction; P < 0.05) and UCP-3 (3.7-fold induction; P < 0.001), mitochondrial proteins that reduce ATP yield and may facilitate the oxidation of fatty acids. |
| 169 | 11473052 | Moreover, bezafibrate reduced the mRNA expression of several adipocyte markers, including PPARgamma (30% reduction; P = 0.05), tumor necrosis factor-alpha (33% reduction; P < 0.05), and the ob gene (26% reduction). |
| 170 | 11473052 | The reduction of the adipocyte markers caused by bezafibrate was accompanied by an increase in the mRNA levels of the preadipocyte marker Pref-1 (1.6-fold induction; P < 0.01). |
| 171 | 11473052 | Similarly, fatty acid translocase (2.6-fold induction; P = 0.002) and Pref-1 (5.6-fold induction) mRNA levels increased, although differences in the latter were not significant because of huge individual variations. |
| 172 | 11499561 | Exposure of MC to rhCTGF significantly increased fibronectin and collagen type I secretion. |
| 173 | 11499561 | However, exposure to TGF-beta, increased glucose concentrations, or cyclic mechanical strain, all causal factors in glomerulosclerosis, markedly induced the expression of CTGF transcripts. |
| 174 | 11499561 | TGF-beta also induced abundant quantities of a small molecular weight form of CTGF (18 kDa). |
| 175 | 11499561 | The induction of CTGF protein by a high glucose concentration was mediated by TGF-beta, since a TGF-beta neutralizing antibody blocked this stimulation. |
| 176 | 11499561 | These results suggest that CTGF upregulation is an important factor in the pathogenesis of mesangial matrix accumulation in both diabetic and non-diabetic glomerulosclerosis, acting downstream of TGF-beta. |
| 177 | 11557774 | PPARalpha (NR1C1) controls lipid oxidation and clearance in hepatocytes and PPARgamma (NR1C3) promotes preadipocyte differentiation and lipogenesis. |
| 178 | 11557774 | PPARgamma agonists increase insulin sensitivity and are used in the management of type 2 diabetes. |
| 179 | 11557774 | Compound F increases the expression of genes involved in lipid uptake and storage such as the class A and B scavenger receptors (SRA, CD36) and adipophilin. |
| 180 | 11574414 | In conclusion, acutely elevated FFA levels 1) induced a significant reduction in tracer-determined GDR paralleled by impaired tyrosine phosphorylation of IRS-1 and reduced IRS-1-associated PI 3-kinase activity and 2) induced a significant reduction in FAT/CD36 total protein. |
| 181 | 11574414 | TZD pretreatment prevented FFA-induced decrements in insulin action and prevented the reduction in FAT/CD36 protein. |
| 182 | 11574414 | In conclusion, acutely elevated FFA levels 1) induced a significant reduction in tracer-determined GDR paralleled by impaired tyrosine phosphorylation of IRS-1 and reduced IRS-1-associated PI 3-kinase activity and 2) induced a significant reduction in FAT/CD36 total protein. |
| 183 | 11574414 | TZD pretreatment prevented FFA-induced decrements in insulin action and prevented the reduction in FAT/CD36 protein. |
| 184 | 11728949 | Platelet collagen receptor alpha2beta1 integrin and glycoprotein IIIa Pl(A1/A2) polymorphisms are not associated with nephropathy in type 2 diabetes. |
| 185 | 11728949 | Clinical factors for investigation included sex, age at diagnosis, duration of diabetes, body mass index (BMI), and fasting plasma glucose, hemoglobin A(1c) (HbA(1c)), total cholesterol, and triglyceride levels. |
| 186 | 11728949 | However, the Bgl II polymorphism of the alpha2beta1 integrin gene and the Apa I polymorphism of the platelet GPIIIa gene do not have a major role in the development of diabetic nephropathy in our population. |
| 187 | 11871150 | In semi-quantitative RT-PCR, scavenger receptor (SR)-AI, macrosialin (MS)/CD68, and receptor for advanced glycation end-products (RAGE) mRNAs showed significant increases at 6 WAI of SZ, and SR-AI and CD36 mRNA obviously increased until 26 WAI, as compared with the control. |
| 188 | 11871150 | Low-density lipoprotein receptor mRNA showed a significant decrease at 14 and 26 WAI, and SR-BI mRNA significantly decreased at 6 and 14 WAI, as compared with the control. |
| 189 | 11889559 | Molecular basis of the Cd36 chromosomal deletion underlying SHR defects in insulin action and fatty acid metabolism. |
| 190 | 11889559 | In the SHR/NCrlBR strain, a chromosomal deletion event that occurred at the Cd36 locus during the evolution of this SHR strain has been proposed as a cause of defective insulin action and fatty acid metabolism. |
| 191 | 11889559 | We conclude that in SHR/NCrlBR, the complex trait of insulin resistance and defective fatty acid metabolism is caused by Cd36 deficiency, resulting from a chromosomal deletion caused by unequal recombination. |
| 192 | 11889559 | Molecular basis of the Cd36 chromosomal deletion underlying SHR defects in insulin action and fatty acid metabolism. |
| 193 | 11889559 | In the SHR/NCrlBR strain, a chromosomal deletion event that occurred at the Cd36 locus during the evolution of this SHR strain has been proposed as a cause of defective insulin action and fatty acid metabolism. |
| 194 | 11889559 | We conclude that in SHR/NCrlBR, the complex trait of insulin resistance and defective fatty acid metabolism is caused by Cd36 deficiency, resulting from a chromosomal deletion caused by unequal recombination. |
| 195 | 11889559 | Molecular basis of the Cd36 chromosomal deletion underlying SHR defects in insulin action and fatty acid metabolism. |
| 196 | 11889559 | In the SHR/NCrlBR strain, a chromosomal deletion event that occurred at the Cd36 locus during the evolution of this SHR strain has been proposed as a cause of defective insulin action and fatty acid metabolism. |
| 197 | 11889559 | We conclude that in SHR/NCrlBR, the complex trait of insulin resistance and defective fatty acid metabolism is caused by Cd36 deficiency, resulting from a chromosomal deletion caused by unequal recombination. |
| 198 | 12031980 | Recently, we have shown that intravenous lipid emulsion (liposyn) infusion during a 120-min euglycemic-hyperinsulinemic clamp led to significant reductions in insulin action and fatty acid translocase (FAT/CD36) skeletal muscle protein expression. |
| 199 | 12031980 | Here, we report that a fourfold elevation in plasma FFA concentration induced a 40% reduction in the insulin-stimulated glucose disposal rate, a 30% decline in insulin-stimulated skeletal muscle insulin substrate receptor-1 (IRS-1) phosphorylation, a 48% decrease in IRS-1-associated phosphatidylinositol (PI) 3-kinase activity, and a 50% reduction in muscle FAT/CD36 protein expression in male rats. |
| 200 | 12031980 | In striking contrast, we found no effect of FFA elevation to cause insulin resistance, changes in IRS-1/PI 3-kinase, or FAT/CD36 protein levels in female animals. |
| 201 | 12031980 | Recently, we have shown that intravenous lipid emulsion (liposyn) infusion during a 120-min euglycemic-hyperinsulinemic clamp led to significant reductions in insulin action and fatty acid translocase (FAT/CD36) skeletal muscle protein expression. |
| 202 | 12031980 | Here, we report that a fourfold elevation in plasma FFA concentration induced a 40% reduction in the insulin-stimulated glucose disposal rate, a 30% decline in insulin-stimulated skeletal muscle insulin substrate receptor-1 (IRS-1) phosphorylation, a 48% decrease in IRS-1-associated phosphatidylinositol (PI) 3-kinase activity, and a 50% reduction in muscle FAT/CD36 protein expression in male rats. |
| 203 | 12031980 | In striking contrast, we found no effect of FFA elevation to cause insulin resistance, changes in IRS-1/PI 3-kinase, or FAT/CD36 protein levels in female animals. |
| 204 | 12031980 | Recently, we have shown that intravenous lipid emulsion (liposyn) infusion during a 120-min euglycemic-hyperinsulinemic clamp led to significant reductions in insulin action and fatty acid translocase (FAT/CD36) skeletal muscle protein expression. |
| 205 | 12031980 | Here, we report that a fourfold elevation in plasma FFA concentration induced a 40% reduction in the insulin-stimulated glucose disposal rate, a 30% decline in insulin-stimulated skeletal muscle insulin substrate receptor-1 (IRS-1) phosphorylation, a 48% decrease in IRS-1-associated phosphatidylinositol (PI) 3-kinase activity, and a 50% reduction in muscle FAT/CD36 protein expression in male rats. |
| 206 | 12031980 | In striking contrast, we found no effect of FFA elevation to cause insulin resistance, changes in IRS-1/PI 3-kinase, or FAT/CD36 protein levels in female animals. |
| 207 | 12054519 | The fatty acid translocase (FAT)/CD36 and the glucose transporter GLUT4 are localized in different cellular compartments in rat cardiac muscle. |
| 208 | 12054519 | We studied the subcellular distribution of FAT/CD36 in rat cardiac muscle after in vivo insulin stimulation by membrane fractionation and immunoisolation of GLUT4- and FAT/CD36-vesicles. |
| 209 | 12054519 | FAT/CD36 was equally present in both plasma and microsomal membranes with no effect of insulin on the cellular distribution, whereas GLUT4 increased 2- to 3-fold in the plasma membrane. |
| 210 | 12054519 | FAT/CD36 resides in one intracellular pool, whereas GLUT4 is present in two distinct pools. |
| 211 | 12054519 | Immunoadsorption of GLUT4-vesicles indicated that FAT/CD36 is undetectable in these vesicles. |
| 212 | 12054519 | Likewise, no GLUT4 could be detected in FAT/CD36-vesicles. |
| 213 | 12054519 | These vesicles contain a high amount of Rab11 that remained unaffected after insulin stimulation, whereas Rab11 increased about 3-fold in the GLUT4-vesicles in response to insulin. |
| 214 | 12054519 | These data show that GLUT4 and FAT/CD36 do not co-localize in cardiac muscle and that FAT/CD36 is not redistributed in response to insulin in the heart. |
| 215 | 12054519 | Rab11 may be involved in endosomal recycling of FAT/CD36, however, insulin-associated Rab11 functions appear to be limited to GLUT4-vesicles. |
| 216 | 12054519 | The fatty acid translocase (FAT)/CD36 and the glucose transporter GLUT4 are localized in different cellular compartments in rat cardiac muscle. |
| 217 | 12054519 | We studied the subcellular distribution of FAT/CD36 in rat cardiac muscle after in vivo insulin stimulation by membrane fractionation and immunoisolation of GLUT4- and FAT/CD36-vesicles. |
| 218 | 12054519 | FAT/CD36 was equally present in both plasma and microsomal membranes with no effect of insulin on the cellular distribution, whereas GLUT4 increased 2- to 3-fold in the plasma membrane. |
| 219 | 12054519 | FAT/CD36 resides in one intracellular pool, whereas GLUT4 is present in two distinct pools. |
| 220 | 12054519 | Immunoadsorption of GLUT4-vesicles indicated that FAT/CD36 is undetectable in these vesicles. |
| 221 | 12054519 | Likewise, no GLUT4 could be detected in FAT/CD36-vesicles. |
| 222 | 12054519 | These vesicles contain a high amount of Rab11 that remained unaffected after insulin stimulation, whereas Rab11 increased about 3-fold in the GLUT4-vesicles in response to insulin. |
| 223 | 12054519 | These data show that GLUT4 and FAT/CD36 do not co-localize in cardiac muscle and that FAT/CD36 is not redistributed in response to insulin in the heart. |
| 224 | 12054519 | Rab11 may be involved in endosomal recycling of FAT/CD36, however, insulin-associated Rab11 functions appear to be limited to GLUT4-vesicles. |
| 225 | 12054519 | The fatty acid translocase (FAT)/CD36 and the glucose transporter GLUT4 are localized in different cellular compartments in rat cardiac muscle. |
| 226 | 12054519 | We studied the subcellular distribution of FAT/CD36 in rat cardiac muscle after in vivo insulin stimulation by membrane fractionation and immunoisolation of GLUT4- and FAT/CD36-vesicles. |
| 227 | 12054519 | FAT/CD36 was equally present in both plasma and microsomal membranes with no effect of insulin on the cellular distribution, whereas GLUT4 increased 2- to 3-fold in the plasma membrane. |
| 228 | 12054519 | FAT/CD36 resides in one intracellular pool, whereas GLUT4 is present in two distinct pools. |
| 229 | 12054519 | Immunoadsorption of GLUT4-vesicles indicated that FAT/CD36 is undetectable in these vesicles. |
| 230 | 12054519 | Likewise, no GLUT4 could be detected in FAT/CD36-vesicles. |
| 231 | 12054519 | These vesicles contain a high amount of Rab11 that remained unaffected after insulin stimulation, whereas Rab11 increased about 3-fold in the GLUT4-vesicles in response to insulin. |
| 232 | 12054519 | These data show that GLUT4 and FAT/CD36 do not co-localize in cardiac muscle and that FAT/CD36 is not redistributed in response to insulin in the heart. |
| 233 | 12054519 | Rab11 may be involved in endosomal recycling of FAT/CD36, however, insulin-associated Rab11 functions appear to be limited to GLUT4-vesicles. |
| 234 | 12054519 | The fatty acid translocase (FAT)/CD36 and the glucose transporter GLUT4 are localized in different cellular compartments in rat cardiac muscle. |
| 235 | 12054519 | We studied the subcellular distribution of FAT/CD36 in rat cardiac muscle after in vivo insulin stimulation by membrane fractionation and immunoisolation of GLUT4- and FAT/CD36-vesicles. |
| 236 | 12054519 | FAT/CD36 was equally present in both plasma and microsomal membranes with no effect of insulin on the cellular distribution, whereas GLUT4 increased 2- to 3-fold in the plasma membrane. |
| 237 | 12054519 | FAT/CD36 resides in one intracellular pool, whereas GLUT4 is present in two distinct pools. |
| 238 | 12054519 | Immunoadsorption of GLUT4-vesicles indicated that FAT/CD36 is undetectable in these vesicles. |
| 239 | 12054519 | Likewise, no GLUT4 could be detected in FAT/CD36-vesicles. |
| 240 | 12054519 | These vesicles contain a high amount of Rab11 that remained unaffected after insulin stimulation, whereas Rab11 increased about 3-fold in the GLUT4-vesicles in response to insulin. |
| 241 | 12054519 | These data show that GLUT4 and FAT/CD36 do not co-localize in cardiac muscle and that FAT/CD36 is not redistributed in response to insulin in the heart. |
| 242 | 12054519 | Rab11 may be involved in endosomal recycling of FAT/CD36, however, insulin-associated Rab11 functions appear to be limited to GLUT4-vesicles. |
| 243 | 12054519 | The fatty acid translocase (FAT)/CD36 and the glucose transporter GLUT4 are localized in different cellular compartments in rat cardiac muscle. |
| 244 | 12054519 | We studied the subcellular distribution of FAT/CD36 in rat cardiac muscle after in vivo insulin stimulation by membrane fractionation and immunoisolation of GLUT4- and FAT/CD36-vesicles. |
| 245 | 12054519 | FAT/CD36 was equally present in both plasma and microsomal membranes with no effect of insulin on the cellular distribution, whereas GLUT4 increased 2- to 3-fold in the plasma membrane. |
| 246 | 12054519 | FAT/CD36 resides in one intracellular pool, whereas GLUT4 is present in two distinct pools. |
| 247 | 12054519 | Immunoadsorption of GLUT4-vesicles indicated that FAT/CD36 is undetectable in these vesicles. |
| 248 | 12054519 | Likewise, no GLUT4 could be detected in FAT/CD36-vesicles. |
| 249 | 12054519 | These vesicles contain a high amount of Rab11 that remained unaffected after insulin stimulation, whereas Rab11 increased about 3-fold in the GLUT4-vesicles in response to insulin. |
| 250 | 12054519 | These data show that GLUT4 and FAT/CD36 do not co-localize in cardiac muscle and that FAT/CD36 is not redistributed in response to insulin in the heart. |
| 251 | 12054519 | Rab11 may be involved in endosomal recycling of FAT/CD36, however, insulin-associated Rab11 functions appear to be limited to GLUT4-vesicles. |
| 252 | 12054519 | The fatty acid translocase (FAT)/CD36 and the glucose transporter GLUT4 are localized in different cellular compartments in rat cardiac muscle. |
| 253 | 12054519 | We studied the subcellular distribution of FAT/CD36 in rat cardiac muscle after in vivo insulin stimulation by membrane fractionation and immunoisolation of GLUT4- and FAT/CD36-vesicles. |
| 254 | 12054519 | FAT/CD36 was equally present in both plasma and microsomal membranes with no effect of insulin on the cellular distribution, whereas GLUT4 increased 2- to 3-fold in the plasma membrane. |
| 255 | 12054519 | FAT/CD36 resides in one intracellular pool, whereas GLUT4 is present in two distinct pools. |
| 256 | 12054519 | Immunoadsorption of GLUT4-vesicles indicated that FAT/CD36 is undetectable in these vesicles. |
| 257 | 12054519 | Likewise, no GLUT4 could be detected in FAT/CD36-vesicles. |
| 258 | 12054519 | These vesicles contain a high amount of Rab11 that remained unaffected after insulin stimulation, whereas Rab11 increased about 3-fold in the GLUT4-vesicles in response to insulin. |
| 259 | 12054519 | These data show that GLUT4 and FAT/CD36 do not co-localize in cardiac muscle and that FAT/CD36 is not redistributed in response to insulin in the heart. |
| 260 | 12054519 | Rab11 may be involved in endosomal recycling of FAT/CD36, however, insulin-associated Rab11 functions appear to be limited to GLUT4-vesicles. |
| 261 | 12054519 | The fatty acid translocase (FAT)/CD36 and the glucose transporter GLUT4 are localized in different cellular compartments in rat cardiac muscle. |
| 262 | 12054519 | We studied the subcellular distribution of FAT/CD36 in rat cardiac muscle after in vivo insulin stimulation by membrane fractionation and immunoisolation of GLUT4- and FAT/CD36-vesicles. |
| 263 | 12054519 | FAT/CD36 was equally present in both plasma and microsomal membranes with no effect of insulin on the cellular distribution, whereas GLUT4 increased 2- to 3-fold in the plasma membrane. |
| 264 | 12054519 | FAT/CD36 resides in one intracellular pool, whereas GLUT4 is present in two distinct pools. |
| 265 | 12054519 | Immunoadsorption of GLUT4-vesicles indicated that FAT/CD36 is undetectable in these vesicles. |
| 266 | 12054519 | Likewise, no GLUT4 could be detected in FAT/CD36-vesicles. |
| 267 | 12054519 | These vesicles contain a high amount of Rab11 that remained unaffected after insulin stimulation, whereas Rab11 increased about 3-fold in the GLUT4-vesicles in response to insulin. |
| 268 | 12054519 | These data show that GLUT4 and FAT/CD36 do not co-localize in cardiac muscle and that FAT/CD36 is not redistributed in response to insulin in the heart. |
| 269 | 12054519 | Rab11 may be involved in endosomal recycling of FAT/CD36, however, insulin-associated Rab11 functions appear to be limited to GLUT4-vesicles. |
| 270 | 12054519 | The fatty acid translocase (FAT)/CD36 and the glucose transporter GLUT4 are localized in different cellular compartments in rat cardiac muscle. |
| 271 | 12054519 | We studied the subcellular distribution of FAT/CD36 in rat cardiac muscle after in vivo insulin stimulation by membrane fractionation and immunoisolation of GLUT4- and FAT/CD36-vesicles. |
| 272 | 12054519 | FAT/CD36 was equally present in both plasma and microsomal membranes with no effect of insulin on the cellular distribution, whereas GLUT4 increased 2- to 3-fold in the plasma membrane. |
| 273 | 12054519 | FAT/CD36 resides in one intracellular pool, whereas GLUT4 is present in two distinct pools. |
| 274 | 12054519 | Immunoadsorption of GLUT4-vesicles indicated that FAT/CD36 is undetectable in these vesicles. |
| 275 | 12054519 | Likewise, no GLUT4 could be detected in FAT/CD36-vesicles. |
| 276 | 12054519 | These vesicles contain a high amount of Rab11 that remained unaffected after insulin stimulation, whereas Rab11 increased about 3-fold in the GLUT4-vesicles in response to insulin. |
| 277 | 12054519 | These data show that GLUT4 and FAT/CD36 do not co-localize in cardiac muscle and that FAT/CD36 is not redistributed in response to insulin in the heart. |
| 278 | 12054519 | Rab11 may be involved in endosomal recycling of FAT/CD36, however, insulin-associated Rab11 functions appear to be limited to GLUT4-vesicles. |
| 279 | 12163016 | The effect of peroxisome proliferator-activated receptor (PPAR)-alpha activators on the liver is well established, but the other effects on muscle and adipose tissue about lipid metabolism and insulin sensitivity are not clear. |
| 280 | 12163016 | We investigated whether PPAR-alpha activation affects adiposity of skeletal muscle as well as adipose tissue and improves insulin sensitivity in spontaneous type 2 diabetes model, Otsuka Long-Evans Tokushima Fatty (OLETF) rats. |
| 281 | 12163016 | The mRNA levels of FAT/CD36 and mitochondrial carnitine palmitoyltransferase I (M-CPT I) in liver were remarkably increased. |
| 282 | 12163016 | Fasting plasma insulin and leptin levels, insulin response after intravenous glucose loading and homeostasis model assessment insulin resistance (HOMA(IR)) index were lowered in treatment group. |
| 283 | 12242049 | Advanced glycation end products (AGE), which are generated through long-term exposure of proteins to glucose, also behave as active ligands for some scavenger receptors, including class A scavenger receptor (SR-A) and class B scavenger receptors such as CD36 and scavenger receptor, class B, type I (SR-BI). |
| 284 | 12242049 | Using Chinese hamster ovary cells overexpressing SR-BI (CHO-SR-BI cells), it was demonstrated that AGE-bovine serum albumin binds to SR-BI and inhibits selective uptake of HDL-CE by CHO-SR-BI cells as well as cholesterol efflux from CHO-SR-BI cells to HDL, suggesting potential roles of AGE in diabetic dyslipidemia and accelerated atherosclerosis in diabetes. |
| 285 | 12297704 | By day 14, neointimal area was significantly increased (0.39 +/- 0.03 vs. 0.18 +/- 0.05 mm(2) at day 7, p = 0.003) characterized by an enhanced number of alpha-actin-positive smooth muscle cells surrounded by extracellular matrix rich in versican and hyaluronan. |
| 286 | 12297704 | This regression phase was accompanied by a marked increase in elastin fibrils and collagen type I. |
| 287 | 12351456 | Insulin stimulates long-chain fatty acid utilization by rat cardiac myocytes through cellular redistribution of FAT/CD36. |
| 288 | 12351456 | The existence of an intracellular pool of fatty acid translocase (FAT/CD36), an 88-kDa membrane transporter for long-chain fatty acids (FAs), and the ability of insulin to induce translocation events prompted us to investigate the direct effects of insulin on cellular uptake of FA by the heart. |
| 289 | 12351456 | This insulin-induced increase in FA uptake was completely blocked by phloretin, sulfo-N-succinimidylpalmitate (SSP), and wortmannin, indicating the involvement of FAT/CD36 and the dependence on phosphatidylinositol-3 (PI-3) kinase activation. |
| 290 | 12351456 | Subcellular fractionation of insulin-stimulated cardiac myocytes demonstrated a 1.5-fold increase in sarcolemmal FAT/CD36 and a 62% decrease in intracellular FAT/CD36 with parallel changes in subcellular distribution of GLUT4. |
| 291 | 12351456 | The addition of insulin to 4 Hz-stimulated cells further stimulated FA uptake to 2.3-fold, indicating that there are at least two functionally independent intracellular FAT/CD36 pools, one recruited by insulin and the other mobilized by contractions. |
| 292 | 12351456 | Malfunctioning of insulin-induced FAT/CD36 translocation may be involved in the development of type 2 diabetic cardiomyopathies. |
| 293 | 12351456 | Insulin stimulates long-chain fatty acid utilization by rat cardiac myocytes through cellular redistribution of FAT/CD36. |
| 294 | 12351456 | The existence of an intracellular pool of fatty acid translocase (FAT/CD36), an 88-kDa membrane transporter for long-chain fatty acids (FAs), and the ability of insulin to induce translocation events prompted us to investigate the direct effects of insulin on cellular uptake of FA by the heart. |
| 295 | 12351456 | This insulin-induced increase in FA uptake was completely blocked by phloretin, sulfo-N-succinimidylpalmitate (SSP), and wortmannin, indicating the involvement of FAT/CD36 and the dependence on phosphatidylinositol-3 (PI-3) kinase activation. |
| 296 | 12351456 | Subcellular fractionation of insulin-stimulated cardiac myocytes demonstrated a 1.5-fold increase in sarcolemmal FAT/CD36 and a 62% decrease in intracellular FAT/CD36 with parallel changes in subcellular distribution of GLUT4. |
| 297 | 12351456 | The addition of insulin to 4 Hz-stimulated cells further stimulated FA uptake to 2.3-fold, indicating that there are at least two functionally independent intracellular FAT/CD36 pools, one recruited by insulin and the other mobilized by contractions. |
| 298 | 12351456 | Malfunctioning of insulin-induced FAT/CD36 translocation may be involved in the development of type 2 diabetic cardiomyopathies. |
| 299 | 12351456 | Insulin stimulates long-chain fatty acid utilization by rat cardiac myocytes through cellular redistribution of FAT/CD36. |
| 300 | 12351456 | The existence of an intracellular pool of fatty acid translocase (FAT/CD36), an 88-kDa membrane transporter for long-chain fatty acids (FAs), and the ability of insulin to induce translocation events prompted us to investigate the direct effects of insulin on cellular uptake of FA by the heart. |
| 301 | 12351456 | This insulin-induced increase in FA uptake was completely blocked by phloretin, sulfo-N-succinimidylpalmitate (SSP), and wortmannin, indicating the involvement of FAT/CD36 and the dependence on phosphatidylinositol-3 (PI-3) kinase activation. |
| 302 | 12351456 | Subcellular fractionation of insulin-stimulated cardiac myocytes demonstrated a 1.5-fold increase in sarcolemmal FAT/CD36 and a 62% decrease in intracellular FAT/CD36 with parallel changes in subcellular distribution of GLUT4. |
| 303 | 12351456 | The addition of insulin to 4 Hz-stimulated cells further stimulated FA uptake to 2.3-fold, indicating that there are at least two functionally independent intracellular FAT/CD36 pools, one recruited by insulin and the other mobilized by contractions. |
| 304 | 12351456 | Malfunctioning of insulin-induced FAT/CD36 translocation may be involved in the development of type 2 diabetic cardiomyopathies. |
| 305 | 12351456 | Insulin stimulates long-chain fatty acid utilization by rat cardiac myocytes through cellular redistribution of FAT/CD36. |
| 306 | 12351456 | The existence of an intracellular pool of fatty acid translocase (FAT/CD36), an 88-kDa membrane transporter for long-chain fatty acids (FAs), and the ability of insulin to induce translocation events prompted us to investigate the direct effects of insulin on cellular uptake of FA by the heart. |
| 307 | 12351456 | This insulin-induced increase in FA uptake was completely blocked by phloretin, sulfo-N-succinimidylpalmitate (SSP), and wortmannin, indicating the involvement of FAT/CD36 and the dependence on phosphatidylinositol-3 (PI-3) kinase activation. |
| 308 | 12351456 | Subcellular fractionation of insulin-stimulated cardiac myocytes demonstrated a 1.5-fold increase in sarcolemmal FAT/CD36 and a 62% decrease in intracellular FAT/CD36 with parallel changes in subcellular distribution of GLUT4. |
| 309 | 12351456 | The addition of insulin to 4 Hz-stimulated cells further stimulated FA uptake to 2.3-fold, indicating that there are at least two functionally independent intracellular FAT/CD36 pools, one recruited by insulin and the other mobilized by contractions. |
| 310 | 12351456 | Malfunctioning of insulin-induced FAT/CD36 translocation may be involved in the development of type 2 diabetic cardiomyopathies. |
| 311 | 12351456 | Insulin stimulates long-chain fatty acid utilization by rat cardiac myocytes through cellular redistribution of FAT/CD36. |
| 312 | 12351456 | The existence of an intracellular pool of fatty acid translocase (FAT/CD36), an 88-kDa membrane transporter for long-chain fatty acids (FAs), and the ability of insulin to induce translocation events prompted us to investigate the direct effects of insulin on cellular uptake of FA by the heart. |
| 313 | 12351456 | This insulin-induced increase in FA uptake was completely blocked by phloretin, sulfo-N-succinimidylpalmitate (SSP), and wortmannin, indicating the involvement of FAT/CD36 and the dependence on phosphatidylinositol-3 (PI-3) kinase activation. |
| 314 | 12351456 | Subcellular fractionation of insulin-stimulated cardiac myocytes demonstrated a 1.5-fold increase in sarcolemmal FAT/CD36 and a 62% decrease in intracellular FAT/CD36 with parallel changes in subcellular distribution of GLUT4. |
| 315 | 12351456 | The addition of insulin to 4 Hz-stimulated cells further stimulated FA uptake to 2.3-fold, indicating that there are at least two functionally independent intracellular FAT/CD36 pools, one recruited by insulin and the other mobilized by contractions. |
| 316 | 12351456 | Malfunctioning of insulin-induced FAT/CD36 translocation may be involved in the development of type 2 diabetic cardiomyopathies. |
| 317 | 12351456 | Insulin stimulates long-chain fatty acid utilization by rat cardiac myocytes through cellular redistribution of FAT/CD36. |
| 318 | 12351456 | The existence of an intracellular pool of fatty acid translocase (FAT/CD36), an 88-kDa membrane transporter for long-chain fatty acids (FAs), and the ability of insulin to induce translocation events prompted us to investigate the direct effects of insulin on cellular uptake of FA by the heart. |
| 319 | 12351456 | This insulin-induced increase in FA uptake was completely blocked by phloretin, sulfo-N-succinimidylpalmitate (SSP), and wortmannin, indicating the involvement of FAT/CD36 and the dependence on phosphatidylinositol-3 (PI-3) kinase activation. |
| 320 | 12351456 | Subcellular fractionation of insulin-stimulated cardiac myocytes demonstrated a 1.5-fold increase in sarcolemmal FAT/CD36 and a 62% decrease in intracellular FAT/CD36 with parallel changes in subcellular distribution of GLUT4. |
| 321 | 12351456 | The addition of insulin to 4 Hz-stimulated cells further stimulated FA uptake to 2.3-fold, indicating that there are at least two functionally independent intracellular FAT/CD36 pools, one recruited by insulin and the other mobilized by contractions. |
| 322 | 12351456 | Malfunctioning of insulin-induced FAT/CD36 translocation may be involved in the development of type 2 diabetic cardiomyopathies. |
| 323 | 12473645 | FEEL-1 and FEEL-2 are endocytic receptors for advanced glycation end products. |
| 324 | 12473645 | Receptors for AGEs include scavenger receptors, which recognize acetylated low density lipoproteins (Ac-LDL) such as scavenger receptor class AI/AII (SR-A), cell surface glycoprotein CD36, scavenger receptor class B type I (SR-BI), and lectin-like oxidized low density lipoprotein receptor-1. |
| 325 | 12473645 | The broad ligand repertoire of these receptors as well as the diversity of the receptors for AGEs have prompted us to examine whether AGEs are also recognized by the novel scavenger receptors, which we have recently isolated from a cDNA library prepared from human umbilical vein endothelial cells, such as the scavenger receptor expressed by endothelial cells-I (SREC-I); the fasciclin EGF-like, laminin-type EGF-like, and link domain-containing scavenger receptor-1 (FEEL-1); and its paralogous protein, FEEL-2. |
| 326 | 12473645 | At 4 degrees C, (125)I-AGE-bovine serum albumin (BSA) exhibited high affinity specific binding to Chinese hamster ovary (CHO) cells overexpressing FEEL-1 (CHO-FEEL-1) and FEEL-2 (CHO-FEEL-2) with K(d) of 2.55 and 1.68 microg/ml, respectively, but not to CHO cells expressing SREC (CHO-SREC) and parent CHO cells. |
| 327 | 12473645 | At 37 degrees C, (125)I-AGE-BSA was taken up and degraded by CHO-FEEL-1 and CHO-FEEL-2 cells but not by CHO-SREC and parent CHO cells. |
| 328 | 12473645 | The (125)I-AGE-BSA binding to CHO-FEEL-1 and CHO-FEEL-2 cells was effectively inhibited by Ac-LDL and polyanionic SR-A inhibitors such as fucoidan, polyinosinic acids, and dextran sulfate but not by native LDL, oxidized LDL, or HDL. |
| 329 | 12479584 | For instance, both muscle contraction and insulin can translocate FAT/CD36 from an intracellular pool to the plasma membrane, thereby increasing fatty acid transport. |
| 330 | 12479587 | Surface expression of fatty acid translocase (FAT/CD36) on platelets in myeloproliferative disorders and non-insulin dependent diabetes mellitus: effect on arachidonic acid uptake. |
| 331 | 12479587 | Expression of CD36 or fatty acid translocase (FAT) and its role in arachidonic acid (AA) uptake by platelets were examined in subjects with myeloproliferative disorders (MPD), those with non-insulin-dependent diabetes mellitus (NIDDM), and in normal, healthy, age-matched controls. |
| 332 | 12479587 | This is consistent with higher surface expression of CD36 in MPD platelets. |
| 333 | 12479587 | Surface expression of fatty acid translocase (FAT/CD36) on platelets in myeloproliferative disorders and non-insulin dependent diabetes mellitus: effect on arachidonic acid uptake. |
| 334 | 12479587 | Expression of CD36 or fatty acid translocase (FAT) and its role in arachidonic acid (AA) uptake by platelets were examined in subjects with myeloproliferative disorders (MPD), those with non-insulin-dependent diabetes mellitus (NIDDM), and in normal, healthy, age-matched controls. |
| 335 | 12479587 | This is consistent with higher surface expression of CD36 in MPD platelets. |
| 336 | 12479587 | Surface expression of fatty acid translocase (FAT/CD36) on platelets in myeloproliferative disorders and non-insulin dependent diabetes mellitus: effect on arachidonic acid uptake. |
| 337 | 12479587 | Expression of CD36 or fatty acid translocase (FAT) and its role in arachidonic acid (AA) uptake by platelets were examined in subjects with myeloproliferative disorders (MPD), those with non-insulin-dependent diabetes mellitus (NIDDM), and in normal, healthy, age-matched controls. |
| 338 | 12479587 | This is consistent with higher surface expression of CD36 in MPD platelets. |
| 339 | 12488363 | This deficit was evident at the molecular level as shown by diminished expression of osteocalcin, collagen types I. |
| 340 | 12488363 | When transcription factors were examined, core-binding factor alpha1 (Cbfa1)/runt domain factor-2 (Runx-2) and human homolog of the drosophila distal-less gene (Dlx5) expression were substantially reduced in the diabetic, compared with control, groups on d 4 and 6. |
| 341 | 12488363 | C-fos but not c-jun expression was also suppressed in the diabetic group but not closely linked to bone formation. |
| 342 | 12488363 | Insulin treatment substantially reversed the effect of diabetes on the expression of bone matrix osteocalcin and collagen type I and transcription factors Cbfa1/Runx2 and Dlx5. |
| 343 | 12488363 | These results indicate that diabetic animals produce sufficient amounts of immature mesenchymal tissue but fail to adequately express genes that regulate osteoblast differentiation, Cbfa1/Runx-2 and Dlx5, which in turn, leads to decreased bone formation. |
| 344 | 12540964 | Diabetes duration may modify the association between genetic variation in the glycoprotein Ia subunit of the platelet collagen receptor and risk of severe diabetic retinopathy: a working hypothesis. |
| 345 | 12540964 | We assessed the associations of the C807T and Glu505Lys variants of the glycoprotein Ia (alpha(2) integrin) subunit of the platelet/endothelial collagen receptor and risk of retinopathy in a population-based survey of 288 diabetic patients in one Swedish community. |
| 346 | 12547883 | Insulin sensitivity and lipid metabolism in human CD36 deficiency. |
| 347 | 12556534 | Here we report the cloning, expression pattern, and subcellular localization of a novel member of the fatty acid transport protein (FATP) family termed FATP6. |
| 348 | 12556534 | FATP6 is principally expressed in the heart where it is the predominant FATP family member. |
| 349 | 12556534 | Similar to other FATPs, transient and stable transfection of FATP6 into 293 cells enhanced uptake of LCFAs. |
| 350 | 12556534 | In these membrane domains FATP6 also colocalizes with another molecule involved in LCFA uptake, CD36. |
| 351 | 12647275 | Compared with placebo values, a 2.4-fold induction in resistin mRNA levels was observed in white adipose tissue of fenofibrate-treated patients, whereas no changes were observed in the mRNA levels of the well-known perosixome proliferator-activated receptor (PPAR) target genes CD36, acyl-CoA oxidase, and carnitine palmitoyltransferase. |
| 352 | 12647275 | These findings indicate that resistin changes were not related to PPAR activation by fenofibrate. |
| 353 | 12704802 | Many of the observed differences, including down-regulation of collagen type I and collagen-processing enzymes, reflect expected patterns and support the relevance of our results. |
| 354 | 12704802 | These include an orphan nuclear receptor DAX1 and a small ras-related GTPase associated with diabetes, both of which increased with increasing differentiation, as well as a high mobility group-box transcription factor, SOX4, that was down-regulated during differentiation. |
| 355 | 12716760 | CD36 deficiency has been linked with insulin resistance. |
| 356 | 12716760 | This study demonstrates that VLDL binds to the platelet receptor CD36, enhances platelet thromboxane A2 production, and causes increased collagen-mediated platelet aggregation. |
| 357 | 12716760 | A monoclonal antibody against CD36 attenuated VLDL-enhanced collagen-induced platelet aggregation by 1) inhibiting binding of VLDL to platelets by 75% (P = 0.041); 2) lengthening lag time to 190% (P < 0.001); and 3) decreasing thromboxane production to 8% of control (P < 0.001). |
| 358 | 12716760 | These data suggest that platelet Cd36 has a key role in VLDL-induced collagen-mediated platelet aggregation, possibly contributing to atherothrombosis associated with increased VLDL levels. |
| 359 | 12716760 | CD36 deficiency has been linked with insulin resistance. |
| 360 | 12716760 | This study demonstrates that VLDL binds to the platelet receptor CD36, enhances platelet thromboxane A2 production, and causes increased collagen-mediated platelet aggregation. |
| 361 | 12716760 | A monoclonal antibody against CD36 attenuated VLDL-enhanced collagen-induced platelet aggregation by 1) inhibiting binding of VLDL to platelets by 75% (P = 0.041); 2) lengthening lag time to 190% (P < 0.001); and 3) decreasing thromboxane production to 8% of control (P < 0.001). |
| 362 | 12716760 | These data suggest that platelet Cd36 has a key role in VLDL-induced collagen-mediated platelet aggregation, possibly contributing to atherothrombosis associated with increased VLDL levels. |
| 363 | 12716760 | CD36 deficiency has been linked with insulin resistance. |
| 364 | 12716760 | This study demonstrates that VLDL binds to the platelet receptor CD36, enhances platelet thromboxane A2 production, and causes increased collagen-mediated platelet aggregation. |
| 365 | 12716760 | A monoclonal antibody against CD36 attenuated VLDL-enhanced collagen-induced platelet aggregation by 1) inhibiting binding of VLDL to platelets by 75% (P = 0.041); 2) lengthening lag time to 190% (P < 0.001); and 3) decreasing thromboxane production to 8% of control (P < 0.001). |
| 366 | 12716760 | These data suggest that platelet Cd36 has a key role in VLDL-induced collagen-mediated platelet aggregation, possibly contributing to atherothrombosis associated with increased VLDL levels. |
| 367 | 12716760 | CD36 deficiency has been linked with insulin resistance. |
| 368 | 12716760 | This study demonstrates that VLDL binds to the platelet receptor CD36, enhances platelet thromboxane A2 production, and causes increased collagen-mediated platelet aggregation. |
| 369 | 12716760 | A monoclonal antibody against CD36 attenuated VLDL-enhanced collagen-induced platelet aggregation by 1) inhibiting binding of VLDL to platelets by 75% (P = 0.041); 2) lengthening lag time to 190% (P < 0.001); and 3) decreasing thromboxane production to 8% of control (P < 0.001). |
| 370 | 12716760 | These data suggest that platelet Cd36 has a key role in VLDL-induced collagen-mediated platelet aggregation, possibly contributing to atherothrombosis associated with increased VLDL levels. |
| 371 | 12716848 | Lipoprotein abnormalities in human genetic CD36 deficiency associated with insulin resistance and abnormal fatty acid metabolism. |
| 372 | 12829625 | Contraction-induced fatty acid translocase/CD36 translocation in rat cardiac myocytes is mediated through AMP-activated protein kinase signaling. |
| 373 | 12829625 | Contraction of rat cardiac myocytes induces translocation of fatty acid translocase (FAT)/CD36 and GLUT4 from intracellular stores to the sarcolemma, leading to enhanced rates of long-chain fatty acid (FA) and glucose uptake, respectively. |
| 374 | 12829625 | Because intracellular AMP/ATP is elevated in contracting cardiac myocytes, we investigated whether activation of AMP-activated protein kinase (AMP kinase) is involved in contraction-inducible FAT/CD36 translocation. |
| 375 | 12829625 | Furthermore, the stimulating effects of both AICAR and oligomycin were antagonized by blocking FAT/CD36 with sulfo-N-succinimidylpalmitate, but not by inhibiting phosphatidylinositol 3-kinase with wortmannin, indicating the involvement of FAT/CD36, but excluding a role for insulin signaling. |
| 376 | 12829625 | Contraction-induced fatty acid translocase/CD36 translocation in rat cardiac myocytes is mediated through AMP-activated protein kinase signaling. |
| 377 | 12829625 | Contraction of rat cardiac myocytes induces translocation of fatty acid translocase (FAT)/CD36 and GLUT4 from intracellular stores to the sarcolemma, leading to enhanced rates of long-chain fatty acid (FA) and glucose uptake, respectively. |
| 378 | 12829625 | Because intracellular AMP/ATP is elevated in contracting cardiac myocytes, we investigated whether activation of AMP-activated protein kinase (AMP kinase) is involved in contraction-inducible FAT/CD36 translocation. |
| 379 | 12829625 | Furthermore, the stimulating effects of both AICAR and oligomycin were antagonized by blocking FAT/CD36 with sulfo-N-succinimidylpalmitate, but not by inhibiting phosphatidylinositol 3-kinase with wortmannin, indicating the involvement of FAT/CD36, but excluding a role for insulin signaling. |
| 380 | 12829625 | Contraction-induced fatty acid translocase/CD36 translocation in rat cardiac myocytes is mediated through AMP-activated protein kinase signaling. |
| 381 | 12829625 | Contraction of rat cardiac myocytes induces translocation of fatty acid translocase (FAT)/CD36 and GLUT4 from intracellular stores to the sarcolemma, leading to enhanced rates of long-chain fatty acid (FA) and glucose uptake, respectively. |
| 382 | 12829625 | Because intracellular AMP/ATP is elevated in contracting cardiac myocytes, we investigated whether activation of AMP-activated protein kinase (AMP kinase) is involved in contraction-inducible FAT/CD36 translocation. |
| 383 | 12829625 | Furthermore, the stimulating effects of both AICAR and oligomycin were antagonized by blocking FAT/CD36 with sulfo-N-succinimidylpalmitate, but not by inhibiting phosphatidylinositol 3-kinase with wortmannin, indicating the involvement of FAT/CD36, but excluding a role for insulin signaling. |
| 384 | 12829625 | Contraction-induced fatty acid translocase/CD36 translocation in rat cardiac myocytes is mediated through AMP-activated protein kinase signaling. |
| 385 | 12829625 | Contraction of rat cardiac myocytes induces translocation of fatty acid translocase (FAT)/CD36 and GLUT4 from intracellular stores to the sarcolemma, leading to enhanced rates of long-chain fatty acid (FA) and glucose uptake, respectively. |
| 386 | 12829625 | Because intracellular AMP/ATP is elevated in contracting cardiac myocytes, we investigated whether activation of AMP-activated protein kinase (AMP kinase) is involved in contraction-inducible FAT/CD36 translocation. |
| 387 | 12829625 | Furthermore, the stimulating effects of both AICAR and oligomycin were antagonized by blocking FAT/CD36 with sulfo-N-succinimidylpalmitate, but not by inhibiting phosphatidylinositol 3-kinase with wortmannin, indicating the involvement of FAT/CD36, but excluding a role for insulin signaling. |
| 388 | 12864739 | Plasmalemmal fatty acid transport is regulated in heart and skeletal muscle by contraction, insulin and leptin, and in obesity and diabetes. |
| 389 | 12864739 | It has recently been found that FAT/CD36 is present in an intracellular (endosomal) compartment from which it can be translocated to the plasma membrane within minutes by muscle contraction and by insulin, to stimulate LCFA uptake. |
| 390 | 12938014 | The BglII gene polymorphism of the alpha2beta1 integrin, which is a platelet collagen receptor, has been suggested as a genetic risk factor for diabetic retinopathy in Japanese subjects. |
| 391 | 12942148 | Peroxisome proliferator-activated receptor-gamma (PPARgamma) ligands have been used for several years as modulators of insulin sensitivity and glucose metabolism. |
| 392 | 12942148 | Also, PPARgamma ligands regulate the expression of SR-A and CD36 receptors that take up lipids in the macrophage. |
| 393 | 12942148 | PPARgamma has also been demonstrated to act through the liver X receptor alpha to increase the activity of reverse cholesterol transport in these cells. |
| 394 | 12946933 | DM induced in the aging heart decreased LV systolic function (LV ejection fraction fell by 25%), increased aortic stiffness, and increased collagen type I and type III protein content. |
| 395 | 12946933 | ALT-711 restored LV ejection fraction, reduced aortic stiffness and LV mass with no reduction in blood glucose level (199 +/- 17 mg/dl), and reversed the upregulation of collagen type I and type III. |
| 396 | 12946933 | DM induced in the aging heart decreased LV systolic function (LV ejection fraction fell by 25%), increased aortic stiffness, and increased collagen type I and type III protein content. |
| 397 | 12946933 | ALT-711 restored LV ejection fraction, reduced aortic stiffness and LV mass with no reduction in blood glucose level (199 +/- 17 mg/dl), and reversed the upregulation of collagen type I and type III. |
| 398 | 14602787 | Oxidative enzyme activities, fatty acid transporters (FAT/CD36 and FABPpm), and TG(m) were measured from basal muscle samples, and total LCACoA content was determined before and after insulin stimulation. |
| 399 | 14602787 | There was a significant relationship between the oxidative capacity of skeletal muscle and insulin sensitivity (citrate synthase, r = 0.71, P < 0.001; beta-hydroxyacyl CoA dehydrogenase, r = 0.61, P = 0.001). |
| 400 | 14633859 | Connective tissue growth factor and igf-I are produced by human renal fibroblasts and cooperate in the induction of collagen production by high glucose. |
| 401 | 14633859 | Here we examined the effects of connective tissue growth factor (CTGF) and IGF-I on collagen type I and III production by human renal fibroblasts and their involvement in glucose-induced matrix accumulation. |
| 402 | 14633859 | We have demonstrated that both CTGF and IGF-I expressions were increased in renal fibroblasts under hyperglycemic conditions, also in the absence of TGF-beta signaling. |
| 403 | 14633859 | Although CTGF alone had no effect on collagen secretion, combined stimulation with IGF-I enhanced collagen accumulation. |
| 404 | 14633859 | Moreover, we observed a partial inhibition in glucose-induced collagen secretion with neutralizing anti-CTGF antibodies, thereby demonstrating for the first time the involvement of endogenous CTGF in glucose-induced effects in human renal fibroblasts. |
| 405 | 14633859 | Therefore, the cooperation between CTGF and IGF-I might be involved in glucose-induced matrix accumulation in tubulointerstitial fibrosis and might contribute to the pathogenesis of diabetic nephropathy. |
| 406 | 15132977 | The altered FAT/CD36 trafficking in muscle from obese subjects and type 2 diabetics juxtaposes the known alterations in GLUT4 trafficking, i.e., GLUT4 is known to be retained in its intracellular depots while FAT/CD36 is retained at the sarcolemma. |
| 407 | 15132977 | This redistribution of FAT/CD36 to the sarcolemma may contribute to the etiology of insulin resistance in human muscle, and hence, FAT/CD36 provides another potential therapeutic target for the prevention and/or treatment of insulin resistance. |
| 408 | 15132977 | The altered FAT/CD36 trafficking in muscle from obese subjects and type 2 diabetics juxtaposes the known alterations in GLUT4 trafficking, i.e., GLUT4 is known to be retained in its intracellular depots while FAT/CD36 is retained at the sarcolemma. |
| 409 | 15132977 | This redistribution of FAT/CD36 to the sarcolemma may contribute to the etiology of insulin resistance in human muscle, and hence, FAT/CD36 provides another potential therapeutic target for the prevention and/or treatment of insulin resistance. |
| 410 | 15220187 | Because LCFA uptake is regulated by insulin and contractions, we examined in cardiac myocytes from lean and obese Zucker rats the effects of insulin and the contraction-mimetic agent oligomycin on the initial rate of LCFA uptake, subcellular distribution of FAT/CD36, and LCFA metabolism. |
| 411 | 15220187 | In cardiac myocytes isolated from lean rats, in vitro administration of insulin induced the translocation of FAT/CD36 to the sarcolemma and stimulated initial rates of LCFA uptake and TAG esterification. |
| 412 | 15220187 | In contrast, in myocytes from obese rats, insulin failed to alter the subcellular localization of FAT/CD36 and the rates of LCFA uptake and TAG esterification. |
| 413 | 15220187 | Because LCFA uptake is regulated by insulin and contractions, we examined in cardiac myocytes from lean and obese Zucker rats the effects of insulin and the contraction-mimetic agent oligomycin on the initial rate of LCFA uptake, subcellular distribution of FAT/CD36, and LCFA metabolism. |
| 414 | 15220187 | In cardiac myocytes isolated from lean rats, in vitro administration of insulin induced the translocation of FAT/CD36 to the sarcolemma and stimulated initial rates of LCFA uptake and TAG esterification. |
| 415 | 15220187 | In contrast, in myocytes from obese rats, insulin failed to alter the subcellular localization of FAT/CD36 and the rates of LCFA uptake and TAG esterification. |
| 416 | 15220187 | Because LCFA uptake is regulated by insulin and contractions, we examined in cardiac myocytes from lean and obese Zucker rats the effects of insulin and the contraction-mimetic agent oligomycin on the initial rate of LCFA uptake, subcellular distribution of FAT/CD36, and LCFA metabolism. |
| 417 | 15220187 | In cardiac myocytes isolated from lean rats, in vitro administration of insulin induced the translocation of FAT/CD36 to the sarcolemma and stimulated initial rates of LCFA uptake and TAG esterification. |
| 418 | 15220187 | In contrast, in myocytes from obese rats, insulin failed to alter the subcellular localization of FAT/CD36 and the rates of LCFA uptake and TAG esterification. |
| 419 | 15221799 | A CD36 nonsense mutation associated with insulin resistance and familial type 2 diabetes. |
| 420 | 15221799 | Mutations in CD36 / fatty acid translocase (FAT) gene are responsible for insulin resistance in the rat but contribution to human Type 2 diabetes is unknown. |
| 421 | 15221799 | Adiponectin levels, as marker of insulin sensitivity, were found to be significantly lower in the p.L360X variant carriers compared to homozygous for wild type CD36. |
| 422 | 15221799 | Thus, our findings suggest a possible role for CD36 in the pathogenesis of T2D associated with reduced insulin sensitivity. |
| 423 | 15221799 | A CD36 nonsense mutation associated with insulin resistance and familial type 2 diabetes. |
| 424 | 15221799 | Mutations in CD36 / fatty acid translocase (FAT) gene are responsible for insulin resistance in the rat but contribution to human Type 2 diabetes is unknown. |
| 425 | 15221799 | Adiponectin levels, as marker of insulin sensitivity, were found to be significantly lower in the p.L360X variant carriers compared to homozygous for wild type CD36. |
| 426 | 15221799 | Thus, our findings suggest a possible role for CD36 in the pathogenesis of T2D associated with reduced insulin sensitivity. |
| 427 | 15221799 | A CD36 nonsense mutation associated with insulin resistance and familial type 2 diabetes. |
| 428 | 15221799 | Mutations in CD36 / fatty acid translocase (FAT) gene are responsible for insulin resistance in the rat but contribution to human Type 2 diabetes is unknown. |
| 429 | 15221799 | Adiponectin levels, as marker of insulin sensitivity, were found to be significantly lower in the p.L360X variant carriers compared to homozygous for wild type CD36. |
| 430 | 15221799 | Thus, our findings suggest a possible role for CD36 in the pathogenesis of T2D associated with reduced insulin sensitivity. |
| 431 | 15221799 | A CD36 nonsense mutation associated with insulin resistance and familial type 2 diabetes. |
| 432 | 15221799 | Mutations in CD36 / fatty acid translocase (FAT) gene are responsible for insulin resistance in the rat but contribution to human Type 2 diabetes is unknown. |
| 433 | 15221799 | Adiponectin levels, as marker of insulin sensitivity, were found to be significantly lower in the p.L360X variant carriers compared to homozygous for wild type CD36. |
| 434 | 15221799 | Thus, our findings suggest a possible role for CD36 in the pathogenesis of T2D associated with reduced insulin sensitivity. |
| 435 | 15231693 | Muscle-specific overexpression of CD36 reverses the insulin resistance and diabetes of MKR mice. |
| 436 | 15231693 | The double-transgenic MKR/CD36 mice showed normalization of the hyperglycemia and the hyperinsulinemia as well as a marked improvement in liver insulin sensitivity. |
| 437 | 15231693 | Muscle-specific overexpression of CD36 reverses the insulin resistance and diabetes of MKR mice. |
| 438 | 15231693 | The double-transgenic MKR/CD36 mice showed normalization of the hyperglycemia and the hyperinsulinemia as well as a marked improvement in liver insulin sensitivity. |
| 439 | 15237193 | In this study, we investigated the influence of collagen type I coating on the cytotoxic effect of glyoxal on rat calvarial osteoblastic cells and on human osteosarcoma cells (Saos-2) grown on titanium alloy, Ti6Al4V. |
| 440 | 15237193 | The present findings demonstrate that osteoblasts treated with glyoxal undergo apoptosis, whereas collagen type I coating of titanium alloys (used for implants) has an antiapoptotic function. |
| 441 | 15237193 | In this study, we investigated the influence of collagen type I coating on the cytotoxic effect of glyoxal on rat calvarial osteoblastic cells and on human osteosarcoma cells (Saos-2) grown on titanium alloy, Ti6Al4V. |
| 442 | 15237193 | The present findings demonstrate that osteoblasts treated with glyoxal undergo apoptosis, whereas collagen type I coating of titanium alloys (used for implants) has an antiapoptotic function. |
| 443 | 15242332 | Extracellular-exposed caveolae-specific proteins CD36 and copper-containing amine oxidase were concealed inside the vesicles and resisted trypsin treatment. |
| 444 | 15277394 | Surface expression of collagen receptor Fc receptor-gamma/glycoprotein VI is enhanced on platelets in type 2 diabetes and mediates release of CD40 ligand and activation of endothelial cells. |
| 445 | 15277394 | In this study, the platelet collagen receptor glycoprotein VI (GPVI) was studied in 385 patients with type 2 diabetes. |
| 446 | 15277394 | Surface expression of the platelet Fc receptor that forms a functional complex with GPVI was significantly increased in patients with diabetes compared with those without diabetes (P = 0.02). |
| 447 | 15277394 | Fc receptor expression correlated with GPVI expression and was found to be independently associated with diabetes (r = 0.529, P < 0.001). |
| 448 | 15277394 | Stimulation of GPVI through a specific anti-GPVI monoclonal antibody significantly enhanced surface expression of CD40L (P = 0.006). |
| 449 | 15277394 | Because CD40L is a potent platelet-derived cytokine that is involved in thrombosis and atherosclerosis, we evaluated the effect of GPVI-mediated release of CD40L on activation of endothelial cells. |
| 450 | 15277394 | Coincubation of GPVI-stimulated platelets resulted in substantial enhanced endothelial surface expression of CD62P, alphavbeta3, and intercellular adhesion molecule 1 (P < 0.05) and secretion of monocyte chemoattractant protein 1 of cultured human umbilical vein endothelial cells (P < 0.01). |
| 451 | 15277394 | These results suggest that the function of collagen receptor GPVI is altered in type 2 diabetes and may play an important role in atherothrombotic complications. |
| 452 | 15284298 | These abnormalities were associated with increased expression of collagen type I and type IV and transforming growth factor-beta1 (TGF-beta1), increased alpha-smooth muscle actin immunostaining and macrophage infiltration, and increased serum and renal AGE. |
| 453 | 15284298 | The two treatments, which attenuated renal AGE accumulation in a disparate manner, were associated with less albuminuria, structural injury, macrophage infiltration, TGF-beta1, and collagen expression. |
| 454 | 15294038 | By repressing FAT/CD36 expression, and thereby lowering the plasmalemmal FAT/CD36 (i.e. leptin-treated animals), the rate of FA transport is reduced. |
| 455 | 15294038 | This increase is a result of the contraction- and insulin-induced translocation of FAT/CD36 from an intracellular depot to the cell surface. |
| 456 | 15294038 | Neither PPAR alpha nor PPAR gamma activation alter FAT/CD36 expression in muscle, despite the fact that PPAR alpha activation increases FAT/CD36 by 80% in liver. |
| 457 | 15294038 | By repressing FAT/CD36 expression, and thereby lowering the plasmalemmal FAT/CD36 (i.e. leptin-treated animals), the rate of FA transport is reduced. |
| 458 | 15294038 | This increase is a result of the contraction- and insulin-induced translocation of FAT/CD36 from an intracellular depot to the cell surface. |
| 459 | 15294038 | Neither PPAR alpha nor PPAR gamma activation alter FAT/CD36 expression in muscle, despite the fact that PPAR alpha activation increases FAT/CD36 by 80% in liver. |
| 460 | 15294038 | By repressing FAT/CD36 expression, and thereby lowering the plasmalemmal FAT/CD36 (i.e. leptin-treated animals), the rate of FA transport is reduced. |
| 461 | 15294038 | This increase is a result of the contraction- and insulin-induced translocation of FAT/CD36 from an intracellular depot to the cell surface. |
| 462 | 15294038 | Neither PPAR alpha nor PPAR gamma activation alter FAT/CD36 expression in muscle, despite the fact that PPAR alpha activation increases FAT/CD36 by 80% in liver. |
| 463 | 15331529 | CD36 in myocytes channels fatty acids to a lipase-accessible triglyceride pool that is related to cell lipid and insulin responsiveness. |
| 464 | 15331529 | We examined whether high CD36 levels would increase lipid content and susceptibility of myocytes to fatty acid-induced insulin resistance. |
| 465 | 15331529 | When +CD36 myotubes were incubated with excess palmitate, CD36 enhancement of glycerol release was blunted, triglyceride content increased above wild-type cells, and insulin resistance of glucose metabolism was observed. |
| 466 | 15331529 | In contrast to palmitate, oleate-treated +CD36 cells exhibited enhanced glycerol release and no alteration in triglyceride content or insulin responsiveness. |
| 467 | 15331529 | Furthermore, increased expression of hormone-sensitive lipase was measured with CD36 expression and with oleate treatment. |
| 468 | 15331529 | CD36 in myocytes channels fatty acids to a lipase-accessible triglyceride pool that is related to cell lipid and insulin responsiveness. |
| 469 | 15331529 | We examined whether high CD36 levels would increase lipid content and susceptibility of myocytes to fatty acid-induced insulin resistance. |
| 470 | 15331529 | When +CD36 myotubes were incubated with excess palmitate, CD36 enhancement of glycerol release was blunted, triglyceride content increased above wild-type cells, and insulin resistance of glucose metabolism was observed. |
| 471 | 15331529 | In contrast to palmitate, oleate-treated +CD36 cells exhibited enhanced glycerol release and no alteration in triglyceride content or insulin responsiveness. |
| 472 | 15331529 | Furthermore, increased expression of hormone-sensitive lipase was measured with CD36 expression and with oleate treatment. |
| 473 | 15331529 | CD36 in myocytes channels fatty acids to a lipase-accessible triglyceride pool that is related to cell lipid and insulin responsiveness. |
| 474 | 15331529 | We examined whether high CD36 levels would increase lipid content and susceptibility of myocytes to fatty acid-induced insulin resistance. |
| 475 | 15331529 | When +CD36 myotubes were incubated with excess palmitate, CD36 enhancement of glycerol release was blunted, triglyceride content increased above wild-type cells, and insulin resistance of glucose metabolism was observed. |
| 476 | 15331529 | In contrast to palmitate, oleate-treated +CD36 cells exhibited enhanced glycerol release and no alteration in triglyceride content or insulin responsiveness. |
| 477 | 15331529 | Furthermore, increased expression of hormone-sensitive lipase was measured with CD36 expression and with oleate treatment. |
| 478 | 15331529 | CD36 in myocytes channels fatty acids to a lipase-accessible triglyceride pool that is related to cell lipid and insulin responsiveness. |
| 479 | 15331529 | We examined whether high CD36 levels would increase lipid content and susceptibility of myocytes to fatty acid-induced insulin resistance. |
| 480 | 15331529 | When +CD36 myotubes were incubated with excess palmitate, CD36 enhancement of glycerol release was blunted, triglyceride content increased above wild-type cells, and insulin resistance of glucose metabolism was observed. |
| 481 | 15331529 | In contrast to palmitate, oleate-treated +CD36 cells exhibited enhanced glycerol release and no alteration in triglyceride content or insulin responsiveness. |
| 482 | 15331529 | Furthermore, increased expression of hormone-sensitive lipase was measured with CD36 expression and with oleate treatment. |
| 483 | 15331529 | CD36 in myocytes channels fatty acids to a lipase-accessible triglyceride pool that is related to cell lipid and insulin responsiveness. |
| 484 | 15331529 | We examined whether high CD36 levels would increase lipid content and susceptibility of myocytes to fatty acid-induced insulin resistance. |
| 485 | 15331529 | When +CD36 myotubes were incubated with excess palmitate, CD36 enhancement of glycerol release was blunted, triglyceride content increased above wild-type cells, and insulin resistance of glucose metabolism was observed. |
| 486 | 15331529 | In contrast to palmitate, oleate-treated +CD36 cells exhibited enhanced glycerol release and no alteration in triglyceride content or insulin responsiveness. |
| 487 | 15331529 | Furthermore, increased expression of hormone-sensitive lipase was measured with CD36 expression and with oleate treatment. |
| 488 | 15492479 | A mutation of the CD36 gene that encodes a fatty acid transporter has been reported to play a role in insulin resistance in spontaneously hypertensive rat (SHR). |
| 489 | 15492479 | The objective of this study was to determine the role of CD36 and the significance of statin therapy in insulin-resistance syndromes. |
| 490 | 15492479 | We determined the isometric relaxation induced by acetylcholine or lecithinized superoxide dismutase (SOD) in aortas obtained from Otsuka Long Evans Tokushima Fatty (OLETF) rats, a model of insulin resistance and dyslipidemia, and normal control (Long Evans Tokushima Otsuka; LETO) rats with or without cerivastatin treatment. |
| 491 | 15492479 | We also determined the effect of cerivastatin on aortic expression of CD36 and PPARgamma. |
| 492 | 15492479 | Cerivastatin increased the aortic expression of CD36 and PPARgamma mRNA in both LETO and OLETF rats. |
| 493 | 15492479 | In conclusion, insulin resistance in OLETF rats may be partially due to an altered expression of CD36. |
| 494 | 15492479 | Increased aortic expression of CD36 in response to cerivastatin could explain the reduction in serum triglyceride concentrations with statin therapy and may have pronounced beneficial effects in insulin-resistance syndromes. |
| 495 | 15492479 | A mutation of the CD36 gene that encodes a fatty acid transporter has been reported to play a role in insulin resistance in spontaneously hypertensive rat (SHR). |
| 496 | 15492479 | The objective of this study was to determine the role of CD36 and the significance of statin therapy in insulin-resistance syndromes. |
| 497 | 15492479 | We determined the isometric relaxation induced by acetylcholine or lecithinized superoxide dismutase (SOD) in aortas obtained from Otsuka Long Evans Tokushima Fatty (OLETF) rats, a model of insulin resistance and dyslipidemia, and normal control (Long Evans Tokushima Otsuka; LETO) rats with or without cerivastatin treatment. |
| 498 | 15492479 | We also determined the effect of cerivastatin on aortic expression of CD36 and PPARgamma. |
| 499 | 15492479 | Cerivastatin increased the aortic expression of CD36 and PPARgamma mRNA in both LETO and OLETF rats. |
| 500 | 15492479 | In conclusion, insulin resistance in OLETF rats may be partially due to an altered expression of CD36. |
| 501 | 15492479 | Increased aortic expression of CD36 in response to cerivastatin could explain the reduction in serum triglyceride concentrations with statin therapy and may have pronounced beneficial effects in insulin-resistance syndromes. |
| 502 | 15492479 | A mutation of the CD36 gene that encodes a fatty acid transporter has been reported to play a role in insulin resistance in spontaneously hypertensive rat (SHR). |
| 503 | 15492479 | The objective of this study was to determine the role of CD36 and the significance of statin therapy in insulin-resistance syndromes. |
| 504 | 15492479 | We determined the isometric relaxation induced by acetylcholine or lecithinized superoxide dismutase (SOD) in aortas obtained from Otsuka Long Evans Tokushima Fatty (OLETF) rats, a model of insulin resistance and dyslipidemia, and normal control (Long Evans Tokushima Otsuka; LETO) rats with or without cerivastatin treatment. |
| 505 | 15492479 | We also determined the effect of cerivastatin on aortic expression of CD36 and PPARgamma. |
| 506 | 15492479 | Cerivastatin increased the aortic expression of CD36 and PPARgamma mRNA in both LETO and OLETF rats. |
| 507 | 15492479 | In conclusion, insulin resistance in OLETF rats may be partially due to an altered expression of CD36. |
| 508 | 15492479 | Increased aortic expression of CD36 in response to cerivastatin could explain the reduction in serum triglyceride concentrations with statin therapy and may have pronounced beneficial effects in insulin-resistance syndromes. |
| 509 | 15492479 | A mutation of the CD36 gene that encodes a fatty acid transporter has been reported to play a role in insulin resistance in spontaneously hypertensive rat (SHR). |
| 510 | 15492479 | The objective of this study was to determine the role of CD36 and the significance of statin therapy in insulin-resistance syndromes. |
| 511 | 15492479 | We determined the isometric relaxation induced by acetylcholine or lecithinized superoxide dismutase (SOD) in aortas obtained from Otsuka Long Evans Tokushima Fatty (OLETF) rats, a model of insulin resistance and dyslipidemia, and normal control (Long Evans Tokushima Otsuka; LETO) rats with or without cerivastatin treatment. |
| 512 | 15492479 | We also determined the effect of cerivastatin on aortic expression of CD36 and PPARgamma. |
| 513 | 15492479 | Cerivastatin increased the aortic expression of CD36 and PPARgamma mRNA in both LETO and OLETF rats. |
| 514 | 15492479 | In conclusion, insulin resistance in OLETF rats may be partially due to an altered expression of CD36. |
| 515 | 15492479 | Increased aortic expression of CD36 in response to cerivastatin could explain the reduction in serum triglyceride concentrations with statin therapy and may have pronounced beneficial effects in insulin-resistance syndromes. |
| 516 | 15492479 | A mutation of the CD36 gene that encodes a fatty acid transporter has been reported to play a role in insulin resistance in spontaneously hypertensive rat (SHR). |
| 517 | 15492479 | The objective of this study was to determine the role of CD36 and the significance of statin therapy in insulin-resistance syndromes. |
| 518 | 15492479 | We determined the isometric relaxation induced by acetylcholine or lecithinized superoxide dismutase (SOD) in aortas obtained from Otsuka Long Evans Tokushima Fatty (OLETF) rats, a model of insulin resistance and dyslipidemia, and normal control (Long Evans Tokushima Otsuka; LETO) rats with or without cerivastatin treatment. |
| 519 | 15492479 | We also determined the effect of cerivastatin on aortic expression of CD36 and PPARgamma. |
| 520 | 15492479 | Cerivastatin increased the aortic expression of CD36 and PPARgamma mRNA in both LETO and OLETF rats. |
| 521 | 15492479 | In conclusion, insulin resistance in OLETF rats may be partially due to an altered expression of CD36. |
| 522 | 15492479 | Increased aortic expression of CD36 in response to cerivastatin could explain the reduction in serum triglyceride concentrations with statin therapy and may have pronounced beneficial effects in insulin-resistance syndromes. |
| 523 | 15492479 | A mutation of the CD36 gene that encodes a fatty acid transporter has been reported to play a role in insulin resistance in spontaneously hypertensive rat (SHR). |
| 524 | 15492479 | The objective of this study was to determine the role of CD36 and the significance of statin therapy in insulin-resistance syndromes. |
| 525 | 15492479 | We determined the isometric relaxation induced by acetylcholine or lecithinized superoxide dismutase (SOD) in aortas obtained from Otsuka Long Evans Tokushima Fatty (OLETF) rats, a model of insulin resistance and dyslipidemia, and normal control (Long Evans Tokushima Otsuka; LETO) rats with or without cerivastatin treatment. |
| 526 | 15492479 | We also determined the effect of cerivastatin on aortic expression of CD36 and PPARgamma. |
| 527 | 15492479 | Cerivastatin increased the aortic expression of CD36 and PPARgamma mRNA in both LETO and OLETF rats. |
| 528 | 15492479 | In conclusion, insulin resistance in OLETF rats may be partially due to an altered expression of CD36. |
| 529 | 15492479 | Increased aortic expression of CD36 in response to cerivastatin could explain the reduction in serum triglyceride concentrations with statin therapy and may have pronounced beneficial effects in insulin-resistance syndromes. |
| 530 | 15525872 | The release of glycerol and free fatty acids from human adipose tissue is mainly dependent on hormone-sensitive lipase which is intensively regulated by hormones and agents, such as insulin (inhibition of lipolysis) and catecholamines (stimulation of lipolysis). |
| 531 | 15525872 | Released into circulation as non-esterified fatty acids by lipoprotein lipase, those are taken up by adipose tissue via specific plasma fatty acid transporters (CD36, FATP, FABPpm) and used for triacylglycerol synthesis. |
| 532 | 15530905 | Gene expression of scavenger receptor class A (SR-A), CD36 and scavenger receptor class B type I (SR-BI) was determined by quantitative reverse transcriptase PCR (RT-PCR). |
| 533 | 15530905 | Glycoxidized LDL was able to significantly induce SR-A and CD36 expression by 3- and 4.5-fold, respectively, in macrophages whereas SR-BI expression was suppressed by glycoxidized LDL, glycated LDL and oxidized LDL. |
| 534 | 15530905 | Gene expression of scavenger receptor class A (SR-A), CD36 and scavenger receptor class B type I (SR-BI) was determined by quantitative reverse transcriptase PCR (RT-PCR). |
| 535 | 15530905 | Glycoxidized LDL was able to significantly induce SR-A and CD36 expression by 3- and 4.5-fold, respectively, in macrophages whereas SR-BI expression was suppressed by glycoxidized LDL, glycated LDL and oxidized LDL. |
| 536 | 15546994 | To dissect and quantitate these two separate effects, we compared the skeletal muscle gene-expression profiles of muscle insulin receptor knockout (MIRKO) mice and their Lox controls in the basal, streptozotocin-induced diabetic, and insulin-treated diabetic states. |
| 537 | 15546994 | Pure deficiency of insulin action as present in the MIRKO mouse results in regulation of 130 genes, with down-regulation of NSF (N-ethylmaleimide-sensitive fusion protein) and VAMP-2 (vesicle-associated membrane protein 2), stearoyl CoA desaturase 1, and cAMP-specific phosphodiesterase 4B, as well as up-regulation of some signaling-related genes, such as Akt2, and the fatty-acid transporter CD36. |
| 538 | 15561953 | Glucose-oxidized LDL resulted in phosphorylation of extracellular signal-regulated kinase and protein kinase B/Akt and stimulated proliferation of isolated macrophages. |
| 539 | 15561953 | The mitogenic effect of glucose-oxidized LDL was mediated by CD36 and by extracellular signal-regulated kinase activation induced by protein kinase C-dependent and phosphatidylinositol 3-kinase-dependent pathways. |
| 540 | 15638783 | Macrophage recruitment by abnormal endothelium over developing atherosclerotic plaques, is aided by endothelial expression of adhesion molecules (ICAM-1, VCAM, ELAM). |
| 541 | 15638783 | Substantial work has clarified macrophage activation by OxLDL via macrophage scavenger receptors (MSRs), especially MSRA and CD36. |
| 542 | 15638783 | Macrophage NO is derived from the high output inducible nitric oxide synthase (iNOS) pathway and upregulates vascular smooth muscle (VSMC) cell surface Fas, priming them for apoptosis. |
| 543 | 15638783 | Existing cardiovascular treatments including angiotensin II receptor antagonists and angiotensin converting enzyme inhibitors, aspirin, cholesterol reduction agents especially statins may inhibit macrophages. |
| 544 | 15677505 | Fatty acid translocase (FAT/CD36) is localized on insulin-containing granules in human pancreatic beta-cells and mediates fatty acid effects on insulin secretion. |
| 545 | 15677505 | In line with the well-known effects of FA metabolism on carbohydrate utilization and insulin responsiveness, altered expression of CD36 has been linked to phenotypic features of the metabolic syndrome including insulin resistance and dyslipidemia. |
| 546 | 15677505 | Fluorescence resonance energy transfer analysis and subcellular protein fractionation indicated that insulin and CD36 are colocalized in the secretory granules of beta-cells. |
| 547 | 15677505 | In conclusion, our study demonstrates that human islets express CD36 in the plasma membrane as well as in the insulin secretory granules. |
| 548 | 15677505 | CD36 activity appears important for uptake of FA into beta-cells as well as for mediating their modulatory effects on insulin secretion. |
| 549 | 15677505 | Fatty acid translocase (FAT/CD36) is localized on insulin-containing granules in human pancreatic beta-cells and mediates fatty acid effects on insulin secretion. |
| 550 | 15677505 | In line with the well-known effects of FA metabolism on carbohydrate utilization and insulin responsiveness, altered expression of CD36 has been linked to phenotypic features of the metabolic syndrome including insulin resistance and dyslipidemia. |
| 551 | 15677505 | Fluorescence resonance energy transfer analysis and subcellular protein fractionation indicated that insulin and CD36 are colocalized in the secretory granules of beta-cells. |
| 552 | 15677505 | In conclusion, our study demonstrates that human islets express CD36 in the plasma membrane as well as in the insulin secretory granules. |
| 553 | 15677505 | CD36 activity appears important for uptake of FA into beta-cells as well as for mediating their modulatory effects on insulin secretion. |
| 554 | 15677505 | Fatty acid translocase (FAT/CD36) is localized on insulin-containing granules in human pancreatic beta-cells and mediates fatty acid effects on insulin secretion. |
| 555 | 15677505 | In line with the well-known effects of FA metabolism on carbohydrate utilization and insulin responsiveness, altered expression of CD36 has been linked to phenotypic features of the metabolic syndrome including insulin resistance and dyslipidemia. |
| 556 | 15677505 | Fluorescence resonance energy transfer analysis and subcellular protein fractionation indicated that insulin and CD36 are colocalized in the secretory granules of beta-cells. |
| 557 | 15677505 | In conclusion, our study demonstrates that human islets express CD36 in the plasma membrane as well as in the insulin secretory granules. |
| 558 | 15677505 | CD36 activity appears important for uptake of FA into beta-cells as well as for mediating their modulatory effects on insulin secretion. |
| 559 | 15677505 | Fatty acid translocase (FAT/CD36) is localized on insulin-containing granules in human pancreatic beta-cells and mediates fatty acid effects on insulin secretion. |
| 560 | 15677505 | In line with the well-known effects of FA metabolism on carbohydrate utilization and insulin responsiveness, altered expression of CD36 has been linked to phenotypic features of the metabolic syndrome including insulin resistance and dyslipidemia. |
| 561 | 15677505 | Fluorescence resonance energy transfer analysis and subcellular protein fractionation indicated that insulin and CD36 are colocalized in the secretory granules of beta-cells. |
| 562 | 15677505 | In conclusion, our study demonstrates that human islets express CD36 in the plasma membrane as well as in the insulin secretory granules. |
| 563 | 15677505 | CD36 activity appears important for uptake of FA into beta-cells as well as for mediating their modulatory effects on insulin secretion. |
| 564 | 15677505 | Fatty acid translocase (FAT/CD36) is localized on insulin-containing granules in human pancreatic beta-cells and mediates fatty acid effects on insulin secretion. |
| 565 | 15677505 | In line with the well-known effects of FA metabolism on carbohydrate utilization and insulin responsiveness, altered expression of CD36 has been linked to phenotypic features of the metabolic syndrome including insulin resistance and dyslipidemia. |
| 566 | 15677505 | Fluorescence resonance energy transfer analysis and subcellular protein fractionation indicated that insulin and CD36 are colocalized in the secretory granules of beta-cells. |
| 567 | 15677505 | In conclusion, our study demonstrates that human islets express CD36 in the plasma membrane as well as in the insulin secretory granules. |
| 568 | 15677505 | CD36 activity appears important for uptake of FA into beta-cells as well as for mediating their modulatory effects on insulin secretion. |
| 569 | 15709716 | The Bgl II gene polymorphism of the alpha2beta1 integrin, which is a platelet collagen receptor, and the -455G/A polymorphism in the beta fibrinogen gene have been suggested as genetic risk factors for MI. |
| 570 | 15713705 | Colectomized subjects exhibited lower insulin sensitivity (homeostatic model assessment model, 33% reduction, P = 0.03; minimal model, 29% reduction, P = 0.05), elevated aldosterone (9-fold, P = 0.003), leptin (2.2-fold, P = 0.03), and an increased rate of nonesterified fatty acid and glycerol release from adipose tissue (P = 0.02) especially in the late postprandial period. |
| 571 | 15713705 | The uptake of fatty acids into muscle was also significantly increased (P = 0.007), as were muscle CD36 and LPL mRNA expression compared with controls. |
| 572 | 15713705 | In adipose tissue, hormone-sensitive lipase mRNA expression was increased (P = 0.015), whereas peroxisome proliferator-activated receptor-gamma expression was decreased (P = 0.02), as was that of CD36 (P = 0.001). |
| 573 | 15713705 | Colectomized subjects exhibited lower insulin sensitivity (homeostatic model assessment model, 33% reduction, P = 0.03; minimal model, 29% reduction, P = 0.05), elevated aldosterone (9-fold, P = 0.003), leptin (2.2-fold, P = 0.03), and an increased rate of nonesterified fatty acid and glycerol release from adipose tissue (P = 0.02) especially in the late postprandial period. |
| 574 | 15713705 | The uptake of fatty acids into muscle was also significantly increased (P = 0.007), as were muscle CD36 and LPL mRNA expression compared with controls. |
| 575 | 15713705 | In adipose tissue, hormone-sensitive lipase mRNA expression was increased (P = 0.015), whereas peroxisome proliferator-activated receptor-gamma expression was decreased (P = 0.02), as was that of CD36 (P = 0.001). |
| 576 | 15713786 | Particularly interesting cases of common or tissue-specific regulation included decorin and CD36, which were upregulated in several tissues, and serum/glucocorticoid-regulated kinase and four and a half LIM domains 2, which were upregulated only in the renal cortex. |
| 577 | 15772429 | In adipose tissue from Rgz-treated rats, FA uptake capacity increased by 2.0-fold, coinciding with increased total contents of fatty acid translocase (FAT/CD36; 2.3-fold) and fatty acid transport protein 1 (1.7-fold) but not of plasmalemmal fatty acid binding protein, whereas only the plasmalemmal content of FAT/CD36 was changed (increase of 1.7-fold). |
| 578 | 15772429 | In conclusion, our study implicates FAT/CD36 in the mechanism by which Rgz increases tissue insulin sensitivity. |
| 579 | 15772429 | In adipose tissue from Rgz-treated rats, FA uptake capacity increased by 2.0-fold, coinciding with increased total contents of fatty acid translocase (FAT/CD36; 2.3-fold) and fatty acid transport protein 1 (1.7-fold) but not of plasmalemmal fatty acid binding protein, whereas only the plasmalemmal content of FAT/CD36 was changed (increase of 1.7-fold). |
| 580 | 15772429 | In conclusion, our study implicates FAT/CD36 in the mechanism by which Rgz increases tissue insulin sensitivity. |
| 581 | 15781223 | Numerous post-translational steps are involved in collagen type I biosynthesis, including residue hydroxylation and glycosylation catalysed by enzymes that work until the protein folds forming the triple helix; therefore, folding rate regulates these processes. |
| 582 | 15790550 | CD36 is a multiligand receptor associated with a broad array of physiological processes and involved in markedly diverse disorders, including atherosclerosis, insulin resistance and diabetes, dyslipidemia, tumor angiogenesis, and host defense against Plasmodium falciparum. |
| 583 | 15790550 | As a receptor for thrombospondin 1, CD36 plays a role in the regulation of angiogenesis, which may be a therapeutic strategy for controlling the dissemination of malignant neoplasms. |
| 584 | 15790550 | CD36 is a multiligand receptor associated with a broad array of physiological processes and involved in markedly diverse disorders, including atherosclerosis, insulin resistance and diabetes, dyslipidemia, tumor angiogenesis, and host defense against Plasmodium falciparum. |
| 585 | 15790550 | As a receptor for thrombospondin 1, CD36 plays a role in the regulation of angiogenesis, which may be a therapeutic strategy for controlling the dissemination of malignant neoplasms. |
| 586 | 15793237 | The renin-angiotensin system with its active metabolite angiotensin (Ang) II has been related not only to hypertension but also to obesity and insulin resistance. |
| 587 | 15793237 | Recent evidence obtained in vitro suggests that the type 2 Ang II receptor (AT2R) mediates the trophic action of Ang II on adipocyte differentiation and lipogenesis. |
| 588 | 15793237 | In muscle, the expression of several genes involved in lipid metabolism, including fatty acid translocase, uncoupling protein-3, peroxisome proliferator-activated receptors (alpha, delta), and carnitine palmitoyl transferase-1, was increased in AT2R-deficient mice. |
| 589 | 15793250 | Consistently, activation of LXRs induced the expression of relevant genes: fatty acid translocase (CD36/FAT), glucose transporters (GLUT1 and -4), sterol regulatory element-binding protein-1c, peroxisome proliferator-activated receptor-gamma, carnitine palmitoyltransferase-1, and uncoupling protein 2 and 3. |
| 590 | 15997096 | Retinoid X receptor (RXR) forms heterodimers with peroxisome proliferator-activated receptors (PPARs, with subtypes of alpha, delta and gamma), and the heterodimers can be activated by either an RXR or a PPAR subtype-specific ligand. |
| 591 | 15997096 | Furthermore, RT-PCR results showed that CS018 induced the expression of the PPARgamma target genes, CD36 and lipoprotein lipase (LPL). |
| 592 | 16037291 | Pathological roles of advanced glycation end product receptors SR-A and CD36. |
| 593 | 16037291 | In this study, we focused on two AGE receptors-specifically, the role of SR-A in pathogenesis of diabetic nephropathy and the role of CD36 in AGE-induced downregulation of leptin by adipocytes. |
| 594 | 16037291 | In terms of SR-A, diabetic wild-type mice exhibited increased urinary albumin excretion, glomerular hypertrophy, and mesangial matrix expansion, whereas SR-A-knockout mice showed reduced glomerular size and mesangial matrix area. |
| 595 | 16037291 | In terms of CD36, incubation of glycolaldehyde-modified bovine serum albumin (GA-BSA) with 3T3-L1 adipocytes reduced leptin secretion by these cells. |
| 596 | 16037291 | These results indicate that the interaction of AGE ligands with 3T3-L1 adipocytes via CD36 induces oxidative stress and leads to inhibition of leptin expression by these cells, suggesting a potential link of this phenomenon to exacerbation of the insulin sensitivity in metabolic syndrome. |
| 597 | 16037291 | Pathological roles of advanced glycation end product receptors SR-A and CD36. |
| 598 | 16037291 | In this study, we focused on two AGE receptors-specifically, the role of SR-A in pathogenesis of diabetic nephropathy and the role of CD36 in AGE-induced downregulation of leptin by adipocytes. |
| 599 | 16037291 | In terms of SR-A, diabetic wild-type mice exhibited increased urinary albumin excretion, glomerular hypertrophy, and mesangial matrix expansion, whereas SR-A-knockout mice showed reduced glomerular size and mesangial matrix area. |
| 600 | 16037291 | In terms of CD36, incubation of glycolaldehyde-modified bovine serum albumin (GA-BSA) with 3T3-L1 adipocytes reduced leptin secretion by these cells. |
| 601 | 16037291 | These results indicate that the interaction of AGE ligands with 3T3-L1 adipocytes via CD36 induces oxidative stress and leads to inhibition of leptin expression by these cells, suggesting a potential link of this phenomenon to exacerbation of the insulin sensitivity in metabolic syndrome. |
| 602 | 16037291 | Pathological roles of advanced glycation end product receptors SR-A and CD36. |
| 603 | 16037291 | In this study, we focused on two AGE receptors-specifically, the role of SR-A in pathogenesis of diabetic nephropathy and the role of CD36 in AGE-induced downregulation of leptin by adipocytes. |
| 604 | 16037291 | In terms of SR-A, diabetic wild-type mice exhibited increased urinary albumin excretion, glomerular hypertrophy, and mesangial matrix expansion, whereas SR-A-knockout mice showed reduced glomerular size and mesangial matrix area. |
| 605 | 16037291 | In terms of CD36, incubation of glycolaldehyde-modified bovine serum albumin (GA-BSA) with 3T3-L1 adipocytes reduced leptin secretion by these cells. |
| 606 | 16037291 | These results indicate that the interaction of AGE ligands with 3T3-L1 adipocytes via CD36 induces oxidative stress and leads to inhibition of leptin expression by these cells, suggesting a potential link of this phenomenon to exacerbation of the insulin sensitivity in metabolic syndrome. |
| 607 | 16037291 | Pathological roles of advanced glycation end product receptors SR-A and CD36. |
| 608 | 16037291 | In this study, we focused on two AGE receptors-specifically, the role of SR-A in pathogenesis of diabetic nephropathy and the role of CD36 in AGE-induced downregulation of leptin by adipocytes. |
| 609 | 16037291 | In terms of SR-A, diabetic wild-type mice exhibited increased urinary albumin excretion, glomerular hypertrophy, and mesangial matrix expansion, whereas SR-A-knockout mice showed reduced glomerular size and mesangial matrix area. |
| 610 | 16037291 | In terms of CD36, incubation of glycolaldehyde-modified bovine serum albumin (GA-BSA) with 3T3-L1 adipocytes reduced leptin secretion by these cells. |
| 611 | 16037291 | These results indicate that the interaction of AGE ligands with 3T3-L1 adipocytes via CD36 induces oxidative stress and leads to inhibition of leptin expression by these cells, suggesting a potential link of this phenomenon to exacerbation of the insulin sensitivity in metabolic syndrome. |
| 612 | 16105663 | Gastric inhibitory polypeptide modulates adiposity and fat oxidation under diminished insulin action. |
| 613 | 16105663 | Gut hormone gastric inhibitory polypeptide (GIP) stimulates insulin secretion from pancreatic beta-cells upon ingestion of nutrients. |
| 614 | 16105663 | Inhibition of GIP signaling prevents the onset of obesity and consequent insulin resistance induced by high-fat diet. |
| 615 | 16105663 | In this study, we investigated the role of GIP in accumulation of triglycerides into adipocytes and in fat oxidation peripherally using insulin receptor substrate (IRS)-1-deficient mice and revealed that IRS-1(-/-)GIPR(-/-) mice exhibited both reduced adiposity and ameliorated insulin resistance. |
| 616 | 16105663 | Furthermore, increased gene expression of CD36 and UCP2 in liver, and increased expression and enzyme activity of 3-hydroxyacyl-CoA dehydrogenase in skeletal muscle of IRS-1(-/-)GIPR(-/-) mice might contribute to the lower respiratory quotient and the higher fat oxidation in light phase. |
| 617 | 16105663 | These results suggest that GIP plays a crucial role in switching from fat oxidation to fat accumulation under the diminished insulin action as a potential target for secondary prevention of insulin resistance. |
| 618 | 16118269 | Gene Ontology (GO) classification indicated that there was a decrease in numerous extracellular matrix genes (e.g., collagen and elastin related) and an increase in oxidative stress-associated genes in the diabetic rat cavernosum. |
| 619 | 16118269 | In addition, PubMatrix literature mining identified differentially expressed genes previously shown to mediate vascular dysfunction [e.g., ceruloplasmin (Cp), lipoprotein lipase, and Cd36] as well as genes involved in the modulation of the smooth muscle phenotype (e.g., Kruppel-like factor 5 and chemokine C-X3-C motif ligand 1). |
| 620 | 16123369 | We investigated the activation state of peripheral blood monocytes in diabetes with respect to scavenger receptor (CD36) expression and monocyte chemoattractant protein-1, intracellular adhesion molecule-1, vascular cell adhesion molecule-1, and peroxisome proliferator-activated receptors mRNA expression. |
| 621 | 16123369 | Both CD68 and peroxisome proliferator-activated receptor-gamma gene expression were increased in the poorly controlled diabetic group (P < 0.05 for each), whose monocytes also displayed increased attachment to endothelial monolayers (P < 0.0005 vs. nondiabetic control subjects). |
| 622 | 16311102 | Insulin signaling and expression of GLUT-4, FAT/CD36, and triglycerides were assessed in muscle biopsies, obtained before the clamp and after 30 minutes of hyperinsulinemia. |
| 623 | 16311102 | No diet effect was found on the expression of the insulin receptor and insulin receptor substrate-1 or on phosphatidylinositol 3'-kinase activity, or on FAT/CD36 expression pattern, GLUT-4 translocation, or triglyceride distribution in either the basal or insulin-stimulated situation. |
| 624 | 16311102 | Accordingly, no changes in activation of phosphatidylinositol 3'-kinase, triglyceride distribution, FAT/CD36 expression, and GLUT-4 translocation were found in skeletal muscle biopsies. |
| 625 | 16311102 | Insulin signaling and expression of GLUT-4, FAT/CD36, and triglycerides were assessed in muscle biopsies, obtained before the clamp and after 30 minutes of hyperinsulinemia. |
| 626 | 16311102 | No diet effect was found on the expression of the insulin receptor and insulin receptor substrate-1 or on phosphatidylinositol 3'-kinase activity, or on FAT/CD36 expression pattern, GLUT-4 translocation, or triglyceride distribution in either the basal or insulin-stimulated situation. |
| 627 | 16311102 | Accordingly, no changes in activation of phosphatidylinositol 3'-kinase, triglyceride distribution, FAT/CD36 expression, and GLUT-4 translocation were found in skeletal muscle biopsies. |
| 628 | 16311102 | Insulin signaling and expression of GLUT-4, FAT/CD36, and triglycerides were assessed in muscle biopsies, obtained before the clamp and after 30 minutes of hyperinsulinemia. |
| 629 | 16311102 | No diet effect was found on the expression of the insulin receptor and insulin receptor substrate-1 or on phosphatidylinositol 3'-kinase activity, or on FAT/CD36 expression pattern, GLUT-4 translocation, or triglyceride distribution in either the basal or insulin-stimulated situation. |
| 630 | 16311102 | Accordingly, no changes in activation of phosphatidylinositol 3'-kinase, triglyceride distribution, FAT/CD36 expression, and GLUT-4 translocation were found in skeletal muscle biopsies. |
| 631 | 16443762 | Islets that had been cultured for 24 h on collagen type I showed an islet survival of 59.7 +/- 8.7%, while islets that had been cultured on collagen type IV and laminin showed an islet survival of 88.6 +/- 10.3 and 94.3 +/- 5.6%, respectively. |
| 632 | 16443762 | When detached from their natural ECM surrounding in the pancreas, islet cells undergo apoptosis, unless islets are cultured on collagen IV or laminin or treated with anti-beta1 integrin antibodies or RGD peptides to mimic ECM ligation. |
| 633 | 16517147 | A recent report demonstrates that Cd36 deficiency underlies insulin resistance, defective fatty acid metabolism and hypertriglyceridemia in spontaneously hypertensive rats (SHRs). |
| 634 | 16517147 | Cd36 is a tightly regulated protein whose expression is modulated through peroxisome proliferator-activated receptor (PPAR) transcription factors, by conditions that alter lipid metabolism such as diabetes mellitus and high-fat feeding. |
| 635 | 16517147 | After 6 weeks of fish oil (FO) administration, this group of SHRs (FO-SHR) presented increased levels of Cd36 mRNA, concomitantly with decreased insulin, free fatty acids (FFAs), triglycerides, cholesterol, LDL, HDL, total lipids and blood pressure, in comparison to control rats that received a corn-canola oil diet. |
| 636 | 16517147 | A recent report demonstrates that Cd36 deficiency underlies insulin resistance, defective fatty acid metabolism and hypertriglyceridemia in spontaneously hypertensive rats (SHRs). |
| 637 | 16517147 | Cd36 is a tightly regulated protein whose expression is modulated through peroxisome proliferator-activated receptor (PPAR) transcription factors, by conditions that alter lipid metabolism such as diabetes mellitus and high-fat feeding. |
| 638 | 16517147 | After 6 weeks of fish oil (FO) administration, this group of SHRs (FO-SHR) presented increased levels of Cd36 mRNA, concomitantly with decreased insulin, free fatty acids (FFAs), triglycerides, cholesterol, LDL, HDL, total lipids and blood pressure, in comparison to control rats that received a corn-canola oil diet. |
| 639 | 16517147 | A recent report demonstrates that Cd36 deficiency underlies insulin resistance, defective fatty acid metabolism and hypertriglyceridemia in spontaneously hypertensive rats (SHRs). |
| 640 | 16517147 | Cd36 is a tightly regulated protein whose expression is modulated through peroxisome proliferator-activated receptor (PPAR) transcription factors, by conditions that alter lipid metabolism such as diabetes mellitus and high-fat feeding. |
| 641 | 16517147 | After 6 weeks of fish oil (FO) administration, this group of SHRs (FO-SHR) presented increased levels of Cd36 mRNA, concomitantly with decreased insulin, free fatty acids (FFAs), triglycerides, cholesterol, LDL, HDL, total lipids and blood pressure, in comparison to control rats that received a corn-canola oil diet. |
| 642 | 16552395 | [The influence of diabetes mellitus and insulin resistance on receptor CD36 expression. |
| 643 | 16552395 | Additionally, increased CD36 expression has been described in diabetes mellitus and insulin resistance and in the pathogenesis of diabetic macro- and microangiopathy. |
| 644 | 16552395 | [The influence of diabetes mellitus and insulin resistance on receptor CD36 expression. |
| 645 | 16552395 | Additionally, increased CD36 expression has been described in diabetes mellitus and insulin resistance and in the pathogenesis of diabetic macro- and microangiopathy. |
| 646 | 16631114 | We measured serum levels of monocyte chemoattractant protein (MCP)-1, fasting plasma glucose (FPG), HbA1c, total cholesterol, triglyceride, body mass index (BMI), high sensitivity CRP (hs-CRP) and evaluated CCR2, CD36, CD68 expression on the surface of monocytes. |
| 647 | 16631114 | The expression levels of CCR2, CD36, and CD68 on monocytes were significantly increased in diabetic patients and were more upregulated by MCP-1 stimulation. |
| 648 | 16631114 | Our data suggest that elevated serum MCP-1 levels and increased monocyte CCR2, CD36, CD68 expression correlate with poor blood glucose control and potentially contribute to increased recruitment of monocytes to the vessel wall in diabetes mellitus. |
| 649 | 16631114 | We measured serum levels of monocyte chemoattractant protein (MCP)-1, fasting plasma glucose (FPG), HbA1c, total cholesterol, triglyceride, body mass index (BMI), high sensitivity CRP (hs-CRP) and evaluated CCR2, CD36, CD68 expression on the surface of monocytes. |
| 650 | 16631114 | The expression levels of CCR2, CD36, and CD68 on monocytes were significantly increased in diabetic patients and were more upregulated by MCP-1 stimulation. |
| 651 | 16631114 | Our data suggest that elevated serum MCP-1 levels and increased monocyte CCR2, CD36, CD68 expression correlate with poor blood glucose control and potentially contribute to increased recruitment of monocytes to the vessel wall in diabetes mellitus. |
| 652 | 16631114 | We measured serum levels of monocyte chemoattractant protein (MCP)-1, fasting plasma glucose (FPG), HbA1c, total cholesterol, triglyceride, body mass index (BMI), high sensitivity CRP (hs-CRP) and evaluated CCR2, CD36, CD68 expression on the surface of monocytes. |
| 653 | 16631114 | The expression levels of CCR2, CD36, and CD68 on monocytes were significantly increased in diabetic patients and were more upregulated by MCP-1 stimulation. |
| 654 | 16631114 | Our data suggest that elevated serum MCP-1 levels and increased monocyte CCR2, CD36, CD68 expression correlate with poor blood glucose control and potentially contribute to increased recruitment of monocytes to the vessel wall in diabetes mellitus. |
| 655 | 16648883 | This process appears to be tightly controlled by AGE clearance receptor complexes containing AGE-R1, AGE-R2 and AGE-R3 and scavenger receptors such as CD36, SR-AII and SR-BI. |
| 656 | 16684853 | Therefore, we examined in Zucker diabetic fatty (ZDF) rats, relative to lean rats, 1) whether rates of fatty acid transport and transporters (FAT/CD36 and FABPpm) were upregulated in skeletal muscle during the transition from insulin resistance (week 6) to type 2 diabetes (weeks 12 and 24), 2) whether such changes occurred primarily in red skeletal muscle, and 3) whether changes in FAT/CD36 and GLUT4 were correlated. |
| 657 | 16684853 | In red muscle only, there was an inverse relationship between FAT/CD36 and GLUT4 protein expression as well as their plasmalemmal content. |
| 658 | 16684853 | Therefore, we examined in Zucker diabetic fatty (ZDF) rats, relative to lean rats, 1) whether rates of fatty acid transport and transporters (FAT/CD36 and FABPpm) were upregulated in skeletal muscle during the transition from insulin resistance (week 6) to type 2 diabetes (weeks 12 and 24), 2) whether such changes occurred primarily in red skeletal muscle, and 3) whether changes in FAT/CD36 and GLUT4 were correlated. |
| 659 | 16684853 | In red muscle only, there was an inverse relationship between FAT/CD36 and GLUT4 protein expression as well as their plasmalemmal content. |
| 660 | 16778384 | We also examined the inhibitory effect of TGF-beta1 siRNAs on the expression of plasminogen activator inhibitor (PAI)-1 and Collagen Type I which are down-regulators of TGF-beta1. |
| 661 | 16778384 | The expression of TGF-beta1, PAI-1 and Collagen Type I was increased in RMCs that were stimulated by 30 mM glucose. |
| 662 | 16778384 | TGF-beta1 siRNAs reduces high glucose-induced TGF-beta1, PAI-1, and Collagen Type I mRNA and protein expression in a dose-dependent manner. |
| 663 | 16778384 | We also examined the inhibitory effect of TGF-beta1 siRNAs on the expression of plasminogen activator inhibitor (PAI)-1 and Collagen Type I which are down-regulators of TGF-beta1. |
| 664 | 16778384 | The expression of TGF-beta1, PAI-1 and Collagen Type I was increased in RMCs that were stimulated by 30 mM glucose. |
| 665 | 16778384 | TGF-beta1 siRNAs reduces high glucose-induced TGF-beta1, PAI-1, and Collagen Type I mRNA and protein expression in a dose-dependent manner. |
| 666 | 16778384 | We also examined the inhibitory effect of TGF-beta1 siRNAs on the expression of plasminogen activator inhibitor (PAI)-1 and Collagen Type I which are down-regulators of TGF-beta1. |
| 667 | 16778384 | The expression of TGF-beta1, PAI-1 and Collagen Type I was increased in RMCs that were stimulated by 30 mM glucose. |
| 668 | 16778384 | TGF-beta1 siRNAs reduces high glucose-induced TGF-beta1, PAI-1, and Collagen Type I mRNA and protein expression in a dose-dependent manner. |
| 669 | 16803864 | Here, we report that SHP(-/-) mice exhibited hypoinsulinemia with age, which was associated with increased peripheral insulin sensitivity and increased response of isolated islets to glucose stimulation, yet maintain normal levels of blood glucose. |
| 670 | 16803864 | Deficiency in SHP function resulted in up-regulation of glucose transporter 4 mRNA and glucose uptake in muscles, and overexpression of SHP in C2C12 cells inhibited both basal and peroxisomal proliferator-activated receptor gamma (PPARgamma) coactivator-1alpha-stimulated glucose transporter 4 expression and glucose uptake. |
| 671 | 16803864 | SHP(-/-) hepatocytes showed markedly decreased basal glucose production in cultures, and SHP(-/-) livers had increased glycogen stores and were more sensitive to insulin inhibition of glucose output, which were concomitant with decreased expression for PPARgamma1, fatty acid translocase, glucose-6-phosphatase, and phosphoenol/pyruvate carboxykinase, and increased mRNAs for glucokinase and pyruvate kinase. |
| 672 | 16803864 | In white fat, SHP deficiency resulted in up-regulation of genes involved in insulin sensitizing, including PPARgamma2 and adiponectin. |
| 673 | 16803864 | We show that, at the transcriptional level, SHP directly represses adiponectin promoter activity by PPARgamma/liver receptor homolog-1. |
| 674 | 16803864 | The results suggest that the increases in insulin sensitivity through multiple signaling pathways in muscle, liver, and fat, with an increase in islet secretory function, represent the complex mechanism whereby SHP deficiency leads to improvement in insulin sensitivity, secretion, and diabetes. |
| 675 | 16838191 | Defects in FAT/CD36 have been linked to the hypertriglyceridemia and insulin resistance. |
| 676 | 16838191 | Expression of FAT/CD36 was reported increase in type 1 diabetes; however, it remains unclear whether serum glucose or insulin plays an important role in this regulation. |
| 677 | 16838191 | To elucidate the individual contribution of plasma glucose and insulin in the regulation of FAT/CD36 mRNA expression, we induced type 1 diabetes in male Sprague-Dawley rats using streptozotocin (STZ) and compared traditional insulin treatment with administration of the orally absorbed chemical agent vanadate, which reduces blood glucose levels via mechanisms that bypass insulin receptor action. |
| 678 | 16838191 | Insulin treatment also corrected increased FAT/CD36 mRNA expression at diabetic rats. |
| 679 | 16838191 | Vanadate significantly reduced serum glucose levels without increasing serum insulin or affecting body weight but reversed increased FAT/CD36 mRNA expression in diabetic rats. |
| 680 | 16838191 | Defects in FAT/CD36 have been linked to the hypertriglyceridemia and insulin resistance. |
| 681 | 16838191 | Expression of FAT/CD36 was reported increase in type 1 diabetes; however, it remains unclear whether serum glucose or insulin plays an important role in this regulation. |
| 682 | 16838191 | To elucidate the individual contribution of plasma glucose and insulin in the regulation of FAT/CD36 mRNA expression, we induced type 1 diabetes in male Sprague-Dawley rats using streptozotocin (STZ) and compared traditional insulin treatment with administration of the orally absorbed chemical agent vanadate, which reduces blood glucose levels via mechanisms that bypass insulin receptor action. |
| 683 | 16838191 | Insulin treatment also corrected increased FAT/CD36 mRNA expression at diabetic rats. |
| 684 | 16838191 | Vanadate significantly reduced serum glucose levels without increasing serum insulin or affecting body weight but reversed increased FAT/CD36 mRNA expression in diabetic rats. |
| 685 | 16838191 | Defects in FAT/CD36 have been linked to the hypertriglyceridemia and insulin resistance. |
| 686 | 16838191 | Expression of FAT/CD36 was reported increase in type 1 diabetes; however, it remains unclear whether serum glucose or insulin plays an important role in this regulation. |
| 687 | 16838191 | To elucidate the individual contribution of plasma glucose and insulin in the regulation of FAT/CD36 mRNA expression, we induced type 1 diabetes in male Sprague-Dawley rats using streptozotocin (STZ) and compared traditional insulin treatment with administration of the orally absorbed chemical agent vanadate, which reduces blood glucose levels via mechanisms that bypass insulin receptor action. |
| 688 | 16838191 | Insulin treatment also corrected increased FAT/CD36 mRNA expression at diabetic rats. |
| 689 | 16838191 | Vanadate significantly reduced serum glucose levels without increasing serum insulin or affecting body weight but reversed increased FAT/CD36 mRNA expression in diabetic rats. |
| 690 | 16838191 | Defects in FAT/CD36 have been linked to the hypertriglyceridemia and insulin resistance. |
| 691 | 16838191 | Expression of FAT/CD36 was reported increase in type 1 diabetes; however, it remains unclear whether serum glucose or insulin plays an important role in this regulation. |
| 692 | 16838191 | To elucidate the individual contribution of plasma glucose and insulin in the regulation of FAT/CD36 mRNA expression, we induced type 1 diabetes in male Sprague-Dawley rats using streptozotocin (STZ) and compared traditional insulin treatment with administration of the orally absorbed chemical agent vanadate, which reduces blood glucose levels via mechanisms that bypass insulin receptor action. |
| 693 | 16838191 | Insulin treatment also corrected increased FAT/CD36 mRNA expression at diabetic rats. |
| 694 | 16838191 | Vanadate significantly reduced serum glucose levels without increasing serum insulin or affecting body weight but reversed increased FAT/CD36 mRNA expression in diabetic rats. |
| 695 | 16838191 | Defects in FAT/CD36 have been linked to the hypertriglyceridemia and insulin resistance. |
| 696 | 16838191 | Expression of FAT/CD36 was reported increase in type 1 diabetes; however, it remains unclear whether serum glucose or insulin plays an important role in this regulation. |
| 697 | 16838191 | To elucidate the individual contribution of plasma glucose and insulin in the regulation of FAT/CD36 mRNA expression, we induced type 1 diabetes in male Sprague-Dawley rats using streptozotocin (STZ) and compared traditional insulin treatment with administration of the orally absorbed chemical agent vanadate, which reduces blood glucose levels via mechanisms that bypass insulin receptor action. |
| 698 | 16838191 | Insulin treatment also corrected increased FAT/CD36 mRNA expression at diabetic rats. |
| 699 | 16838191 | Vanadate significantly reduced serum glucose levels without increasing serum insulin or affecting body weight but reversed increased FAT/CD36 mRNA expression in diabetic rats. |
| 700 | 16870193 | THP-1 MDM incubated with oleic acid (OA) and a BODIPY-conjugated NEFA, accumulate, respectively, intracellular inclusions that are positive for oil red O and BODIPY-labeling. |
| 701 | 16870193 | Parallel studies with [(14)C]OA show dose-dependent accumulation of intracellular (14)C-labeled neutral lipid, almost exclusively as triglyceride; the rate of [(3)H]OA uptake increases as THP-1 MDM convert to foam cells. |
| 702 | 16870193 | Preincubation of THP-1 MDM with higher concentrations of OA (1.8mM versus 0.2mM) was associated with enhanced uptake of Ac-LDL, and increased expression of adipocyte fatty acid binding protein, FAT/CD36, and cyclooxygenase-2 (COX-2); COX-2 mass and activity also increased. |
| 703 | 16929141 | Leptin is primarily metabolized in the kidney, presumably by binding to megalin, a multiligand receptor in the proximal tubule, tubular uptake and endocytosis. |
| 704 | 16929141 | In contrast, leptin did not influence TGF-beta1 production in mesangial cells, but the peptide stimulates glucose transport in these cells, increased collagen type I synthesis, and lead to an upregulation of surface TGF-beta type II receptors through signal transduction pathways involving phosphatidylinositol-3-kinase. |
| 705 | 16929141 | In addition, transgenic mice with leptin overexpression demonstrated a increase in collagen type IV and fibronectin mRNA in the kidney. |
| 706 | 16952981 | Identification of the oxidized low-density lipoprotein scavenger receptor CD36 in plasma: a novel marker of insulin resistance. |
| 707 | 16988889 | The cellular uptake of both LCFA and glucose is regulated by the sarcolemmal amount of specific transport proteins, i.e., fatty acid translocase (FAT)/CD36 and GLUT4, respectively. |
| 708 | 16988889 | Both an increased workload and the hormone insulin induce translocation of FAT/CD36 and GLUT4 to the sarcolemma. |
| 709 | 16988889 | In the early stages of T2DM, relocation of FAT/CD36 to the sarcolemma is associated with the myocardial accumulation of triacylglycerols (TAGs) eventually leading to an impaired insulin-stimulated GLUT4-translocation. |
| 710 | 16988889 | The cellular uptake of both LCFA and glucose is regulated by the sarcolemmal amount of specific transport proteins, i.e., fatty acid translocase (FAT)/CD36 and GLUT4, respectively. |
| 711 | 16988889 | Both an increased workload and the hormone insulin induce translocation of FAT/CD36 and GLUT4 to the sarcolemma. |
| 712 | 16988889 | In the early stages of T2DM, relocation of FAT/CD36 to the sarcolemma is associated with the myocardial accumulation of triacylglycerols (TAGs) eventually leading to an impaired insulin-stimulated GLUT4-translocation. |
| 713 | 16988889 | The cellular uptake of both LCFA and glucose is regulated by the sarcolemmal amount of specific transport proteins, i.e., fatty acid translocase (FAT)/CD36 and GLUT4, respectively. |
| 714 | 16988889 | Both an increased workload and the hormone insulin induce translocation of FAT/CD36 and GLUT4 to the sarcolemma. |
| 715 | 16988889 | In the early stages of T2DM, relocation of FAT/CD36 to the sarcolemma is associated with the myocardial accumulation of triacylglycerols (TAGs) eventually leading to an impaired insulin-stimulated GLUT4-translocation. |
| 716 | 17127041 | Modulation of CD36 protein expression by AGEs and insulin in aortic VSMCs from diabetic and non-diabetic rats. |
| 717 | 17166616 | The total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C), and the mRNAs expression of monocyte chemoattractant protein (MCP)-1, intercellular adhesion molecule (ICAM)-1 and CD36 mRNA in aorta were determined. |
| 718 | 17166616 | The results demonstrated that DBT could regulate blood lipid, inhibit the genes expression of MCP-1, ICAM-1 and CD36 in aorta. |
| 719 | 17166616 | The total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C), and the mRNAs expression of monocyte chemoattractant protein (MCP)-1, intercellular adhesion molecule (ICAM)-1 and CD36 mRNA in aorta were determined. |
| 720 | 17166616 | The results demonstrated that DBT could regulate blood lipid, inhibit the genes expression of MCP-1, ICAM-1 and CD36 in aorta. |
| 721 | 17186996 | The findings suggest that in this case the CD36 deficiency type 1 was the pathogenic mechanism of acute coronary syndrome relative to insulin resistance and modification of the lipid profile. |
| 722 | 17258748 | Mouse peritoneal macrophages (MPMs) isolated from Balb-C streptozotocin-induced diabetic mice, exhibited significantly higher total peroxides, lipid peroxides and paraoxonase 2 (PON2) activity by 290%, 61% and 55%, respectively, compared to non-diabetic mice. |
| 723 | 17258748 | In vitro studies revealed that glucose-induced oxidative stress was obtained by D-glucose, but not by L-glucose and it involved activation of the NADPH oxidase complex, and up-regulation of the macrophage PON2. |
| 724 | 17258748 | These effects on cellular cholesterol metabolism were associated with up-regulation of the scavenger receptors for Ox-LDL (CD-36 and SR-A), and of HMG-CoA reductase (cholesterol biosynthesis rate limiting enzyme). |
| 725 | 17258748 | In conclusion, macrophages from diabetic mice demonstrate increased oxidative stress associated with activation of NADPH oxidase and up-regulation of cellular PON2, as well as increased macrophages cholesterol uptake and biosynthesis (increased expression of CD-36 and HMG-CoA reductase). |
| 726 | 17363697 | Mice with cardiac-restricted overexpression of PPARalpha (myosin heavy chain [MHC]-PPARalpha) exhibit myocyte lipid accumulation and cardiac dysfunction. |
| 727 | 17363697 | As predicted by the metabolic changes, the activation of PPARalpha target genes involved in myocardial FA-oxidation pathways in the hearts of the MHC-PPARalpha mice was unchanged in the CD36-deficient background. |
| 728 | 17369521 | Loss of stearoyl-CoA desaturase-1 improves insulin sensitivity in lean mice but worsens diabetes in leptin-deficient obese mice. |
| 729 | 17369521 | The lipogenic gene stearoyl-CoA desaturase (SCD)1 appears to be a promising new target for obesity-related diabetes, as mice deficient in this enzyme are resistant to diet- and leptin deficiency-induced obesity. |
| 730 | 17369521 | Using the hyperinsulinemic-euglycemic clamp technique, we determined that insulin sensitivity was improved in heart, soleus muscle, adipose tissue, and liver of BTBR SCD1-deficient mice. |
| 731 | 17369521 | We next determined whether SCD1 deficiency could prevent diabetes in leptin-deficient BTBR mice. |
| 732 | 17369521 | Loss of SCD1 in leptin(ob/ob) mice unexpectedly accelerated the progression to severe diabetes; 6-week fasting glucose increased approximately 70%. |
| 733 | 17369521 | In response to a glucose challenge, Scd1(-/-) leptin(ob/ob) mice had insufficient insulin secretion, resulting in glucose intolerance. |
| 734 | 17369521 | A morphologically distinct class of islets isolated from the Scd1(-/-) leptin(ob/ob) mice had reduced insulin content and increased triglycerides, free fatty acids, esterified cholesterol, and free cholesterol and also a much higher content of saturated fatty acids. |
| 735 | 17369521 | We believe the accumulation of lipid is due to an upregulation of lipoprotein lipase (20-fold) and Cd36 (167-fold) and downregulation of lipid oxidation genes in this class of islets. |
| 736 | 17374701 | HF-fed ZDF rats developed hyperglycemia (mean: 24.4 +/- 2.1 mM), impairments in muscle insulin-stimulated glucose transport, increases in the FA transporter FAT/CD36, and increases in total ceramide and DAG content. |
| 737 | 17374701 | Interestingly, improvements in insulin-stimulated glucose transport and increased GLUT4 transporter expression in isolated muscle were seen only in conditions that included exercise training. |
| 738 | 17374701 | However, exercise did induce modest increases in peroxisome proliferator-activated receptor-gamma coactivator-1alpha, citrate synthase, and beta-hydroxyacyl-CoA dehydrogenase activity. |
| 739 | 17374701 | Thus reduction of skeletal muscle FAT/CD36 and content of ceramide and DAG may be important mechanisms by which exercise training blunts the progression of diet-induced insulin resistance in skeletal muscle. |
| 740 | 17374701 | HF-fed ZDF rats developed hyperglycemia (mean: 24.4 +/- 2.1 mM), impairments in muscle insulin-stimulated glucose transport, increases in the FA transporter FAT/CD36, and increases in total ceramide and DAG content. |
| 741 | 17374701 | Interestingly, improvements in insulin-stimulated glucose transport and increased GLUT4 transporter expression in isolated muscle were seen only in conditions that included exercise training. |
| 742 | 17374701 | However, exercise did induce modest increases in peroxisome proliferator-activated receptor-gamma coactivator-1alpha, citrate synthase, and beta-hydroxyacyl-CoA dehydrogenase activity. |
| 743 | 17374701 | Thus reduction of skeletal muscle FAT/CD36 and content of ceramide and DAG may be important mechanisms by which exercise training blunts the progression of diet-induced insulin resistance in skeletal muscle. |
| 744 | 17412916 | These CD14(-)CD36(+)CD61(+) nonadherent cells expressed general markers of hematopoietic and progenitor cells (CD45 and CD7) but no stem cell, T cell, B cell, NK cell, monocytes or dendritic cell markers. |
| 745 | 17437042 | Blood glucose, kidney weight/body weight and 24-hour urine protein in the control and DN rats were examined; the expressions of BMP-7, Smad6 and Smad7 were detected by using immunohistochemical techniques, Western blot and real-time PCR. |
| 746 | 17437042 | The expressions of BMP-7 and Smad6 proteins in DN rats were elevated, while BMP-7 mRNA expression was increased 2 weeks after STZ injection and decreased 16 weeks after STZ injection. |
| 747 | 17437042 | In addition, the expressions of transforming growth factor-beta1 (TGF-beta1) and collagen type I (COL-I) mRNA were increased in DN rats. |
| 748 | 17440173 | CD36-facilitated fatty acid uptake inhibits leptin production and signaling in adipose tissue. |
| 749 | 17440173 | Fatty acid inhibition of basal and insulin-stimulated leptin release is linked to CD36-facilitated fatty acid flux, which is important for fatty acid activation of peroxisome proliferator-activated receptor gamma and likely contributes to the nutrient sensing function of adipocytes. |
| 750 | 17440173 | Fatty acid uptake also may modulate adipocyte leptin signaling. |
| 751 | 17440173 | The ratio of phosphorylated to unphosphorylated signal transducer and activator of transcription 3, an index of leptin activity, is increased in CD36-null fat tissue disproportionately to leptin levels. |
| 752 | 17440173 | Targeting adipocyte CD36 may offer a way to uncouple leptin production and adiposity. |
| 753 | 17440173 | CD36-facilitated fatty acid uptake inhibits leptin production and signaling in adipose tissue. |
| 754 | 17440173 | Fatty acid inhibition of basal and insulin-stimulated leptin release is linked to CD36-facilitated fatty acid flux, which is important for fatty acid activation of peroxisome proliferator-activated receptor gamma and likely contributes to the nutrient sensing function of adipocytes. |
| 755 | 17440173 | Fatty acid uptake also may modulate adipocyte leptin signaling. |
| 756 | 17440173 | The ratio of phosphorylated to unphosphorylated signal transducer and activator of transcription 3, an index of leptin activity, is increased in CD36-null fat tissue disproportionately to leptin levels. |
| 757 | 17440173 | Targeting adipocyte CD36 may offer a way to uncouple leptin production and adiposity. |
| 758 | 17440173 | CD36-facilitated fatty acid uptake inhibits leptin production and signaling in adipose tissue. |
| 759 | 17440173 | Fatty acid inhibition of basal and insulin-stimulated leptin release is linked to CD36-facilitated fatty acid flux, which is important for fatty acid activation of peroxisome proliferator-activated receptor gamma and likely contributes to the nutrient sensing function of adipocytes. |
| 760 | 17440173 | Fatty acid uptake also may modulate adipocyte leptin signaling. |
| 761 | 17440173 | The ratio of phosphorylated to unphosphorylated signal transducer and activator of transcription 3, an index of leptin activity, is increased in CD36-null fat tissue disproportionately to leptin levels. |
| 762 | 17440173 | Targeting adipocyte CD36 may offer a way to uncouple leptin production and adiposity. |
| 763 | 17456847 | This was related to impaired activation of genes involved in lipid metabolism, including those for peroxisome proliferator-activated receptor coactivator-1alpha (PGC1alpha) and fatty acid translocase (FAT)/CD36 (P < 0.05). |
| 764 | 17456847 | Of interest, adiponectin receptor-1 expression decreased 23% after the high-fat meal in both groups, but it was not changed after the high-carbohydrate meal. |
| 765 | 17456847 | PGC1alpha and FAT/CD36 are likely candidates in mediating this response. |
| 766 | 17456847 | This was related to impaired activation of genes involved in lipid metabolism, including those for peroxisome proliferator-activated receptor coactivator-1alpha (PGC1alpha) and fatty acid translocase (FAT)/CD36 (P < 0.05). |
| 767 | 17456847 | Of interest, adiponectin receptor-1 expression decreased 23% after the high-fat meal in both groups, but it was not changed after the high-carbohydrate meal. |
| 768 | 17456847 | PGC1alpha and FAT/CD36 are likely candidates in mediating this response. |
| 769 | 17516074 | Defects in fatty acid translocase (FAT/CD36) have been identified as a major factor in insulin resistance and defective fatty acid and glucose metabolism. |
| 770 | 17516074 | We differentiated 3T3-L1 preadipocytes into matured adipocytes and examined the roles of insulin and long chain fatty acids on FAT/CD36 expression and function. |
| 771 | 17516074 | Our results indicate that FAT/CD36 mRNA expression was not detected at preadipocyte but was significantly increased at matured adipocyte. |
| 772 | 17516074 | In fully differentiated 3T3-L1 adipocytes, insulin significantly increased FAT/CD36 mRNA and protein expression in a dose dependent manner. |
| 773 | 17516074 | Mechanism analysis indicated that the effect of insulin and 2-BP on the FAT/CD36 mRNA gene expression may be mediated through activation of PPAR-gamma, suggesting that FAT/CD36 may have important implications in the pathophysiology of defective fatty acid metabolism. |
| 774 | 17516074 | Defects in fatty acid translocase (FAT/CD36) have been identified as a major factor in insulin resistance and defective fatty acid and glucose metabolism. |
| 775 | 17516074 | We differentiated 3T3-L1 preadipocytes into matured adipocytes and examined the roles of insulin and long chain fatty acids on FAT/CD36 expression and function. |
| 776 | 17516074 | Our results indicate that FAT/CD36 mRNA expression was not detected at preadipocyte but was significantly increased at matured adipocyte. |
| 777 | 17516074 | In fully differentiated 3T3-L1 adipocytes, insulin significantly increased FAT/CD36 mRNA and protein expression in a dose dependent manner. |
| 778 | 17516074 | Mechanism analysis indicated that the effect of insulin and 2-BP on the FAT/CD36 mRNA gene expression may be mediated through activation of PPAR-gamma, suggesting that FAT/CD36 may have important implications in the pathophysiology of defective fatty acid metabolism. |
| 779 | 17516074 | Defects in fatty acid translocase (FAT/CD36) have been identified as a major factor in insulin resistance and defective fatty acid and glucose metabolism. |
| 780 | 17516074 | We differentiated 3T3-L1 preadipocytes into matured adipocytes and examined the roles of insulin and long chain fatty acids on FAT/CD36 expression and function. |
| 781 | 17516074 | Our results indicate that FAT/CD36 mRNA expression was not detected at preadipocyte but was significantly increased at matured adipocyte. |
| 782 | 17516074 | In fully differentiated 3T3-L1 adipocytes, insulin significantly increased FAT/CD36 mRNA and protein expression in a dose dependent manner. |
| 783 | 17516074 | Mechanism analysis indicated that the effect of insulin and 2-BP on the FAT/CD36 mRNA gene expression may be mediated through activation of PPAR-gamma, suggesting that FAT/CD36 may have important implications in the pathophysiology of defective fatty acid metabolism. |
| 784 | 17516074 | Defects in fatty acid translocase (FAT/CD36) have been identified as a major factor in insulin resistance and defective fatty acid and glucose metabolism. |
| 785 | 17516074 | We differentiated 3T3-L1 preadipocytes into matured adipocytes and examined the roles of insulin and long chain fatty acids on FAT/CD36 expression and function. |
| 786 | 17516074 | Our results indicate that FAT/CD36 mRNA expression was not detected at preadipocyte but was significantly increased at matured adipocyte. |
| 787 | 17516074 | In fully differentiated 3T3-L1 adipocytes, insulin significantly increased FAT/CD36 mRNA and protein expression in a dose dependent manner. |
| 788 | 17516074 | Mechanism analysis indicated that the effect of insulin and 2-BP on the FAT/CD36 mRNA gene expression may be mediated through activation of PPAR-gamma, suggesting that FAT/CD36 may have important implications in the pathophysiology of defective fatty acid metabolism. |
| 789 | 17516074 | Defects in fatty acid translocase (FAT/CD36) have been identified as a major factor in insulin resistance and defective fatty acid and glucose metabolism. |
| 790 | 17516074 | We differentiated 3T3-L1 preadipocytes into matured adipocytes and examined the roles of insulin and long chain fatty acids on FAT/CD36 expression and function. |
| 791 | 17516074 | Our results indicate that FAT/CD36 mRNA expression was not detected at preadipocyte but was significantly increased at matured adipocyte. |
| 792 | 17516074 | In fully differentiated 3T3-L1 adipocytes, insulin significantly increased FAT/CD36 mRNA and protein expression in a dose dependent manner. |
| 793 | 17516074 | Mechanism analysis indicated that the effect of insulin and 2-BP on the FAT/CD36 mRNA gene expression may be mediated through activation of PPAR-gamma, suggesting that FAT/CD36 may have important implications in the pathophysiology of defective fatty acid metabolism. |
| 794 | 17551591 | Phagocytosis of cholesteryl ester is amplified in diabetic mouse macrophages and is largely mediated by CD36 and SR-A. |
| 795 | 17551591 | However, IP administration of CD36 and SR-A blocking antibodies led to 37% and 25% reductions in cholesteryl ester accumulation in PerMPhi. |
| 796 | 17551591 | Importantly, db/db PerMPhis showed a 43% increase in CD36 expression and an 80% increase in SR-A expression. |
| 797 | 17551591 | Taken together, these data indicate that direct cholesteryl ester accumulation in mouse macrophages is mediated by CD36 and SR-A, and the magnitude of accumulation is increased in db/db macrophages due to increased scavenger receptor expression. |
| 798 | 17551591 | Phagocytosis of cholesteryl ester is amplified in diabetic mouse macrophages and is largely mediated by CD36 and SR-A. |
| 799 | 17551591 | However, IP administration of CD36 and SR-A blocking antibodies led to 37% and 25% reductions in cholesteryl ester accumulation in PerMPhi. |
| 800 | 17551591 | Importantly, db/db PerMPhis showed a 43% increase in CD36 expression and an 80% increase in SR-A expression. |
| 801 | 17551591 | Taken together, these data indicate that direct cholesteryl ester accumulation in mouse macrophages is mediated by CD36 and SR-A, and the magnitude of accumulation is increased in db/db macrophages due to increased scavenger receptor expression. |
| 802 | 17551591 | Phagocytosis of cholesteryl ester is amplified in diabetic mouse macrophages and is largely mediated by CD36 and SR-A. |
| 803 | 17551591 | However, IP administration of CD36 and SR-A blocking antibodies led to 37% and 25% reductions in cholesteryl ester accumulation in PerMPhi. |
| 804 | 17551591 | Importantly, db/db PerMPhis showed a 43% increase in CD36 expression and an 80% increase in SR-A expression. |
| 805 | 17551591 | Taken together, these data indicate that direct cholesteryl ester accumulation in mouse macrophages is mediated by CD36 and SR-A, and the magnitude of accumulation is increased in db/db macrophages due to increased scavenger receptor expression. |
| 806 | 17551591 | Phagocytosis of cholesteryl ester is amplified in diabetic mouse macrophages and is largely mediated by CD36 and SR-A. |
| 807 | 17551591 | However, IP administration of CD36 and SR-A blocking antibodies led to 37% and 25% reductions in cholesteryl ester accumulation in PerMPhi. |
| 808 | 17551591 | Importantly, db/db PerMPhis showed a 43% increase in CD36 expression and an 80% increase in SR-A expression. |
| 809 | 17551591 | Taken together, these data indicate that direct cholesteryl ester accumulation in mouse macrophages is mediated by CD36 and SR-A, and the magnitude of accumulation is increased in db/db macrophages due to increased scavenger receptor expression. |
| 810 | 17588473 | Identification of CD13+CD36+ cells as a common progenitor for erythroid and myeloid lineages in human bone marrow. |
| 811 | 17639306 | Cardiac contractile dysfunction in insulin-resistant rats fed a high-fat diet is associated with elevated CD36-mediated fatty acid uptake and esterification. |
| 812 | 17658475 | Moreover, mRNA levels of PPARgamma target genes such as LPL, aP2, CD36 and LXRalpha are up-regulated by phloretin. |
| 813 | 17658475 | Taken together, these results suggest that phloretin may be beneficial for reducing insulin resistance through its potency to regulate adipocyte differentiation and function. |
| 814 | 17686959 | Diabetes was associated with an increase in urine albumin excretion, glomerulosclerosis, tubulointerstitial fibrosis, renal cortical collagen type I and IV, laminin, plasminogen activator inhibitor-1, tissue inhibitors of metalloproteinase-1 and -2, transforming growth factor (TGF)-beta, TGF-beta receptor type I and II, Smad2/3, phosphorylated Smad2/3, and Smad4 protein expression, and CD68-positive cell abundance. |
| 815 | 17686959 | Decreases in matrix metalloproteinase (MMP)-2 protein expression and activity and decreases in Smad6 and Smad7 protein expression were also associated with diabetes. |
| 816 | 17905828 | It has an equally diverse range of ligands and physiological functions, which has implicated Cd36 in a number of diseases including insulin resistance, diabetes, and, most notably, atherosclerosis. |
| 817 | 18259041 | Diabetes was associated with the following increases: 3.2-fold in urine albumin excretion, 6.3-fold in glomerulosclerosis, 6.0-fold in tubulointerstitial fibrosis, 1.6-fold in collagen type I, 1.2-fold in collagen type IV, 1.3-fold in transforming growth factor-beta protein expression, and 32.7-fold in CD68-positive cell abundance. |
| 818 | 18288286 | Uncovering the biologic roles of PPARgamma and its mechanism of action has greatly advanced our understanding of the transcriptional control of lipid and glucose metabolism, and compounds such as thiazolidinediones which directly regulate PPARgamma have proven to exhibit potent insulin-sensitizer effects in the treatment of diabetes. |
| 819 | 18288286 | We review here recent advances on the emerging role of growth hormone releasing peptides in regulating PPARgamma through interaction with scavenger receptor CD36 and ghrelin GHS-R1a receptor. |
| 820 | 18308721 | CD36-dependent regulation of muscle FoxO1 and PDK4 in the PPAR delta/beta-mediated adaptation to metabolic stress. |
| 821 | 18308721 | Increased fatty acid flux or enforced CD36 expression in C(2)C(12) cells is sufficient to induce FoxO1 and PDK4, whereas CD36 knockdown has opposite effects. |
| 822 | 18308721 | In vivo, CD36 loss blunts fasting induction of FoxO1 and PDK4 and the associated suppression of glucose oxidation. |
| 823 | 18308721 | Loss of PPARdelta/beta phenocopies CD36 deficiency in blunting fasting induction of muscle FoxO1 and PDK4 in vivo. |
| 824 | 18308721 | FoxO1 in turn can regulate CD36, lipoprotein lipase, and PDK4, reinforcing the action of PPARdelta/beta to increase muscle reliance on FA. |
| 825 | 18308721 | CD36-dependent regulation of muscle FoxO1 and PDK4 in the PPAR delta/beta-mediated adaptation to metabolic stress. |
| 826 | 18308721 | Increased fatty acid flux or enforced CD36 expression in C(2)C(12) cells is sufficient to induce FoxO1 and PDK4, whereas CD36 knockdown has opposite effects. |
| 827 | 18308721 | In vivo, CD36 loss blunts fasting induction of FoxO1 and PDK4 and the associated suppression of glucose oxidation. |
| 828 | 18308721 | Loss of PPARdelta/beta phenocopies CD36 deficiency in blunting fasting induction of muscle FoxO1 and PDK4 in vivo. |
| 829 | 18308721 | FoxO1 in turn can regulate CD36, lipoprotein lipase, and PDK4, reinforcing the action of PPARdelta/beta to increase muscle reliance on FA. |
| 830 | 18308721 | CD36-dependent regulation of muscle FoxO1 and PDK4 in the PPAR delta/beta-mediated adaptation to metabolic stress. |
| 831 | 18308721 | Increased fatty acid flux or enforced CD36 expression in C(2)C(12) cells is sufficient to induce FoxO1 and PDK4, whereas CD36 knockdown has opposite effects. |
| 832 | 18308721 | In vivo, CD36 loss blunts fasting induction of FoxO1 and PDK4 and the associated suppression of glucose oxidation. |
| 833 | 18308721 | Loss of PPARdelta/beta phenocopies CD36 deficiency in blunting fasting induction of muscle FoxO1 and PDK4 in vivo. |
| 834 | 18308721 | FoxO1 in turn can regulate CD36, lipoprotein lipase, and PDK4, reinforcing the action of PPARdelta/beta to increase muscle reliance on FA. |
| 835 | 18308721 | CD36-dependent regulation of muscle FoxO1 and PDK4 in the PPAR delta/beta-mediated adaptation to metabolic stress. |
| 836 | 18308721 | Increased fatty acid flux or enforced CD36 expression in C(2)C(12) cells is sufficient to induce FoxO1 and PDK4, whereas CD36 knockdown has opposite effects. |
| 837 | 18308721 | In vivo, CD36 loss blunts fasting induction of FoxO1 and PDK4 and the associated suppression of glucose oxidation. |
| 838 | 18308721 | Loss of PPARdelta/beta phenocopies CD36 deficiency in blunting fasting induction of muscle FoxO1 and PDK4 in vivo. |
| 839 | 18308721 | FoxO1 in turn can regulate CD36, lipoprotein lipase, and PDK4, reinforcing the action of PPARdelta/beta to increase muscle reliance on FA. |
| 840 | 18308721 | CD36-dependent regulation of muscle FoxO1 and PDK4 in the PPAR delta/beta-mediated adaptation to metabolic stress. |
| 841 | 18308721 | Increased fatty acid flux or enforced CD36 expression in C(2)C(12) cells is sufficient to induce FoxO1 and PDK4, whereas CD36 knockdown has opposite effects. |
| 842 | 18308721 | In vivo, CD36 loss blunts fasting induction of FoxO1 and PDK4 and the associated suppression of glucose oxidation. |
| 843 | 18308721 | Loss of PPARdelta/beta phenocopies CD36 deficiency in blunting fasting induction of muscle FoxO1 and PDK4 in vivo. |
| 844 | 18308721 | FoxO1 in turn can regulate CD36, lipoprotein lipase, and PDK4, reinforcing the action of PPARdelta/beta to increase muscle reliance on FA. |
| 845 | 18441389 | Insulin acutely upregulates protein expression of the fatty acid transporter CD36 in human skeletal muscle in vivo. |
| 846 | 18441389 | The fatty acid transporter FAT/CD36 protein content increased 1.5-fold (P < 0.05) after 3-hrs of insulin stimulation with no difference between IGT and control subjects. |
| 847 | 18441389 | The increase in FAT/CD36 protein content was positively related to insulin resistance as measured during the clamp (r = 0.56, P < 0.05). |
| 848 | 18441389 | We conclude that also in obese humans the FAT/CD36 protein content in skeletal muscle is dynamically regulated by insulin in vivo on the short term. |
| 849 | 18441389 | Insulin acutely upregulates protein expression of the fatty acid transporter CD36 in human skeletal muscle in vivo. |
| 850 | 18441389 | The fatty acid transporter FAT/CD36 protein content increased 1.5-fold (P < 0.05) after 3-hrs of insulin stimulation with no difference between IGT and control subjects. |
| 851 | 18441389 | The increase in FAT/CD36 protein content was positively related to insulin resistance as measured during the clamp (r = 0.56, P < 0.05). |
| 852 | 18441389 | We conclude that also in obese humans the FAT/CD36 protein content in skeletal muscle is dynamically regulated by insulin in vivo on the short term. |
| 853 | 18441389 | Insulin acutely upregulates protein expression of the fatty acid transporter CD36 in human skeletal muscle in vivo. |
| 854 | 18441389 | The fatty acid transporter FAT/CD36 protein content increased 1.5-fold (P < 0.05) after 3-hrs of insulin stimulation with no difference between IGT and control subjects. |
| 855 | 18441389 | The increase in FAT/CD36 protein content was positively related to insulin resistance as measured during the clamp (r = 0.56, P < 0.05). |
| 856 | 18441389 | We conclude that also in obese humans the FAT/CD36 protein content in skeletal muscle is dynamically regulated by insulin in vivo on the short term. |
| 857 | 18441389 | Insulin acutely upregulates protein expression of the fatty acid transporter CD36 in human skeletal muscle in vivo. |
| 858 | 18441389 | The fatty acid transporter FAT/CD36 protein content increased 1.5-fold (P < 0.05) after 3-hrs of insulin stimulation with no difference between IGT and control subjects. |
| 859 | 18441389 | The increase in FAT/CD36 protein content was positively related to insulin resistance as measured during the clamp (r = 0.56, P < 0.05). |
| 860 | 18441389 | We conclude that also in obese humans the FAT/CD36 protein content in skeletal muscle is dynamically regulated by insulin in vivo on the short term. |
| 861 | 18456735 | Microvessel vascular smooth muscle cells contribute to collagen type I deposition through ERK1/2 MAP kinase, alphavbeta3-integrin, and TGF-beta1 in response to ANG II and high glucose. |
| 862 | 18456735 | This study determines that vascular smooth muscle cell (VSMC) signaling through extracellular signal-regulated kinase (ERK) 1/2-mitogen-activated protein (MAP) kinase, alphavbeta(3)-integrin, and transforming growth factor (TGF)-beta1 dictates collagen type I network induction in mesenteric resistance arteries (MRA) from type 1 diabetic (streptozotocin) or hypertensive (HT; ANG II) mice. |
| 863 | 18456735 | Pressure-passive-diameter relationship reduction was associated with increased collagen type I deposition in MRA from HT and diabetic mice compared with control. |
| 864 | 18456735 | Treatment of HT and diabetic mice with neutralizing TGF-beta1 antibody reduced MRA stiffness and collagen type I deposition. |
| 865 | 18456735 | Cultured VSMC stimulated with HG or ANG II for 5 min increased ERK1/2-MAP kinase phosphorylation, whereas a 48-h stimulation induced latent TGF-beta1, alphavbeta(3)-integrin, and collagen type 1 release in the conditioned media. |
| 866 | 18456735 | TGF-beta1 bioactivity and Smad2 phosphorylation were alphavbeta(3)-integrin-dependent, since beta(3)-integrin antibody and alphavbeta(3)-integrin inhibitor (SB-223245, 10 microM) significantly prevented TGF-beta1 bioactivity and Smad2 phosphorylation. |
| 867 | 18456735 | Pretreatment of VSMC with ERK1/2-MAP kinase inhibitor (U-0126, 1 microM) reduced alphavbeta(3)-integrin, TGF-beta1, and collagen type 1 content. |
| 868 | 18456735 | Additionally, alphavbeta(3)-integrin antibody, SB-223245, TGF-beta1-small-intefering RNA (siRNA), and Smad2-siRNA (40 nM) prevented collagen type I network formation in response to ANG II and HG. |
| 869 | 18456735 | Together, these data provide evidence that resistance artery fibrosis in type 1 diabetes and hypertension is a consequence of abnormal collagen type I release by VSMC and involves ERK1/2, alphavbeta(3)-integrin, and TGF-beta1 signaling. |
| 870 | 18456735 | Microvessel vascular smooth muscle cells contribute to collagen type I deposition through ERK1/2 MAP kinase, alphavbeta3-integrin, and TGF-beta1 in response to ANG II and high glucose. |
| 871 | 18456735 | This study determines that vascular smooth muscle cell (VSMC) signaling through extracellular signal-regulated kinase (ERK) 1/2-mitogen-activated protein (MAP) kinase, alphavbeta(3)-integrin, and transforming growth factor (TGF)-beta1 dictates collagen type I network induction in mesenteric resistance arteries (MRA) from type 1 diabetic (streptozotocin) or hypertensive (HT; ANG II) mice. |
| 872 | 18456735 | Pressure-passive-diameter relationship reduction was associated with increased collagen type I deposition in MRA from HT and diabetic mice compared with control. |
| 873 | 18456735 | Treatment of HT and diabetic mice with neutralizing TGF-beta1 antibody reduced MRA stiffness and collagen type I deposition. |
| 874 | 18456735 | Cultured VSMC stimulated with HG or ANG II for 5 min increased ERK1/2-MAP kinase phosphorylation, whereas a 48-h stimulation induced latent TGF-beta1, alphavbeta(3)-integrin, and collagen type 1 release in the conditioned media. |
| 875 | 18456735 | TGF-beta1 bioactivity and Smad2 phosphorylation were alphavbeta(3)-integrin-dependent, since beta(3)-integrin antibody and alphavbeta(3)-integrin inhibitor (SB-223245, 10 microM) significantly prevented TGF-beta1 bioactivity and Smad2 phosphorylation. |
| 876 | 18456735 | Pretreatment of VSMC with ERK1/2-MAP kinase inhibitor (U-0126, 1 microM) reduced alphavbeta(3)-integrin, TGF-beta1, and collagen type 1 content. |
| 877 | 18456735 | Additionally, alphavbeta(3)-integrin antibody, SB-223245, TGF-beta1-small-intefering RNA (siRNA), and Smad2-siRNA (40 nM) prevented collagen type I network formation in response to ANG II and HG. |
| 878 | 18456735 | Together, these data provide evidence that resistance artery fibrosis in type 1 diabetes and hypertension is a consequence of abnormal collagen type I release by VSMC and involves ERK1/2, alphavbeta(3)-integrin, and TGF-beta1 signaling. |
| 879 | 18456735 | Microvessel vascular smooth muscle cells contribute to collagen type I deposition through ERK1/2 MAP kinase, alphavbeta3-integrin, and TGF-beta1 in response to ANG II and high glucose. |
| 880 | 18456735 | This study determines that vascular smooth muscle cell (VSMC) signaling through extracellular signal-regulated kinase (ERK) 1/2-mitogen-activated protein (MAP) kinase, alphavbeta(3)-integrin, and transforming growth factor (TGF)-beta1 dictates collagen type I network induction in mesenteric resistance arteries (MRA) from type 1 diabetic (streptozotocin) or hypertensive (HT; ANG II) mice. |
| 881 | 18456735 | Pressure-passive-diameter relationship reduction was associated with increased collagen type I deposition in MRA from HT and diabetic mice compared with control. |
| 882 | 18456735 | Treatment of HT and diabetic mice with neutralizing TGF-beta1 antibody reduced MRA stiffness and collagen type I deposition. |
| 883 | 18456735 | Cultured VSMC stimulated with HG or ANG II for 5 min increased ERK1/2-MAP kinase phosphorylation, whereas a 48-h stimulation induced latent TGF-beta1, alphavbeta(3)-integrin, and collagen type 1 release in the conditioned media. |
| 884 | 18456735 | TGF-beta1 bioactivity and Smad2 phosphorylation were alphavbeta(3)-integrin-dependent, since beta(3)-integrin antibody and alphavbeta(3)-integrin inhibitor (SB-223245, 10 microM) significantly prevented TGF-beta1 bioactivity and Smad2 phosphorylation. |
| 885 | 18456735 | Pretreatment of VSMC with ERK1/2-MAP kinase inhibitor (U-0126, 1 microM) reduced alphavbeta(3)-integrin, TGF-beta1, and collagen type 1 content. |
| 886 | 18456735 | Additionally, alphavbeta(3)-integrin antibody, SB-223245, TGF-beta1-small-intefering RNA (siRNA), and Smad2-siRNA (40 nM) prevented collagen type I network formation in response to ANG II and HG. |
| 887 | 18456735 | Together, these data provide evidence that resistance artery fibrosis in type 1 diabetes and hypertension is a consequence of abnormal collagen type I release by VSMC and involves ERK1/2, alphavbeta(3)-integrin, and TGF-beta1 signaling. |
| 888 | 18456735 | Microvessel vascular smooth muscle cells contribute to collagen type I deposition through ERK1/2 MAP kinase, alphavbeta3-integrin, and TGF-beta1 in response to ANG II and high glucose. |
| 889 | 18456735 | This study determines that vascular smooth muscle cell (VSMC) signaling through extracellular signal-regulated kinase (ERK) 1/2-mitogen-activated protein (MAP) kinase, alphavbeta(3)-integrin, and transforming growth factor (TGF)-beta1 dictates collagen type I network induction in mesenteric resistance arteries (MRA) from type 1 diabetic (streptozotocin) or hypertensive (HT; ANG II) mice. |
| 890 | 18456735 | Pressure-passive-diameter relationship reduction was associated with increased collagen type I deposition in MRA from HT and diabetic mice compared with control. |
| 891 | 18456735 | Treatment of HT and diabetic mice with neutralizing TGF-beta1 antibody reduced MRA stiffness and collagen type I deposition. |
| 892 | 18456735 | Cultured VSMC stimulated with HG or ANG II for 5 min increased ERK1/2-MAP kinase phosphorylation, whereas a 48-h stimulation induced latent TGF-beta1, alphavbeta(3)-integrin, and collagen type 1 release in the conditioned media. |
| 893 | 18456735 | TGF-beta1 bioactivity and Smad2 phosphorylation were alphavbeta(3)-integrin-dependent, since beta(3)-integrin antibody and alphavbeta(3)-integrin inhibitor (SB-223245, 10 microM) significantly prevented TGF-beta1 bioactivity and Smad2 phosphorylation. |
| 894 | 18456735 | Pretreatment of VSMC with ERK1/2-MAP kinase inhibitor (U-0126, 1 microM) reduced alphavbeta(3)-integrin, TGF-beta1, and collagen type 1 content. |
| 895 | 18456735 | Additionally, alphavbeta(3)-integrin antibody, SB-223245, TGF-beta1-small-intefering RNA (siRNA), and Smad2-siRNA (40 nM) prevented collagen type I network formation in response to ANG II and HG. |
| 896 | 18456735 | Together, these data provide evidence that resistance artery fibrosis in type 1 diabetes and hypertension is a consequence of abnormal collagen type I release by VSMC and involves ERK1/2, alphavbeta(3)-integrin, and TGF-beta1 signaling. |
| 897 | 18456735 | Microvessel vascular smooth muscle cells contribute to collagen type I deposition through ERK1/2 MAP kinase, alphavbeta3-integrin, and TGF-beta1 in response to ANG II and high glucose. |
| 898 | 18456735 | This study determines that vascular smooth muscle cell (VSMC) signaling through extracellular signal-regulated kinase (ERK) 1/2-mitogen-activated protein (MAP) kinase, alphavbeta(3)-integrin, and transforming growth factor (TGF)-beta1 dictates collagen type I network induction in mesenteric resistance arteries (MRA) from type 1 diabetic (streptozotocin) or hypertensive (HT; ANG II) mice. |
| 899 | 18456735 | Pressure-passive-diameter relationship reduction was associated with increased collagen type I deposition in MRA from HT and diabetic mice compared with control. |
| 900 | 18456735 | Treatment of HT and diabetic mice with neutralizing TGF-beta1 antibody reduced MRA stiffness and collagen type I deposition. |
| 901 | 18456735 | Cultured VSMC stimulated with HG or ANG II for 5 min increased ERK1/2-MAP kinase phosphorylation, whereas a 48-h stimulation induced latent TGF-beta1, alphavbeta(3)-integrin, and collagen type 1 release in the conditioned media. |
| 902 | 18456735 | TGF-beta1 bioactivity and Smad2 phosphorylation were alphavbeta(3)-integrin-dependent, since beta(3)-integrin antibody and alphavbeta(3)-integrin inhibitor (SB-223245, 10 microM) significantly prevented TGF-beta1 bioactivity and Smad2 phosphorylation. |
| 903 | 18456735 | Pretreatment of VSMC with ERK1/2-MAP kinase inhibitor (U-0126, 1 microM) reduced alphavbeta(3)-integrin, TGF-beta1, and collagen type 1 content. |
| 904 | 18456735 | Additionally, alphavbeta(3)-integrin antibody, SB-223245, TGF-beta1-small-intefering RNA (siRNA), and Smad2-siRNA (40 nM) prevented collagen type I network formation in response to ANG II and HG. |
| 905 | 18456735 | Together, these data provide evidence that resistance artery fibrosis in type 1 diabetes and hypertension is a consequence of abnormal collagen type I release by VSMC and involves ERK1/2, alphavbeta(3)-integrin, and TGF-beta1 signaling. |
| 906 | 18456735 | Microvessel vascular smooth muscle cells contribute to collagen type I deposition through ERK1/2 MAP kinase, alphavbeta3-integrin, and TGF-beta1 in response to ANG II and high glucose. |
| 907 | 18456735 | This study determines that vascular smooth muscle cell (VSMC) signaling through extracellular signal-regulated kinase (ERK) 1/2-mitogen-activated protein (MAP) kinase, alphavbeta(3)-integrin, and transforming growth factor (TGF)-beta1 dictates collagen type I network induction in mesenteric resistance arteries (MRA) from type 1 diabetic (streptozotocin) or hypertensive (HT; ANG II) mice. |
| 908 | 18456735 | Pressure-passive-diameter relationship reduction was associated with increased collagen type I deposition in MRA from HT and diabetic mice compared with control. |
| 909 | 18456735 | Treatment of HT and diabetic mice with neutralizing TGF-beta1 antibody reduced MRA stiffness and collagen type I deposition. |
| 910 | 18456735 | Cultured VSMC stimulated with HG or ANG II for 5 min increased ERK1/2-MAP kinase phosphorylation, whereas a 48-h stimulation induced latent TGF-beta1, alphavbeta(3)-integrin, and collagen type 1 release in the conditioned media. |
| 911 | 18456735 | TGF-beta1 bioactivity and Smad2 phosphorylation were alphavbeta(3)-integrin-dependent, since beta(3)-integrin antibody and alphavbeta(3)-integrin inhibitor (SB-223245, 10 microM) significantly prevented TGF-beta1 bioactivity and Smad2 phosphorylation. |
| 912 | 18456735 | Pretreatment of VSMC with ERK1/2-MAP kinase inhibitor (U-0126, 1 microM) reduced alphavbeta(3)-integrin, TGF-beta1, and collagen type 1 content. |
| 913 | 18456735 | Additionally, alphavbeta(3)-integrin antibody, SB-223245, TGF-beta1-small-intefering RNA (siRNA), and Smad2-siRNA (40 nM) prevented collagen type I network formation in response to ANG II and HG. |
| 914 | 18456735 | Together, these data provide evidence that resistance artery fibrosis in type 1 diabetes and hypertension is a consequence of abnormal collagen type I release by VSMC and involves ERK1/2, alphavbeta(3)-integrin, and TGF-beta1 signaling. |
| 915 | 18502258 | The heart expression of lipid-metabolizing genes (peroxisomal proliferator-activated receptor alpha, lipoprotein lipase, fatty acid translocase, and fatty acid transport protein 1) was reduced in offspring from Ins2(Akita) mothers with high blood glucose levels and were closely intercorrelated, suggesting coordinated down-regulation. |
| 916 | 18502258 | In contrast, on day 1 postnatally where the lipid availability to the heart is markedly increased, heart triglycerides and expression of several lipid-metabolizing genes (including lipoprotein lipase and fatty acid transport protein 1) were increased in offspring from wild-type mice. |
| 917 | 18726071 | Differential regulation of collagen types I and III expression in cardiac fibroblasts by AGEs through TRB3/MAPK signaling pathway. |
| 918 | 18726071 | We demonstrated that AGEs induce collagen type I expression but inhibit collagen type III expression, accompanied by increased TRB3 expression. |
| 919 | 18726071 | Furthermore, the collagen type I induced byAGEs was down-regulated after inhibition of ERK and p38-MAPK, the collagen type III reduced by AGEs was up-regulated after inhibition of ERK. |
| 920 | 18726071 | The expression of collagen types I and III regulated by AGEs through MAPK was partly reversed after treatment with TRB3 siRNA. |
| 921 | 18726071 | It suggests that the TRB3/MAPK signaling pathway participates in the regulation of collagen types I and III by AGEs and may provide new therapeutic strategies for diabetic cardiomyopathy. |
| 922 | 18726071 | Differential regulation of collagen types I and III expression in cardiac fibroblasts by AGEs through TRB3/MAPK signaling pathway. |
| 923 | 18726071 | We demonstrated that AGEs induce collagen type I expression but inhibit collagen type III expression, accompanied by increased TRB3 expression. |
| 924 | 18726071 | Furthermore, the collagen type I induced byAGEs was down-regulated after inhibition of ERK and p38-MAPK, the collagen type III reduced by AGEs was up-regulated after inhibition of ERK. |
| 925 | 18726071 | The expression of collagen types I and III regulated by AGEs through MAPK was partly reversed after treatment with TRB3 siRNA. |
| 926 | 18726071 | It suggests that the TRB3/MAPK signaling pathway participates in the regulation of collagen types I and III by AGEs and may provide new therapeutic strategies for diabetic cardiomyopathy. |
| 927 | 18772361 | The high concentration of glucose enhanced the protein expression of the critical cholesterol transporter NPC1L1 and that of CD36 (P < 0.02) and concomitantly decreased SR-BI protein mass (P < 0.02). |
| 928 | 18772361 | No significant changes were observed in the protein expression of ABCA1 and ABCG8, which act as efflux pumps favoring cholesterol export out of absorptive cells. |
| 929 | 18772361 | Finally, increases were noted in the transcription factors LXR-alpha, LXR-beta, PPAR-beta, and PPAR-gamma along with a drop in the protein expression of SREBP-2. |
| 930 | 18779868 | We examined changes in the ultrastructure and localization of major extracellular matrix components, including 5 types of collagen (type I, III, IV, VI, and VIII), laminin, fibronectin, and heparan sulfate proteoglycan in Descemet's membrane of the cornea of diabetic GK rats. |
| 931 | 18820218 | Elevated plasma plasminogen activator inhibitor-1 in CD36 deficiency. |
| 932 | 18849545 | Ritonavir increases CD36, ABCA1 and CYP27 expression in THP-1 macrophages. |
| 933 | 18948972 | In this study, we show that isorhamnetin inhibits adipocyte differentiation, as evidenced by reduced triglyceride (TG) accumulation and glycerol-3-phosphate dehydrogenase (GPDH) activity. |
| 934 | 18948972 | At the molecular level, the mRNA expression levels of peroxidase proliferator-activated receptor-gamma (PPAR-gamma) and CCAAT/enhancer-binding protein-alpha (C/EBP-alpha), which are the major adipogenic transcription factors, were markedly reduced by isorhamnetin. |
| 935 | 18948972 | However, the mRNA levels of C/EBP-beta and -delta, the upstream regulators of PPAR-gamma and C/EBP-alpha, were not reduced by isorhamnetin. |
| 936 | 18948972 | Moreover, the mRNA levels of PPAR-gamma target genes such as lipoprotein lipase (LPL), CD36, aP2, and liver X receptor-alpha (LXR-alpha) were downregulated by isorhamnetin. |
| 937 | 18948972 | We also showed that isorhamnetin inhibits the expression and secretion of adiponectin, and the results of adiponectin promoter assays suggest the inhibition of PPAR-gamma expression as a possible mechanism underlying the isorhamnetin-mediated effects. |
| 938 | 18948972 | Taken together, these results indicate that isorhamnetin inhibits adipogenesis through downregulation of PPAR-gamma and C/EBP-alpha. |
| 939 | 19052104 | In addition, D+canola attenuated D-associated increase in collagen type I and type IV, IL-6, MCP-1, transforming growth factor-beta, and CD68 expression. |
| 940 | 19066218 | Paradoxical effects of increased expression of PGC-1alpha on muscle mitochondrial function and insulin-stimulated muscle glucose metabolism. |
| 941 | 19066218 | To determine the effect of increased muscle-specific PGC-1alpha expression on muscle mitochondrial function and glucose and lipid metabolism in vivo, we examined body composition, energy balance, and liver and muscle insulin sensitivity by hyperinsulinemic-euglycemic clamp studies and muscle energetics by using (31)P magnetic resonance spectroscopy in transgenic mice. |
| 942 | 19066218 | Surprisingly, there was no effect of increased muscle PGC-1alpha expression on whole-body energy expenditure, and PGC-1alpha transgenic mice were more prone to fat-induced insulin resistance because of decreased insulin-stimulated muscle glucose uptake. |
| 943 | 19066218 | The reduced insulin-stimulated muscle glucose uptake could most likely be attributed to a relative increase in fatty acid delivery/triglyceride reesterfication, as reflected by increased expression of CD36, acyl-CoA:diacylglycerol acyltransferase1, and mitochondrial acyl-CoA:glycerol-sn-3-phosphate acyltransferase, that may have exceeded mitochondrial fatty acid oxidation, resulting in increased intracellular lipid accumulation and an increase in the membrane to cytosol diacylglycerol content. |
| 944 | 19096709 | Peroxisome proliferator-activated receptors (PPARs) are transcriptional factors involved in the regulation of insulin resistance and adipogenesis. |
| 945 | 19096709 | Cinnamon, a widely used spice in food preparation and traditional antidiabetic remedy, is found to activate PPARgamma and alpha, resulting in improved insulin resistance, reduced fasted glucose, FFA, LDL-c, and AST levels in high-caloric diet-induced obesity (DIO) and db/db mice in its water extract form. |
| 946 | 19096709 | In vitro studies demonstrate that cinnamon increases the expression of peroxisome proliferator-activated receptors gamma and alpha (PPARgamma/alpha) and their target genes such as LPL, CD36, GLUT4, and ACO in 3T3-L1 adipocyte. |
| 947 | 19096709 | The transactivities of both full length and ligand-binding domain (LBD) of PPARgamma and PPARalpha are activated by cinnamon as evidenced by reporter gene assays. |
| 948 | 19230716 | After APS/NS administration at a dose of 1 g/kg per day for 10 weeks, hemodynamic parameters, levels of insulin (INS), C-peptide (C-P), glycosylated serum protein (GSP), lipoproteins, myocardial enzymes, and Ang II (plasma and myocardial) were tested; myocardial collagen (type I and III), myocardial ultrastructure, and activities of matrix metalloproteinase (MMPs) were measured; activities and expression of cardiac chymase and ACE were detected by using quantitative real-time RT-PCR and RIA; protein expression of cardiac phosphoric extracellular signal-regulated kinase 1/2 (p-ERK1/2) was measured by Western blot. |
| 949 | 19230716 | AP-administrated diabetic hamsters had lower levels of GSP, lipoproteins, myocardial enzymes, myocardial Ang II, expression of collagen I and I/ III, activities of pro-MMP-2 and MMP-2, activities and expression of chymase, and expression of p-ERK1/2 than NS-administrated diabetic hamsters and could better protect the myocardial ultrastructure. |
| 950 | 19350199 | In this study, we investigated the effects of APS treatment on cardiac function, myocardial collagen expression, cardiac ultrastructure, cardiac matrix metalloproteinase (MMP) activity, levels of plasma glycosylated serum protein (GSP), and myocardial enzymes, and the expression of Ang II, chymase, and angiotensin-converting enzyme (ACE) in the diabetic hamster myocardium. |
| 951 | 19350199 | Compared with insulin treatment, APS treatment significantly reduced myocardial collagen (type I and III) expression and lowered cardiac MMP-2 activity, myocardial Ang II levels, myocardial chymase expression, and p-ERK1/2 kinase expression. |
| 952 | 19350199 | In diabetic hamsters, myocardial ACE expression and plasma Ang II levels was not altered by insulin or APS treatment. |
| 953 | 19375767 | Increased carnitine palmitoyl transferase 1 expression and decreased sterol regulatory element-binding protein 1c expression are associated with reduced intramuscular triglyceride accumulation after insulin therapy in high-fat-diet and streptozotocin-induced diabetic rats. |
| 954 | 19375767 | Compared with normal rats, untreated diabetic rats had a 30% and 61% increase in lipoprotein lipase protein expression and activity, which were decreased by insulin and gliclazide (P < .05). |
| 955 | 19375767 | Fatty acid translocase protein was down-regulated by 45% in untreated diabetic rats, which was up-regulated by 31% and 26% with insulin and gliclazide, respectively (P < .05). |
| 956 | 19375767 | Insulin failed to affect fatty acid transport protein 1 and fatty acid binding protein expressions. |
| 957 | 19375767 | Moreover, compared with normal rats, untreated diabetic rats had higher expressions of sterol regulatory element-binding protein 1c, tumor necrosis factor alpha, and Tyr(705) phosphorylation of signal transducer and activator of transcription 3 levels, which all were down-regulated after insulin treatment. |
| 958 | 19448691 | The peroxisome proliferator-activated receptor gamma (PPARgamma) coactivator 1alpha (PGC-1alpha), a nuclear encoded transcriptional coactivator, increases the expression of many genes in skeletal muscle, including those involved with fatty acid oxidation and oxidative phosphorylation. |
| 959 | 19448691 | PGC-1alpha reductions in humans have been observed in type 2 diabetes, while, in cell lines, PGC-1alpha mimics the exercise-induced improvement in insulin sensitivity. |
| 960 | 19448691 | However, unexpectedly, in mammalian muscle, PGC-1alpha overexpression contributed to the development of diet-induced insulin resistance. |
| 961 | 19448691 | This may have been related to the massive overexpression of PGC-1alpha, which induced the upregulation of the fatty acid transporter FAT/CD36 and led to an increase in intramuscular lipids, which interfere with insulin signalling. |
| 962 | 19448691 | In contrast, when PGC-1alpha was overexpressed modestly, within physiological limits, mitochondrial fatty acid oxidation was increased, GLUT4 expression was upregulated, and insulin-stimulated glucose transport was increased. |
| 963 | 19448691 | These studies suggest that massive PGC-1alpha overexpression, but not physiologic PGC-1alpha overexpression, induces deleterious metabolic effects, and that exercise-induced improvements in insulin sensitivity are induced, in part, by the exercise-induced upregulation of PGC-1alpha. |
| 964 | 19448717 | In the insulin-resistant heart, the abundance of the LCFA transporters CD36 and FABPpm at the sarcolemma of cardiac myocytes appears to be markedly increased. |
| 965 | 19448717 | Carnitine palmitoyltransferase (CPT)-I has long been considered to be this rate-limiting site and, accordingly, pharmacological inhibition of CPT-I, or beta-oxidation enzymes, has been proposed as an insulin-resistance-antagonizing strategy. |
| 966 | 19448717 | In this review, it is proposed that a pharmacologically imposed net internalization of CD36 and FABPpm is the preferable strategy to limit LCFA entry and accumulation of LCFA metabolites, to regress cardiac insulin resistance and, eventually, prevent diabetic heart failure. |
| 967 | 19448717 | In the insulin-resistant heart, the abundance of the LCFA transporters CD36 and FABPpm at the sarcolemma of cardiac myocytes appears to be markedly increased. |
| 968 | 19448717 | Carnitine palmitoyltransferase (CPT)-I has long been considered to be this rate-limiting site and, accordingly, pharmacological inhibition of CPT-I, or beta-oxidation enzymes, has been proposed as an insulin-resistance-antagonizing strategy. |
| 969 | 19448717 | In this review, it is proposed that a pharmacologically imposed net internalization of CD36 and FABPpm is the preferable strategy to limit LCFA entry and accumulation of LCFA metabolites, to regress cardiac insulin resistance and, eventually, prevent diabetic heart failure. |
| 970 | 19471024 | On microvascular endothelial cells, CD36 is a receptor for thrombospondin-1 and related proteins and functions as a negative regulator of angiogenesis. |
| 971 | 19521352 | Lipid-induced insulin resistance is associated with increased monocyte expression of scavenger receptor CD36 and internalization of oxidized LDL. |
| 972 | 19521352 | We tested the relationship among lipid-induced insulin resistance, endothelial dysfunction, and monocyte capacity to form foam cells through scavenger receptor A (SRA) and CD36. |
| 973 | 19521352 | Surface expression and function of CD36 and SRA to take up oxidized low-density lipoprotein (oxLDL) was determined by flow cytometry and quantitative confocal imaging. |
| 974 | 19521352 | These data support a role for FFAs in induction of insulin resistance and provide a link to atherogenic mechanisms mediated by expression of scavenger receptor CD36. |
| 975 | 19521352 | Lipid-induced insulin resistance is associated with increased monocyte expression of scavenger receptor CD36 and internalization of oxidized LDL. |
| 976 | 19521352 | We tested the relationship among lipid-induced insulin resistance, endothelial dysfunction, and monocyte capacity to form foam cells through scavenger receptor A (SRA) and CD36. |
| 977 | 19521352 | Surface expression and function of CD36 and SRA to take up oxidized low-density lipoprotein (oxLDL) was determined by flow cytometry and quantitative confocal imaging. |
| 978 | 19521352 | These data support a role for FFAs in induction of insulin resistance and provide a link to atherogenic mechanisms mediated by expression of scavenger receptor CD36. |
| 979 | 19521352 | Lipid-induced insulin resistance is associated with increased monocyte expression of scavenger receptor CD36 and internalization of oxidized LDL. |
| 980 | 19521352 | We tested the relationship among lipid-induced insulin resistance, endothelial dysfunction, and monocyte capacity to form foam cells through scavenger receptor A (SRA) and CD36. |
| 981 | 19521352 | Surface expression and function of CD36 and SRA to take up oxidized low-density lipoprotein (oxLDL) was determined by flow cytometry and quantitative confocal imaging. |
| 982 | 19521352 | These data support a role for FFAs in induction of insulin resistance and provide a link to atherogenic mechanisms mediated by expression of scavenger receptor CD36. |
| 983 | 19521352 | Lipid-induced insulin resistance is associated with increased monocyte expression of scavenger receptor CD36 and internalization of oxidized LDL. |
| 984 | 19521352 | We tested the relationship among lipid-induced insulin resistance, endothelial dysfunction, and monocyte capacity to form foam cells through scavenger receptor A (SRA) and CD36. |
| 985 | 19521352 | Surface expression and function of CD36 and SRA to take up oxidized low-density lipoprotein (oxLDL) was determined by flow cytometry and quantitative confocal imaging. |
| 986 | 19521352 | These data support a role for FFAs in induction of insulin resistance and provide a link to atherogenic mechanisms mediated by expression of scavenger receptor CD36. |
| 987 | 19666541 | TR4 nuclear receptor functions as a fatty acid sensor to modulate CD36 expression and foam cell formation. |
| 988 | 19666541 | Testicular orphan nuclear receptor 4 (TR4) is an orphan member of the nuclear receptor superfamily with diverse physiological functions. |
| 989 | 19666541 | Mechanistic dissection suggests that TR4 induces CD36 protein and mRNA expression via a transcriptional regulation. |
| 990 | 19666541 | Interestingly, we found this TR4-mediated CD36 transactivation can be further enhanced by polyunsaturated fatty acids (PUFAs), such as omega-3 and -6 fatty acids, and their metabolites such as 15-hydroxyeico-satetraonic acid (15-HETE) and 13-hydroxy octa-deca dieonic acid (13-HODE) and thiazolidinedione (TZD)-rosiglitazone. |
| 991 | 19666541 | Both electrophoretic mobility shift assays (EMSA) and chromatin immunoprecipitation (ChIP) assays demonstrate that TR4 binds to the TR4 response element located on the CD36 5'-promoter region for the induction of CD36 expression. |
| 992 | 19666541 | Stably transfected TR4-siRNA or functional TR4 cDNA in the RAW264.7 macrophage cells resulted in either decreased or increased CD36 expression with decreased or increased foam cell formation. |
| 993 | 19666541 | Restoring functional CD36 cDNA in the TR4 knockdown macrophage cells reversed the decreased foam cell formation. |
| 994 | 19666541 | Together, these results reveal an important signaling pathway controlling CD36-mediated foam cell formation/cardiovascular diseases, and findings that TR4 transactivation can be activated via its ligands/activators, such as PUFA metabolites and TZD, may provide a platform to screen new drug(s) to battle the metabolism syndrome, diabetes, and cardiovascular diseases. |
| 995 | 19666541 | TR4 nuclear receptor functions as a fatty acid sensor to modulate CD36 expression and foam cell formation. |
| 996 | 19666541 | Testicular orphan nuclear receptor 4 (TR4) is an orphan member of the nuclear receptor superfamily with diverse physiological functions. |
| 997 | 19666541 | Mechanistic dissection suggests that TR4 induces CD36 protein and mRNA expression via a transcriptional regulation. |
| 998 | 19666541 | Interestingly, we found this TR4-mediated CD36 transactivation can be further enhanced by polyunsaturated fatty acids (PUFAs), such as omega-3 and -6 fatty acids, and their metabolites such as 15-hydroxyeico-satetraonic acid (15-HETE) and 13-hydroxy octa-deca dieonic acid (13-HODE) and thiazolidinedione (TZD)-rosiglitazone. |
| 999 | 19666541 | Both electrophoretic mobility shift assays (EMSA) and chromatin immunoprecipitation (ChIP) assays demonstrate that TR4 binds to the TR4 response element located on the CD36 5'-promoter region for the induction of CD36 expression. |
| 1000 | 19666541 | Stably transfected TR4-siRNA or functional TR4 cDNA in the RAW264.7 macrophage cells resulted in either decreased or increased CD36 expression with decreased or increased foam cell formation. |
| 1001 | 19666541 | Restoring functional CD36 cDNA in the TR4 knockdown macrophage cells reversed the decreased foam cell formation. |
| 1002 | 19666541 | Together, these results reveal an important signaling pathway controlling CD36-mediated foam cell formation/cardiovascular diseases, and findings that TR4 transactivation can be activated via its ligands/activators, such as PUFA metabolites and TZD, may provide a platform to screen new drug(s) to battle the metabolism syndrome, diabetes, and cardiovascular diseases. |
| 1003 | 19666541 | TR4 nuclear receptor functions as a fatty acid sensor to modulate CD36 expression and foam cell formation. |
| 1004 | 19666541 | Testicular orphan nuclear receptor 4 (TR4) is an orphan member of the nuclear receptor superfamily with diverse physiological functions. |
| 1005 | 19666541 | Mechanistic dissection suggests that TR4 induces CD36 protein and mRNA expression via a transcriptional regulation. |
| 1006 | 19666541 | Interestingly, we found this TR4-mediated CD36 transactivation can be further enhanced by polyunsaturated fatty acids (PUFAs), such as omega-3 and -6 fatty acids, and their metabolites such as 15-hydroxyeico-satetraonic acid (15-HETE) and 13-hydroxy octa-deca dieonic acid (13-HODE) and thiazolidinedione (TZD)-rosiglitazone. |
| 1007 | 19666541 | Both electrophoretic mobility shift assays (EMSA) and chromatin immunoprecipitation (ChIP) assays demonstrate that TR4 binds to the TR4 response element located on the CD36 5'-promoter region for the induction of CD36 expression. |
| 1008 | 19666541 | Stably transfected TR4-siRNA or functional TR4 cDNA in the RAW264.7 macrophage cells resulted in either decreased or increased CD36 expression with decreased or increased foam cell formation. |
| 1009 | 19666541 | Restoring functional CD36 cDNA in the TR4 knockdown macrophage cells reversed the decreased foam cell formation. |
| 1010 | 19666541 | Together, these results reveal an important signaling pathway controlling CD36-mediated foam cell formation/cardiovascular diseases, and findings that TR4 transactivation can be activated via its ligands/activators, such as PUFA metabolites and TZD, may provide a platform to screen new drug(s) to battle the metabolism syndrome, diabetes, and cardiovascular diseases. |
| 1011 | 19666541 | TR4 nuclear receptor functions as a fatty acid sensor to modulate CD36 expression and foam cell formation. |
| 1012 | 19666541 | Testicular orphan nuclear receptor 4 (TR4) is an orphan member of the nuclear receptor superfamily with diverse physiological functions. |
| 1013 | 19666541 | Mechanistic dissection suggests that TR4 induces CD36 protein and mRNA expression via a transcriptional regulation. |
| 1014 | 19666541 | Interestingly, we found this TR4-mediated CD36 transactivation can be further enhanced by polyunsaturated fatty acids (PUFAs), such as omega-3 and -6 fatty acids, and their metabolites such as 15-hydroxyeico-satetraonic acid (15-HETE) and 13-hydroxy octa-deca dieonic acid (13-HODE) and thiazolidinedione (TZD)-rosiglitazone. |
| 1015 | 19666541 | Both electrophoretic mobility shift assays (EMSA) and chromatin immunoprecipitation (ChIP) assays demonstrate that TR4 binds to the TR4 response element located on the CD36 5'-promoter region for the induction of CD36 expression. |
| 1016 | 19666541 | Stably transfected TR4-siRNA or functional TR4 cDNA in the RAW264.7 macrophage cells resulted in either decreased or increased CD36 expression with decreased or increased foam cell formation. |
| 1017 | 19666541 | Restoring functional CD36 cDNA in the TR4 knockdown macrophage cells reversed the decreased foam cell formation. |
| 1018 | 19666541 | Together, these results reveal an important signaling pathway controlling CD36-mediated foam cell formation/cardiovascular diseases, and findings that TR4 transactivation can be activated via its ligands/activators, such as PUFA metabolites and TZD, may provide a platform to screen new drug(s) to battle the metabolism syndrome, diabetes, and cardiovascular diseases. |
| 1019 | 19666541 | TR4 nuclear receptor functions as a fatty acid sensor to modulate CD36 expression and foam cell formation. |
| 1020 | 19666541 | Testicular orphan nuclear receptor 4 (TR4) is an orphan member of the nuclear receptor superfamily with diverse physiological functions. |
| 1021 | 19666541 | Mechanistic dissection suggests that TR4 induces CD36 protein and mRNA expression via a transcriptional regulation. |
| 1022 | 19666541 | Interestingly, we found this TR4-mediated CD36 transactivation can be further enhanced by polyunsaturated fatty acids (PUFAs), such as omega-3 and -6 fatty acids, and their metabolites such as 15-hydroxyeico-satetraonic acid (15-HETE) and 13-hydroxy octa-deca dieonic acid (13-HODE) and thiazolidinedione (TZD)-rosiglitazone. |
| 1023 | 19666541 | Both electrophoretic mobility shift assays (EMSA) and chromatin immunoprecipitation (ChIP) assays demonstrate that TR4 binds to the TR4 response element located on the CD36 5'-promoter region for the induction of CD36 expression. |
| 1024 | 19666541 | Stably transfected TR4-siRNA or functional TR4 cDNA in the RAW264.7 macrophage cells resulted in either decreased or increased CD36 expression with decreased or increased foam cell formation. |
| 1025 | 19666541 | Restoring functional CD36 cDNA in the TR4 knockdown macrophage cells reversed the decreased foam cell formation. |
| 1026 | 19666541 | Together, these results reveal an important signaling pathway controlling CD36-mediated foam cell formation/cardiovascular diseases, and findings that TR4 transactivation can be activated via its ligands/activators, such as PUFA metabolites and TZD, may provide a platform to screen new drug(s) to battle the metabolism syndrome, diabetes, and cardiovascular diseases. |
| 1027 | 19666541 | TR4 nuclear receptor functions as a fatty acid sensor to modulate CD36 expression and foam cell formation. |
| 1028 | 19666541 | Testicular orphan nuclear receptor 4 (TR4) is an orphan member of the nuclear receptor superfamily with diverse physiological functions. |
| 1029 | 19666541 | Mechanistic dissection suggests that TR4 induces CD36 protein and mRNA expression via a transcriptional regulation. |
| 1030 | 19666541 | Interestingly, we found this TR4-mediated CD36 transactivation can be further enhanced by polyunsaturated fatty acids (PUFAs), such as omega-3 and -6 fatty acids, and their metabolites such as 15-hydroxyeico-satetraonic acid (15-HETE) and 13-hydroxy octa-deca dieonic acid (13-HODE) and thiazolidinedione (TZD)-rosiglitazone. |
| 1031 | 19666541 | Both electrophoretic mobility shift assays (EMSA) and chromatin immunoprecipitation (ChIP) assays demonstrate that TR4 binds to the TR4 response element located on the CD36 5'-promoter region for the induction of CD36 expression. |
| 1032 | 19666541 | Stably transfected TR4-siRNA or functional TR4 cDNA in the RAW264.7 macrophage cells resulted in either decreased or increased CD36 expression with decreased or increased foam cell formation. |
| 1033 | 19666541 | Restoring functional CD36 cDNA in the TR4 knockdown macrophage cells reversed the decreased foam cell formation. |
| 1034 | 19666541 | Together, these results reveal an important signaling pathway controlling CD36-mediated foam cell formation/cardiovascular diseases, and findings that TR4 transactivation can be activated via its ligands/activators, such as PUFA metabolites and TZD, may provide a platform to screen new drug(s) to battle the metabolism syndrome, diabetes, and cardiovascular diseases. |
| 1035 | 19666541 | TR4 nuclear receptor functions as a fatty acid sensor to modulate CD36 expression and foam cell formation. |
| 1036 | 19666541 | Testicular orphan nuclear receptor 4 (TR4) is an orphan member of the nuclear receptor superfamily with diverse physiological functions. |
| 1037 | 19666541 | Mechanistic dissection suggests that TR4 induces CD36 protein and mRNA expression via a transcriptional regulation. |
| 1038 | 19666541 | Interestingly, we found this TR4-mediated CD36 transactivation can be further enhanced by polyunsaturated fatty acids (PUFAs), such as omega-3 and -6 fatty acids, and their metabolites such as 15-hydroxyeico-satetraonic acid (15-HETE) and 13-hydroxy octa-deca dieonic acid (13-HODE) and thiazolidinedione (TZD)-rosiglitazone. |
| 1039 | 19666541 | Both electrophoretic mobility shift assays (EMSA) and chromatin immunoprecipitation (ChIP) assays demonstrate that TR4 binds to the TR4 response element located on the CD36 5'-promoter region for the induction of CD36 expression. |
| 1040 | 19666541 | Stably transfected TR4-siRNA or functional TR4 cDNA in the RAW264.7 macrophage cells resulted in either decreased or increased CD36 expression with decreased or increased foam cell formation. |
| 1041 | 19666541 | Restoring functional CD36 cDNA in the TR4 knockdown macrophage cells reversed the decreased foam cell formation. |
| 1042 | 19666541 | Together, these results reveal an important signaling pathway controlling CD36-mediated foam cell formation/cardiovascular diseases, and findings that TR4 transactivation can be activated via its ligands/activators, such as PUFA metabolites and TZD, may provide a platform to screen new drug(s) to battle the metabolism syndrome, diabetes, and cardiovascular diseases. |
| 1043 | 19675275 | Thus, in red, but not white, muscle of insulin-resistant and type 2 diabetic animals, a marked upregulation in fatty acid transport and intramuscular triacylglycerol was associated with increased levels of FAT/CD36 expression and plasmalemmal content. |
| 1044 | 19675275 | Thus insulin resistance and type 2 diabetes are accompanied by tissue-specific differences in FAT/CD36 and fatty acid transport and metabolism. |
| 1045 | 19675275 | Thus, in red, but not white, muscle of insulin-resistant and type 2 diabetic animals, a marked upregulation in fatty acid transport and intramuscular triacylglycerol was associated with increased levels of FAT/CD36 expression and plasmalemmal content. |
| 1046 | 19675275 | Thus insulin resistance and type 2 diabetes are accompanied by tissue-specific differences in FAT/CD36 and fatty acid transport and metabolism. |
| 1047 | 19699280 | Furthermore, the results of quantitative RT-PCR analysis showed that emodin significantly elevated the mRNA expression level of PPARgamma and regulated the mRNA expressions of LPL, FAT/CD36, resistin and FABPs (ap2) in liver and adipocyte tissues. |
| 1048 | 19819977 | Expression of the orphan nuclear receptor Nur77, which is induced by beta-adrenergic signaling and is associated with insulin sensitivity, was lower in LCR (P < 0.05). |
| 1049 | 19819977 | Muscle protein content of Nur77 target genes, including uncoupling protein 3, fatty acid translocase/CD36, and the AMPK gamma3 subunit were also lower in LCR (P < 0.05). |
| 1050 | 19865095 | AGE-modified collagens I and III induce keratinocyte terminal differentiation through AGE receptor CD36: epidermal-dermal interaction in acquired perforating dermatosis. |
| 1051 | 19865095 | The expression of involucrin (INV) and keratin 10 was significantly enhanced in normal human KCs grown on AGE-modified collagen I or III compared with cells grown on unmodified collagen I or III. |
| 1052 | 19865095 | Glycated collagens I and III preferentially induced the expression of AGE receptor CD36, but not of other AGE receptors. |
| 1053 | 19865095 | Glycated collagen I- and III-induced INV expression was partially blocked by the anti-CD36 antibody (Ab). |
| 1054 | 19865095 | These results suggest that exposing KCs to AGE-modified interstitial collagen (types I and III) by scratching induces terminal differentiation of KCs via the AGE receptor (CD36), leading to the upward movement of KCs together with glycated collagen. |
| 1055 | 19865095 | AGE-modified collagens I and III induce keratinocyte terminal differentiation through AGE receptor CD36: epidermal-dermal interaction in acquired perforating dermatosis. |
| 1056 | 19865095 | The expression of involucrin (INV) and keratin 10 was significantly enhanced in normal human KCs grown on AGE-modified collagen I or III compared with cells grown on unmodified collagen I or III. |
| 1057 | 19865095 | Glycated collagens I and III preferentially induced the expression of AGE receptor CD36, but not of other AGE receptors. |
| 1058 | 19865095 | Glycated collagen I- and III-induced INV expression was partially blocked by the anti-CD36 antibody (Ab). |
| 1059 | 19865095 | These results suggest that exposing KCs to AGE-modified interstitial collagen (types I and III) by scratching induces terminal differentiation of KCs via the AGE receptor (CD36), leading to the upward movement of KCs together with glycated collagen. |
| 1060 | 19865095 | AGE-modified collagens I and III induce keratinocyte terminal differentiation through AGE receptor CD36: epidermal-dermal interaction in acquired perforating dermatosis. |
| 1061 | 19865095 | The expression of involucrin (INV) and keratin 10 was significantly enhanced in normal human KCs grown on AGE-modified collagen I or III compared with cells grown on unmodified collagen I or III. |
| 1062 | 19865095 | Glycated collagens I and III preferentially induced the expression of AGE receptor CD36, but not of other AGE receptors. |
| 1063 | 19865095 | Glycated collagen I- and III-induced INV expression was partially blocked by the anti-CD36 antibody (Ab). |
| 1064 | 19865095 | These results suggest that exposing KCs to AGE-modified interstitial collagen (types I and III) by scratching induces terminal differentiation of KCs via the AGE receptor (CD36), leading to the upward movement of KCs together with glycated collagen. |
| 1065 | 20008269 | Coculture with HVSMCs increased CD36 expression in THP-1 cells, and this was significantly augmented by treatment of HVSMCs with S100B or HG. |
| 1066 | 20013249 | In this model, the use of whole genome sequencing and gene expression profiling techniques, linkage and correlation analyses in recombinant inbred strains, and in vitro and in vivo functional studies in congenic and transgenic lines has recently enabled molecular identification of quantitative trait loci (QTLs) relevant to the metabolic syndrome: (1) a deletion variant in Cd36 (fatty acid translocase) responsible for QTLs on chromosome 4 associated with dyslipidemia, insulin resistance and hypertension, (2) mutated Srebf1 (sterol regulatory element binding factor 1) as a QTL on chromosome 10 influencing dietary-induced changes in hepatic cholesterol levels, and (3) Ogn (osteoglycin) as a QTL on chromosome 17 associated with left ventricular hypertrophy. |
| 1067 | 20094041 | Although germ-line deletion of c-Jun NH(2)-terminal kinase (JNK) improves overall insulin sensitivity in mice, those studies could not reveal the underlying molecular mechanism and the tissue site(s) in which reduced JNK activity elicits the observed phenotype. |
| 1068 | 20094041 | Given its importance in nonesterified fatty acids (NEFA) and glucose utilization, we hypothesized that the insulin-sensitive phenotype associated with Jnk deletion originates from loss of JNK function in skeletal muscle. |
| 1069 | 20094041 | We show for the first time that cellular JNK2- and JNK1/JNK2-deficiency divert glucose from oxidation to glycogenesis due to increased glycogen synthase (GS) activity and induction of Pdk4. |
| 1070 | 20094041 | We further show that JNK2- and JNK1/JNK2-deficiency profoundly increase cellular NEFA oxidation, and their conversion to phospholipids and triglyceride. |
| 1071 | 20094041 | The increased NEFA utilization was coupled to increased expressions of selective NEFA handling genes including Cd36, Acsl4, and Chka, and enhanced palmitic acid (PA)-dependent suppression of acetyl-CoA carboxylase (Acc). |
| 1072 | 20094041 | In JNK-intact cells, PA inhibited insulin signaling and glycogenesis. |
| 1073 | 20094041 | Although silencing Jnk1 and/or Jnk2 prevented PA-induced inhibition of insulin signaling, it did not completely block decreased insulin-mediated glycogenesis, thus indicating JNK-independent pathways in the suppression of glycogenesis by PA. |
| 1074 | 20094041 | Muscle-specific inhibition of JNK2 (or total JNK) improves the capacity of NEFA utilization and glycogenesis, and is a potential therapeutic target for improving systemic insulin sensitivity in type 2 diabetes (T2D). |
| 1075 | 20134099 | Atorvastatin downregulates monocyte CD36 expression, nuclear NFkappaB and TNFalpha levels in type 2 diabetes. |
| 1076 | 20158099 | Peroxisome proliferator-activated receptor (PPAR) gamma is a nuclear receptor and ligand-activated transcription factor which plays important roles in the control of energy balance. |
| 1077 | 20158099 | The thiazolidinediones (TZDs), in use as an insulin-sensitizing agent, are well known as the PPARgamma agonist. |
| 1078 | 20158099 | Recent studies reported that PPARgamma agonists involve in lipid metabolism through regulating genes including lipoprotein lipase, CD36, and ABCA1. |
| 1079 | 20159856 | These abnormalities were associated with reduced Glut4 mRNA expression and increased Cd36 mRNA expression and mitochondrial carnitine palmitoyltransferase 1 activity (P < 0.05). |
| 1080 | 20332082 | Some of these novel candidate proteins such as GFPT1, CD36, PLAA (phospholipase A(2)-activating protein), METTL7B, SLC30A1, several G signaling proteins, and the sulfide-metabolizing ETHE1 and SQRDL (sulfide-quinone reductase-like) might be considered as drug targets for the treatment of metabolic syndrome. |
| 1081 | 20693579 | The mRNA levels of peroxidase proliferator-activated receptor (PPAR) γ and CCAAT/enhancer-binding protein α (C/EBPα), but not CCAAT/enhancer-binding protein ((C/EBP) β and δ, were reduced by UVA. |
| 1082 | 20693579 | Moreover, the mRNA levels of PPAR γ target genes (lipoprotein lipase (LPL), CD36, adipocyte protein (aP2), and liver X receptor α (LXR)) were down-regulated by UVA. |
| 1083 | 20693579 | Additionally, attempts to elucidate a possible mechanism underlying the UVA-mediated effects revealed that UVA induced migration inhibitory factor (MIF) gene expression, and this was mediated through activation of AP-1 (especially JNK and p42/44 MAPK) and nuclear factor-κB. |
| 1084 | 20693579 | AMP-activated protein kinase phosphorylation and up-regulation of Kruppel-like factor 2 (KLF2) were induced by UVA. |
| 1085 | 20693579 | Taken together, these findings suggest that the inhibition of adipogenic differentiation of human adipose tissue-derived mesenchymal stem cells by UVA occurs primarily through the reduced expression of PPAR γ, which is mediated by up-regulation of KLF2 via the activation of MIF-AMP-activated protein kinase signaling. |
| 1086 | 20966915 | Variants in the CD36 gene locus determine whole-body adiposity, but have no independent effect on insulin sensitivity. |
| 1087 | 20966915 | In contrast, the effect of single-nucleotide polymorphisms (SNPs) in CD36 on insulin resistance is controversial in literature. |
| 1088 | 20966915 | Therefore, we investigated whether genetic variation within the CD36 gene locus affects insulin resistance in a well-phenotyped cohort of white European subjects at increased risk for type 2 diabetes. |
| 1089 | 20966915 | No reliable association was detected between the six CD36 SNPs and insulin sensitivity or ectopic hepatic lipid accumulation after adjustment for age, gender, and BMI. |
| 1090 | 20966915 | In the long run, genetic variation within the CD36 locus may contribute to metabolic disease via its effect on body adiposity, but not via an independent effect on insulin sensitivity. |
| 1091 | 20966915 | Variants in the CD36 gene locus determine whole-body adiposity, but have no independent effect on insulin sensitivity. |
| 1092 | 20966915 | In contrast, the effect of single-nucleotide polymorphisms (SNPs) in CD36 on insulin resistance is controversial in literature. |
| 1093 | 20966915 | Therefore, we investigated whether genetic variation within the CD36 gene locus affects insulin resistance in a well-phenotyped cohort of white European subjects at increased risk for type 2 diabetes. |
| 1094 | 20966915 | No reliable association was detected between the six CD36 SNPs and insulin sensitivity or ectopic hepatic lipid accumulation after adjustment for age, gender, and BMI. |
| 1095 | 20966915 | In the long run, genetic variation within the CD36 locus may contribute to metabolic disease via its effect on body adiposity, but not via an independent effect on insulin sensitivity. |
| 1096 | 20966915 | Variants in the CD36 gene locus determine whole-body adiposity, but have no independent effect on insulin sensitivity. |
| 1097 | 20966915 | In contrast, the effect of single-nucleotide polymorphisms (SNPs) in CD36 on insulin resistance is controversial in literature. |
| 1098 | 20966915 | Therefore, we investigated whether genetic variation within the CD36 gene locus affects insulin resistance in a well-phenotyped cohort of white European subjects at increased risk for type 2 diabetes. |
| 1099 | 20966915 | No reliable association was detected between the six CD36 SNPs and insulin sensitivity or ectopic hepatic lipid accumulation after adjustment for age, gender, and BMI. |
| 1100 | 20966915 | In the long run, genetic variation within the CD36 locus may contribute to metabolic disease via its effect on body adiposity, but not via an independent effect on insulin sensitivity. |
| 1101 | 20966915 | Variants in the CD36 gene locus determine whole-body adiposity, but have no independent effect on insulin sensitivity. |
| 1102 | 20966915 | In contrast, the effect of single-nucleotide polymorphisms (SNPs) in CD36 on insulin resistance is controversial in literature. |
| 1103 | 20966915 | Therefore, we investigated whether genetic variation within the CD36 gene locus affects insulin resistance in a well-phenotyped cohort of white European subjects at increased risk for type 2 diabetes. |
| 1104 | 20966915 | No reliable association was detected between the six CD36 SNPs and insulin sensitivity or ectopic hepatic lipid accumulation after adjustment for age, gender, and BMI. |
| 1105 | 20966915 | In the long run, genetic variation within the CD36 locus may contribute to metabolic disease via its effect on body adiposity, but not via an independent effect on insulin sensitivity. |
| 1106 | 20966915 | Variants in the CD36 gene locus determine whole-body adiposity, but have no independent effect on insulin sensitivity. |
| 1107 | 20966915 | In contrast, the effect of single-nucleotide polymorphisms (SNPs) in CD36 on insulin resistance is controversial in literature. |
| 1108 | 20966915 | Therefore, we investigated whether genetic variation within the CD36 gene locus affects insulin resistance in a well-phenotyped cohort of white European subjects at increased risk for type 2 diabetes. |
| 1109 | 20966915 | No reliable association was detected between the six CD36 SNPs and insulin sensitivity or ectopic hepatic lipid accumulation after adjustment for age, gender, and BMI. |
| 1110 | 20966915 | In the long run, genetic variation within the CD36 locus may contribute to metabolic disease via its effect on body adiposity, but not via an independent effect on insulin sensitivity. |
| 1111 | 21031614 | IOWE stimulated gene expression of C/EBPα (CCAAT/enhancer-binding protein α) and PPARγ (peroxisome proliferator-activated receptors γ) during adipocyte differentiation, and induced the expression of PPARγ target genes such as aP2 (adipocyte protein 2), LPL (lipoprotein lipase) and CD36 (fatty acid translocase). |
| 1112 | 21136146 | The myocardial expression of LXRα target genes, long-chain acyl-CoA synthetase 3 (ACSL3), fatty acid transporter protein (FAT/CD36), ATP-binding cassette transporter A1 (ABCA1), and ABCG1 were also detected. |
| 1113 | 21136146 | The mRNA expression levels of ACSL3 and FAT/CD36 and the protein expression levels of ABCA1 and ABCG1 were also markedly increased in different heart chambers of diabetic rats. |
| 1114 | 21136146 | The myocardial expression of LXRα target genes, long-chain acyl-CoA synthetase 3 (ACSL3), fatty acid transporter protein (FAT/CD36), ATP-binding cassette transporter A1 (ABCA1), and ABCG1 were also detected. |
| 1115 | 21136146 | The mRNA expression levels of ACSL3 and FAT/CD36 and the protein expression levels of ABCA1 and ABCG1 were also markedly increased in different heart chambers of diabetic rats. |
| 1116 | 21186102 | Evidence has been reported that chemokine CXCL16, rather than CD36, is the main scavenger receptor in human podocytes mediating the uptake of ox-LDL. |
| 1117 | 21186102 | It has been recently shown that nephrin once phosphorilated associates with PI3K and stimulates the Akt dependent signaling. |
| 1118 | 21186102 | Notably CXCL16 are the main receptors for the uptake of ox-LDL in podocytes, whereas CD36 plays this role in tubular renal cells. |
| 1119 | 21186102 | Evidence has been reported that chemokine CXCL16, rather than CD36, is the main scavenger receptor in human podocytes mediating the uptake of ox-LDL. |
| 1120 | 21186102 | It has been recently shown that nephrin once phosphorilated associates with PI3K and stimulates the Akt dependent signaling. |
| 1121 | 21186102 | Notably CXCL16 are the main receptors for the uptake of ox-LDL in podocytes, whereas CD36 plays this role in tubular renal cells. |
| 1122 | 21216462 | Impairments in leptin-melanocortin signaling are associated with insulin-deficient diabetes and leptin treatment has been shown to be effective in reversing hyperglycemia in animal models of type 1 diabetes. |
| 1123 | 21216462 | MTII treatment did not alter expression levels of genes encoding gluconeogenic enzymes including glucose-6-phosphatase (G6Pase) and phosphoenolpyruvate carboxykinase (PEPCK), in the liver of diabetic mice. |
| 1124 | 21216462 | MTII treatment also significantly reduced expression levels of hormone sensitive lipase (HSL) and adipose triglyceride lipase (ATGL) mRNA in white adipose tissue of diabetic mice without a significant change in serum insulin levels. |
| 1125 | 21216462 | Expression levels of lipoprotein lipase (LPL) and fatty acid translocase (FAT/CD36) mRNA in white adipose tissue and skeletal muscle were not changed by MTII treatment. |
| 1126 | 21250778 | Recent literature has implicated CD36 in the pathogenesis of metabolic dysregulation such as found in obesity, insulin resistance, and atherosclerosis. |
| 1127 | 21262584 | The macrophage Ox-LDL receptor, CD36 and its association with type II diabetes mellitus. |
| 1128 | 21262584 | In addition to Ox-LDL, raised levels of glucose, insulin resistance, low HDL cholesterol, increased levels of free fatty acid (FFA) all result in increased expression of CD36, thereby contributing to T2DM and related atherosclerosis. |
| 1129 | 21262584 | Adipocytokines such as tumor necrosis factor-alpha (TNF-α), C-reactive protein (CRP), adiponectin, leptin, resistin along with peroxisome proliferator activated receptor-γ (PPAR-γ) are important mediators in glucose homeostasis in association with CD36 and can be used as markers for T2DM and atherosclerosis. |
| 1130 | 21262584 | The macrophage Ox-LDL receptor, CD36 and its association with type II diabetes mellitus. |
| 1131 | 21262584 | In addition to Ox-LDL, raised levels of glucose, insulin resistance, low HDL cholesterol, increased levels of free fatty acid (FFA) all result in increased expression of CD36, thereby contributing to T2DM and related atherosclerosis. |
| 1132 | 21262584 | Adipocytokines such as tumor necrosis factor-alpha (TNF-α), C-reactive protein (CRP), adiponectin, leptin, resistin along with peroxisome proliferator activated receptor-γ (PPAR-γ) are important mediators in glucose homeostasis in association with CD36 and can be used as markers for T2DM and atherosclerosis. |
| 1133 | 21262584 | The macrophage Ox-LDL receptor, CD36 and its association with type II diabetes mellitus. |
| 1134 | 21262584 | In addition to Ox-LDL, raised levels of glucose, insulin resistance, low HDL cholesterol, increased levels of free fatty acid (FFA) all result in increased expression of CD36, thereby contributing to T2DM and related atherosclerosis. |
| 1135 | 21262584 | Adipocytokines such as tumor necrosis factor-alpha (TNF-α), C-reactive protein (CRP), adiponectin, leptin, resistin along with peroxisome proliferator activated receptor-γ (PPAR-γ) are important mediators in glucose homeostasis in association with CD36 and can be used as markers for T2DM and atherosclerosis. |
| 1136 | 21296063 | Metoprolol inhibited CPT-1 without affecting CD36 translocation, associated with increased accumulation of triglycerides and long chain acyl CoA in the cytoplasm, and no effect on oxidative stress. |
| 1137 | 21296063 | Metoprolol induced a shift from protein kinase A to protein kinase B-mediated signaling, associated with a shift in the phosphorylation patterns of BCl-2 and Bad which favored BCl-2 action. |
| 1138 | 21296212 | Inter Cellular Adhesion Molecule (ICAM-1), CD31, CD36 and glycans are potential receptors for PfEMP1 of RBCs parasited by plasmodium falciparum. |
| 1139 | 21296212 | This mutation stimulates erythropoiesis and is the cause of Lu/BCAM (CD239) phosphorylation, which potentiated the interaction with laminin alpha 5. |
| 1140 | 21296212 | The couple laminin alpha 5 endothelial and phosphorylated Lu/BCAM explained the increased adhesion of RBCs from patients PV to endothelium. |
| 1141 | 21347706 | Some differentially expressed proteins in particular, including fatty acid translocase (FAT)/CD36, fatty acid binding protein, lipoprotein lipase, acetyl CoA acyltransferase, carnitine O-palmitoyltransferase 2, sterol carrier protein, adiponectin, and phosphoenolpyruvate carboxykinase could explain the current action mechanism of TZDs. |
| 1142 | 21347706 | Furthermore, this study is the first to report on two potential target proteins of rosiglitazone, such as adenomatosis polyposis coli 2 (APC2), and eukaryotic translation initiation factor 5A-1 (eIF5A) related to apoptosis and cell division. |
| 1143 | 21378177 | Hematopoietic cell-restricted deletion of CD36 reduces high-fat diet-induced macrophage infiltration and improves insulin signaling in adipose tissue. |
| 1144 | 21454644 | CD36 protein is involved in store-operated calcium flux, phospholipase A2 activation, and production of prostaglandin E2. |
| 1145 | 21454644 | Calcium influx after ER calcium release resulted in phosphorylation of cPLA(2) and its translocation to membranes in a CD36-dependent manner. |
| 1146 | 21454644 | Peritoneal macrophages from CD36(-/-) mice exhibited diminished calcium transients and reduced AA release after thapsigargin or UTP treatment with decreased ERK1/2 and cPLA(2) phosphorylation. |
| 1147 | 21454644 | CD36 protein is involved in store-operated calcium flux, phospholipase A2 activation, and production of prostaglandin E2. |
| 1148 | 21454644 | Calcium influx after ER calcium release resulted in phosphorylation of cPLA(2) and its translocation to membranes in a CD36-dependent manner. |
| 1149 | 21454644 | Peritoneal macrophages from CD36(-/-) mice exhibited diminished calcium transients and reduced AA release after thapsigargin or UTP treatment with decreased ERK1/2 and cPLA(2) phosphorylation. |
| 1150 | 21454644 | CD36 protein is involved in store-operated calcium flux, phospholipase A2 activation, and production of prostaglandin E2. |
| 1151 | 21454644 | Calcium influx after ER calcium release resulted in phosphorylation of cPLA(2) and its translocation to membranes in a CD36-dependent manner. |
| 1152 | 21454644 | Peritoneal macrophages from CD36(-/-) mice exhibited diminished calcium transients and reduced AA release after thapsigargin or UTP treatment with decreased ERK1/2 and cPLA(2) phosphorylation. |
| 1153 | 21491468 | Immunocytochemical analyses of fibroblasts isolated from these biopsies confirmed a significant increase of the epidermal and connective wound-healing markers such as collagen type I, collagen type IV, cytokeratin 1 (CK1), CK5, CK10 and CK14 versus controls. |
| 1154 | 21547502 | Subcellular trafficking of the substrate transporters GLUT4 and CD36 in cardiomyocytes. |
| 1155 | 21547502 | These substrates are transported into the cell by glucose transporter 4 (GLUT4) and the fatty acid transporter CD36. |
| 1156 | 21547502 | Besides being located at the sarcolemma, GLUT4 and CD36 are stored in intracellular compartments. |
| 1157 | 21547502 | Raised plasma insulin concentrations and increased cardiac work will stimulate GLUT4 as well as CD36 to translocate to the sarcolemma. |
| 1158 | 21547502 | As so far studied, signaling pathways that regulate GLUT4 translocation similarly affect CD36 translocation. |
| 1159 | 21547502 | During the development of insulin resistance and type 2 diabetes, CD36 becomes permanently localized at the sarcolemma, whereas GLUT4 internalizes. |
| 1160 | 21547502 | This juxtaposed positioning of GLUT4 and CD36 is important for aberrant substrate uptake in the diabetic heart: chronically increased fatty acid uptake at the expense of glucose. |
| 1161 | 21547502 | To explain the differences in subcellular localization of GLUT4 and CD36 in type 2 diabetes, recent research has focused on the role of proteins involved in trafficking of cargo between subcellular compartments. |
| 1162 | 21547502 | Several of these proteins appear to be similarly involved in both GLUT4 and CD36 translocation. |
| 1163 | 21547502 | Others, however, have different roles in either GLUT4 or CD36 translocation. |
| 1164 | 21547502 | These trafficking components, which are differently involved in GLUT4 or CD36 translocation, may be considered novel targets for the development of therapies to restore the imbalanced substrate utilization that occurs in obesity, insulin resistance and diabetic cardiomyopathy. |
| 1165 | 21547502 | Subcellular trafficking of the substrate transporters GLUT4 and CD36 in cardiomyocytes. |
| 1166 | 21547502 | These substrates are transported into the cell by glucose transporter 4 (GLUT4) and the fatty acid transporter CD36. |
| 1167 | 21547502 | Besides being located at the sarcolemma, GLUT4 and CD36 are stored in intracellular compartments. |
| 1168 | 21547502 | Raised plasma insulin concentrations and increased cardiac work will stimulate GLUT4 as well as CD36 to translocate to the sarcolemma. |
| 1169 | 21547502 | As so far studied, signaling pathways that regulate GLUT4 translocation similarly affect CD36 translocation. |
| 1170 | 21547502 | During the development of insulin resistance and type 2 diabetes, CD36 becomes permanently localized at the sarcolemma, whereas GLUT4 internalizes. |
| 1171 | 21547502 | This juxtaposed positioning of GLUT4 and CD36 is important for aberrant substrate uptake in the diabetic heart: chronically increased fatty acid uptake at the expense of glucose. |
| 1172 | 21547502 | To explain the differences in subcellular localization of GLUT4 and CD36 in type 2 diabetes, recent research has focused on the role of proteins involved in trafficking of cargo between subcellular compartments. |
| 1173 | 21547502 | Several of these proteins appear to be similarly involved in both GLUT4 and CD36 translocation. |
| 1174 | 21547502 | Others, however, have different roles in either GLUT4 or CD36 translocation. |
| 1175 | 21547502 | These trafficking components, which are differently involved in GLUT4 or CD36 translocation, may be considered novel targets for the development of therapies to restore the imbalanced substrate utilization that occurs in obesity, insulin resistance and diabetic cardiomyopathy. |
| 1176 | 21547502 | Subcellular trafficking of the substrate transporters GLUT4 and CD36 in cardiomyocytes. |
| 1177 | 21547502 | These substrates are transported into the cell by glucose transporter 4 (GLUT4) and the fatty acid transporter CD36. |
| 1178 | 21547502 | Besides being located at the sarcolemma, GLUT4 and CD36 are stored in intracellular compartments. |
| 1179 | 21547502 | Raised plasma insulin concentrations and increased cardiac work will stimulate GLUT4 as well as CD36 to translocate to the sarcolemma. |
| 1180 | 21547502 | As so far studied, signaling pathways that regulate GLUT4 translocation similarly affect CD36 translocation. |
| 1181 | 21547502 | During the development of insulin resistance and type 2 diabetes, CD36 becomes permanently localized at the sarcolemma, whereas GLUT4 internalizes. |
| 1182 | 21547502 | This juxtaposed positioning of GLUT4 and CD36 is important for aberrant substrate uptake in the diabetic heart: chronically increased fatty acid uptake at the expense of glucose. |
| 1183 | 21547502 | To explain the differences in subcellular localization of GLUT4 and CD36 in type 2 diabetes, recent research has focused on the role of proteins involved in trafficking of cargo between subcellular compartments. |
| 1184 | 21547502 | Several of these proteins appear to be similarly involved in both GLUT4 and CD36 translocation. |
| 1185 | 21547502 | Others, however, have different roles in either GLUT4 or CD36 translocation. |
| 1186 | 21547502 | These trafficking components, which are differently involved in GLUT4 or CD36 translocation, may be considered novel targets for the development of therapies to restore the imbalanced substrate utilization that occurs in obesity, insulin resistance and diabetic cardiomyopathy. |
| 1187 | 21547502 | Subcellular trafficking of the substrate transporters GLUT4 and CD36 in cardiomyocytes. |
| 1188 | 21547502 | These substrates are transported into the cell by glucose transporter 4 (GLUT4) and the fatty acid transporter CD36. |
| 1189 | 21547502 | Besides being located at the sarcolemma, GLUT4 and CD36 are stored in intracellular compartments. |
| 1190 | 21547502 | Raised plasma insulin concentrations and increased cardiac work will stimulate GLUT4 as well as CD36 to translocate to the sarcolemma. |
| 1191 | 21547502 | As so far studied, signaling pathways that regulate GLUT4 translocation similarly affect CD36 translocation. |
| 1192 | 21547502 | During the development of insulin resistance and type 2 diabetes, CD36 becomes permanently localized at the sarcolemma, whereas GLUT4 internalizes. |
| 1193 | 21547502 | This juxtaposed positioning of GLUT4 and CD36 is important for aberrant substrate uptake in the diabetic heart: chronically increased fatty acid uptake at the expense of glucose. |
| 1194 | 21547502 | To explain the differences in subcellular localization of GLUT4 and CD36 in type 2 diabetes, recent research has focused on the role of proteins involved in trafficking of cargo between subcellular compartments. |
| 1195 | 21547502 | Several of these proteins appear to be similarly involved in both GLUT4 and CD36 translocation. |
| 1196 | 21547502 | Others, however, have different roles in either GLUT4 or CD36 translocation. |
| 1197 | 21547502 | These trafficking components, which are differently involved in GLUT4 or CD36 translocation, may be considered novel targets for the development of therapies to restore the imbalanced substrate utilization that occurs in obesity, insulin resistance and diabetic cardiomyopathy. |
| 1198 | 21547502 | Subcellular trafficking of the substrate transporters GLUT4 and CD36 in cardiomyocytes. |
| 1199 | 21547502 | These substrates are transported into the cell by glucose transporter 4 (GLUT4) and the fatty acid transporter CD36. |
| 1200 | 21547502 | Besides being located at the sarcolemma, GLUT4 and CD36 are stored in intracellular compartments. |
| 1201 | 21547502 | Raised plasma insulin concentrations and increased cardiac work will stimulate GLUT4 as well as CD36 to translocate to the sarcolemma. |
| 1202 | 21547502 | As so far studied, signaling pathways that regulate GLUT4 translocation similarly affect CD36 translocation. |
| 1203 | 21547502 | During the development of insulin resistance and type 2 diabetes, CD36 becomes permanently localized at the sarcolemma, whereas GLUT4 internalizes. |
| 1204 | 21547502 | This juxtaposed positioning of GLUT4 and CD36 is important for aberrant substrate uptake in the diabetic heart: chronically increased fatty acid uptake at the expense of glucose. |
| 1205 | 21547502 | To explain the differences in subcellular localization of GLUT4 and CD36 in type 2 diabetes, recent research has focused on the role of proteins involved in trafficking of cargo between subcellular compartments. |
| 1206 | 21547502 | Several of these proteins appear to be similarly involved in both GLUT4 and CD36 translocation. |
| 1207 | 21547502 | Others, however, have different roles in either GLUT4 or CD36 translocation. |
| 1208 | 21547502 | These trafficking components, which are differently involved in GLUT4 or CD36 translocation, may be considered novel targets for the development of therapies to restore the imbalanced substrate utilization that occurs in obesity, insulin resistance and diabetic cardiomyopathy. |
| 1209 | 21547502 | Subcellular trafficking of the substrate transporters GLUT4 and CD36 in cardiomyocytes. |
| 1210 | 21547502 | These substrates are transported into the cell by glucose transporter 4 (GLUT4) and the fatty acid transporter CD36. |
| 1211 | 21547502 | Besides being located at the sarcolemma, GLUT4 and CD36 are stored in intracellular compartments. |
| 1212 | 21547502 | Raised plasma insulin concentrations and increased cardiac work will stimulate GLUT4 as well as CD36 to translocate to the sarcolemma. |
| 1213 | 21547502 | As so far studied, signaling pathways that regulate GLUT4 translocation similarly affect CD36 translocation. |
| 1214 | 21547502 | During the development of insulin resistance and type 2 diabetes, CD36 becomes permanently localized at the sarcolemma, whereas GLUT4 internalizes. |
| 1215 | 21547502 | This juxtaposed positioning of GLUT4 and CD36 is important for aberrant substrate uptake in the diabetic heart: chronically increased fatty acid uptake at the expense of glucose. |
| 1216 | 21547502 | To explain the differences in subcellular localization of GLUT4 and CD36 in type 2 diabetes, recent research has focused on the role of proteins involved in trafficking of cargo between subcellular compartments. |
| 1217 | 21547502 | Several of these proteins appear to be similarly involved in both GLUT4 and CD36 translocation. |
| 1218 | 21547502 | Others, however, have different roles in either GLUT4 or CD36 translocation. |
| 1219 | 21547502 | These trafficking components, which are differently involved in GLUT4 or CD36 translocation, may be considered novel targets for the development of therapies to restore the imbalanced substrate utilization that occurs in obesity, insulin resistance and diabetic cardiomyopathy. |
| 1220 | 21547502 | Subcellular trafficking of the substrate transporters GLUT4 and CD36 in cardiomyocytes. |
| 1221 | 21547502 | These substrates are transported into the cell by glucose transporter 4 (GLUT4) and the fatty acid transporter CD36. |
| 1222 | 21547502 | Besides being located at the sarcolemma, GLUT4 and CD36 are stored in intracellular compartments. |
| 1223 | 21547502 | Raised plasma insulin concentrations and increased cardiac work will stimulate GLUT4 as well as CD36 to translocate to the sarcolemma. |
| 1224 | 21547502 | As so far studied, signaling pathways that regulate GLUT4 translocation similarly affect CD36 translocation. |
| 1225 | 21547502 | During the development of insulin resistance and type 2 diabetes, CD36 becomes permanently localized at the sarcolemma, whereas GLUT4 internalizes. |
| 1226 | 21547502 | This juxtaposed positioning of GLUT4 and CD36 is important for aberrant substrate uptake in the diabetic heart: chronically increased fatty acid uptake at the expense of glucose. |
| 1227 | 21547502 | To explain the differences in subcellular localization of GLUT4 and CD36 in type 2 diabetes, recent research has focused on the role of proteins involved in trafficking of cargo between subcellular compartments. |
| 1228 | 21547502 | Several of these proteins appear to be similarly involved in both GLUT4 and CD36 translocation. |
| 1229 | 21547502 | Others, however, have different roles in either GLUT4 or CD36 translocation. |
| 1230 | 21547502 | These trafficking components, which are differently involved in GLUT4 or CD36 translocation, may be considered novel targets for the development of therapies to restore the imbalanced substrate utilization that occurs in obesity, insulin resistance and diabetic cardiomyopathy. |
| 1231 | 21547502 | Subcellular trafficking of the substrate transporters GLUT4 and CD36 in cardiomyocytes. |
| 1232 | 21547502 | These substrates are transported into the cell by glucose transporter 4 (GLUT4) and the fatty acid transporter CD36. |
| 1233 | 21547502 | Besides being located at the sarcolemma, GLUT4 and CD36 are stored in intracellular compartments. |
| 1234 | 21547502 | Raised plasma insulin concentrations and increased cardiac work will stimulate GLUT4 as well as CD36 to translocate to the sarcolemma. |
| 1235 | 21547502 | As so far studied, signaling pathways that regulate GLUT4 translocation similarly affect CD36 translocation. |
| 1236 | 21547502 | During the development of insulin resistance and type 2 diabetes, CD36 becomes permanently localized at the sarcolemma, whereas GLUT4 internalizes. |
| 1237 | 21547502 | This juxtaposed positioning of GLUT4 and CD36 is important for aberrant substrate uptake in the diabetic heart: chronically increased fatty acid uptake at the expense of glucose. |
| 1238 | 21547502 | To explain the differences in subcellular localization of GLUT4 and CD36 in type 2 diabetes, recent research has focused on the role of proteins involved in trafficking of cargo between subcellular compartments. |
| 1239 | 21547502 | Several of these proteins appear to be similarly involved in both GLUT4 and CD36 translocation. |
| 1240 | 21547502 | Others, however, have different roles in either GLUT4 or CD36 translocation. |
| 1241 | 21547502 | These trafficking components, which are differently involved in GLUT4 or CD36 translocation, may be considered novel targets for the development of therapies to restore the imbalanced substrate utilization that occurs in obesity, insulin resistance and diabetic cardiomyopathy. |
| 1242 | 21547502 | Subcellular trafficking of the substrate transporters GLUT4 and CD36 in cardiomyocytes. |
| 1243 | 21547502 | These substrates are transported into the cell by glucose transporter 4 (GLUT4) and the fatty acid transporter CD36. |
| 1244 | 21547502 | Besides being located at the sarcolemma, GLUT4 and CD36 are stored in intracellular compartments. |
| 1245 | 21547502 | Raised plasma insulin concentrations and increased cardiac work will stimulate GLUT4 as well as CD36 to translocate to the sarcolemma. |
| 1246 | 21547502 | As so far studied, signaling pathways that regulate GLUT4 translocation similarly affect CD36 translocation. |
| 1247 | 21547502 | During the development of insulin resistance and type 2 diabetes, CD36 becomes permanently localized at the sarcolemma, whereas GLUT4 internalizes. |
| 1248 | 21547502 | This juxtaposed positioning of GLUT4 and CD36 is important for aberrant substrate uptake in the diabetic heart: chronically increased fatty acid uptake at the expense of glucose. |
| 1249 | 21547502 | To explain the differences in subcellular localization of GLUT4 and CD36 in type 2 diabetes, recent research has focused on the role of proteins involved in trafficking of cargo between subcellular compartments. |
| 1250 | 21547502 | Several of these proteins appear to be similarly involved in both GLUT4 and CD36 translocation. |
| 1251 | 21547502 | Others, however, have different roles in either GLUT4 or CD36 translocation. |
| 1252 | 21547502 | These trafficking components, which are differently involved in GLUT4 or CD36 translocation, may be considered novel targets for the development of therapies to restore the imbalanced substrate utilization that occurs in obesity, insulin resistance and diabetic cardiomyopathy. |
| 1253 | 21547502 | Subcellular trafficking of the substrate transporters GLUT4 and CD36 in cardiomyocytes. |
| 1254 | 21547502 | These substrates are transported into the cell by glucose transporter 4 (GLUT4) and the fatty acid transporter CD36. |
| 1255 | 21547502 | Besides being located at the sarcolemma, GLUT4 and CD36 are stored in intracellular compartments. |
| 1256 | 21547502 | Raised plasma insulin concentrations and increased cardiac work will stimulate GLUT4 as well as CD36 to translocate to the sarcolemma. |
| 1257 | 21547502 | As so far studied, signaling pathways that regulate GLUT4 translocation similarly affect CD36 translocation. |
| 1258 | 21547502 | During the development of insulin resistance and type 2 diabetes, CD36 becomes permanently localized at the sarcolemma, whereas GLUT4 internalizes. |
| 1259 | 21547502 | This juxtaposed positioning of GLUT4 and CD36 is important for aberrant substrate uptake in the diabetic heart: chronically increased fatty acid uptake at the expense of glucose. |
| 1260 | 21547502 | To explain the differences in subcellular localization of GLUT4 and CD36 in type 2 diabetes, recent research has focused on the role of proteins involved in trafficking of cargo between subcellular compartments. |
| 1261 | 21547502 | Several of these proteins appear to be similarly involved in both GLUT4 and CD36 translocation. |
| 1262 | 21547502 | Others, however, have different roles in either GLUT4 or CD36 translocation. |
| 1263 | 21547502 | These trafficking components, which are differently involved in GLUT4 or CD36 translocation, may be considered novel targets for the development of therapies to restore the imbalanced substrate utilization that occurs in obesity, insulin resistance and diabetic cardiomyopathy. |
| 1264 | 21547502 | Subcellular trafficking of the substrate transporters GLUT4 and CD36 in cardiomyocytes. |
| 1265 | 21547502 | These substrates are transported into the cell by glucose transporter 4 (GLUT4) and the fatty acid transporter CD36. |
| 1266 | 21547502 | Besides being located at the sarcolemma, GLUT4 and CD36 are stored in intracellular compartments. |
| 1267 | 21547502 | Raised plasma insulin concentrations and increased cardiac work will stimulate GLUT4 as well as CD36 to translocate to the sarcolemma. |
| 1268 | 21547502 | As so far studied, signaling pathways that regulate GLUT4 translocation similarly affect CD36 translocation. |
| 1269 | 21547502 | During the development of insulin resistance and type 2 diabetes, CD36 becomes permanently localized at the sarcolemma, whereas GLUT4 internalizes. |
| 1270 | 21547502 | This juxtaposed positioning of GLUT4 and CD36 is important for aberrant substrate uptake in the diabetic heart: chronically increased fatty acid uptake at the expense of glucose. |
| 1271 | 21547502 | To explain the differences in subcellular localization of GLUT4 and CD36 in type 2 diabetes, recent research has focused on the role of proteins involved in trafficking of cargo between subcellular compartments. |
| 1272 | 21547502 | Several of these proteins appear to be similarly involved in both GLUT4 and CD36 translocation. |
| 1273 | 21547502 | Others, however, have different roles in either GLUT4 or CD36 translocation. |
| 1274 | 21547502 | These trafficking components, which are differently involved in GLUT4 or CD36 translocation, may be considered novel targets for the development of therapies to restore the imbalanced substrate utilization that occurs in obesity, insulin resistance and diabetic cardiomyopathy. |
| 1275 | 21571515 | This switch in metabolic substrate uptake is accompanied by an increased presence of the FA transporter CD36 at the cardiac plasma membrane and over time results in the development of cardiac insulin resistance and ultimately diabetic cardiomyopathy. |
| 1276 | 21669879 | In this study, we investigated the physiological function of sphingomyelin synthase 2 (SMS2) using SMS2 knock-out mice, and we found that SMS2 deficiency prevents high fat diet-induced obesity and insulin resistance. |
| 1277 | 21669879 | Additionally, the siRNA of SMS2 decreased the accumulation of triglyceride in liver of leptin-deficient (ob/ob) mice, strongly suggesting that SMS2 is involved in lipid droplet formation. |
| 1278 | 21669879 | Furthermore, we found that SMS2 exists in lipid microdomains and partially associates with the fatty acid transporter CD36/FAT and with caveolin 1, a scaffolding protein of caveolae. |
| 1279 | 21669879 | Because CD36/FAT and caveolin 1 exist in lipid microdomains and are coordinately involved in lipid droplet formation, SMS2 is implicated in the modulation of the SM in lipid microdomains, resulting in the regulation of CD36/FAT and caveolae. |
| 1280 | 21669879 | Here, we established new cell lines, in which we can completely distinguish SMS2 activity from SMS1 activity, and we demonstrated that SMS2 could convert ceramide produced in the outer leaflet of the plasma membrane into SM. |
| 1281 | 21669879 | In this study, we investigated the physiological function of sphingomyelin synthase 2 (SMS2) using SMS2 knock-out mice, and we found that SMS2 deficiency prevents high fat diet-induced obesity and insulin resistance. |
| 1282 | 21669879 | Additionally, the siRNA of SMS2 decreased the accumulation of triglyceride in liver of leptin-deficient (ob/ob) mice, strongly suggesting that SMS2 is involved in lipid droplet formation. |
| 1283 | 21669879 | Furthermore, we found that SMS2 exists in lipid microdomains and partially associates with the fatty acid transporter CD36/FAT and with caveolin 1, a scaffolding protein of caveolae. |
| 1284 | 21669879 | Because CD36/FAT and caveolin 1 exist in lipid microdomains and are coordinately involved in lipid droplet formation, SMS2 is implicated in the modulation of the SM in lipid microdomains, resulting in the regulation of CD36/FAT and caveolae. |
| 1285 | 21669879 | Here, we established new cell lines, in which we can completely distinguish SMS2 activity from SMS1 activity, and we demonstrated that SMS2 could convert ceramide produced in the outer leaflet of the plasma membrane into SM. |
| 1286 | 21674150 | Macrophage expression of CD36, scavenger receptor A (SR-A) and stearoyl-CoA desaturase (SCD) was increased, most prominently in macrophages exposed to hypertriglyceridemic diabetic serum (twofold increase in CD36 and fourfold increase in SCD, p < 0.05). |
| 1287 | 21674150 | Increased expression of CD36 and SR-A would facilitate macrophage lipid uptake, while increased expression of SCD could block compensatory upregulation of ABCA1 and cholesterol efflux. |
| 1288 | 21674150 | Macrophage expression of CD36, scavenger receptor A (SR-A) and stearoyl-CoA desaturase (SCD) was increased, most prominently in macrophages exposed to hypertriglyceridemic diabetic serum (twofold increase in CD36 and fourfold increase in SCD, p < 0.05). |
| 1289 | 21674150 | Increased expression of CD36 and SR-A would facilitate macrophage lipid uptake, while increased expression of SCD could block compensatory upregulation of ABCA1 and cholesterol efflux. |
| 1290 | 21679697 | Lactogens (prolactin, placental lactogen and growth hormone) improve β-cell survival via STAT5 activation but the molecular targets are incompletely characterized. |
| 1291 | 21679697 | The aim of this study was to examine the effect of human growth hormone (hGH) on mRNAs of fatty acid transport and binding proteins expressed in pancreatic β-cells, and to examine this in relation to β-cell survival after exposure to fatty acids. hGH decreased mRNA levels of FAT/CD36, whereas mRNAs of GPR40, FASN, FABP2, FATP1 and FATP4 were unchanged. |
| 1292 | 21679697 | Over-expression of constitutively active STAT5 was able to mimic hGH's suppression of FAT/CD36 expression, whereas dominant negative STAT5 was unable to block the effect of hGH indicating that STAT5 did not bind directly to the FAT/CD36 promoter. |
| 1293 | 21679697 | The hGH-mediated suppression of FAT/CD36 mRNA was associated with a decrease in palmitate uptake and fatty acid-induced basal hyper-secretion of insulin resulting in improved glucose-stimulated insulin secretion. |
| 1294 | 21679697 | Lactogens (prolactin, placental lactogen and growth hormone) improve β-cell survival via STAT5 activation but the molecular targets are incompletely characterized. |
| 1295 | 21679697 | The aim of this study was to examine the effect of human growth hormone (hGH) on mRNAs of fatty acid transport and binding proteins expressed in pancreatic β-cells, and to examine this in relation to β-cell survival after exposure to fatty acids. hGH decreased mRNA levels of FAT/CD36, whereas mRNAs of GPR40, FASN, FABP2, FATP1 and FATP4 were unchanged. |
| 1296 | 21679697 | Over-expression of constitutively active STAT5 was able to mimic hGH's suppression of FAT/CD36 expression, whereas dominant negative STAT5 was unable to block the effect of hGH indicating that STAT5 did not bind directly to the FAT/CD36 promoter. |
| 1297 | 21679697 | The hGH-mediated suppression of FAT/CD36 mRNA was associated with a decrease in palmitate uptake and fatty acid-induced basal hyper-secretion of insulin resulting in improved glucose-stimulated insulin secretion. |
| 1298 | 21679697 | Lactogens (prolactin, placental lactogen and growth hormone) improve β-cell survival via STAT5 activation but the molecular targets are incompletely characterized. |
| 1299 | 21679697 | The aim of this study was to examine the effect of human growth hormone (hGH) on mRNAs of fatty acid transport and binding proteins expressed in pancreatic β-cells, and to examine this in relation to β-cell survival after exposure to fatty acids. hGH decreased mRNA levels of FAT/CD36, whereas mRNAs of GPR40, FASN, FABP2, FATP1 and FATP4 were unchanged. |
| 1300 | 21679697 | Over-expression of constitutively active STAT5 was able to mimic hGH's suppression of FAT/CD36 expression, whereas dominant negative STAT5 was unable to block the effect of hGH indicating that STAT5 did not bind directly to the FAT/CD36 promoter. |
| 1301 | 21679697 | The hGH-mediated suppression of FAT/CD36 mRNA was associated with a decrease in palmitate uptake and fatty acid-induced basal hyper-secretion of insulin resulting in improved glucose-stimulated insulin secretion. |
| 1302 | 21803601 | Mo/Mp isolated from excisional wounds in non-diabetic db/+ mice exhibited a pro-inflammatory phenotype on day 5 post-injury, with high level expression of the pro-inflammatory molecules interleukin-1β, matrix metalloprotease-9 and inducible nitric oxide synthase. |
| 1303 | 21803601 | Wound Mo/Mp exhibited a less inflammatory phenotype on day 10 post-injury, with decreased expression of the pro-inflammatory molecules and increased expression of the alternative activation markers CD206 and CD36. |
| 1304 | 21803601 | In contrast, in db/db mice, the pro-inflammatory phenotype persisted through day 10 post-injury and was associated with reduced expression of insulin-like growth factor-1, transforming growth factor-β1 and vascular endothelial growth factor. |
| 1305 | 21803601 | The persistent pro-inflammatory wound Mo/Mp phenotype in db/db mice may have resulted from elevated levels of pro-inflammatory interleukin-1β and interferon-γ and reduced levels of anti-inflammatory interleukin-10 in the wound environment. |
| 1306 | 21823052 | The purpose of this study was to explore whether mechanical loading by exercise over a 1-year period in postmenopausal women had an effect on the receptor activator for nuclear factor kappa B ligand/osteoprotegerin (RANKL/OPG) system or the levels of the Wnt-signaling antagonist sclerostin. |
| 1307 | 21823052 | Blood samples were taken from participants at baseline and after 1 year and serum levels of OPG, RANKL and sclerostin were quantified together with the bone metabolism markers C-terminal telopeptide of collagen type I (CTX) and bone-specific alkaline phosphatase (BALP). |
| 1308 | 21823052 | Although our study is limited in number of participating women, we have been able to show an OPG-associated, and RANKL- and sclerostin-independent, training-induced inhibition of postmenopausal bone loss. |
| 1309 | 21871459 | In wild-type C57Bl6-mice, 3weeks of treatment with sitagliptin had no effect on body weight and glucose tolerance nor on phosphorylation of AMP-activated protein kinase (AMPK) and acetyl-CoAcarboxylase (ACC), phosphofructokinase-2 (PFK2) or tuberin-2 (TSC2) in the left ventricular myocardium. |
| 1310 | 21871459 | The myocardium of untreated db/db-/- mice exhibited a marked increase of the phosphorylation of AMPK, ACC, TSC2, expression of p53 and fatty acid translocase (FAT/CD36) membrane expression. |
| 1311 | 21898473 | The nonsalivary gland protein fragments identified in saliva were mainly derived from collagen and extracellular matrix proteins, namely collagen type I. |
| 1312 | 21898473 | The cleavage site frequency analysis showed significant differences between healthy and type 1 diabetic individuals, highlighting the activity of proteases such as matrix metalloproteinase-9 and cathepsin D. |
| 1313 | 21904540 | During atherosclerosis monocyte-derived macrophages accumulate cholesteryl esters from low-density lipoproteins (LDLs) via lectin-like oxidised LDL receptor-1 (LOX-1) and class AI and AII (SR-AI, SR-AII) and class B (SR-BI, CD36) scavenger receptors. |
| 1314 | 21904540 | High glucose elevated LOX1 mRNA, but decreased SR-AI, SR-BI, LDLR, and CD36 mRNA. |
| 1315 | 21904540 | SR-BI and CD36 protein levels were decreased. |
| 1316 | 21904540 | During atherosclerosis monocyte-derived macrophages accumulate cholesteryl esters from low-density lipoproteins (LDLs) via lectin-like oxidised LDL receptor-1 (LOX-1) and class AI and AII (SR-AI, SR-AII) and class B (SR-BI, CD36) scavenger receptors. |
| 1317 | 21904540 | High glucose elevated LOX1 mRNA, but decreased SR-AI, SR-BI, LDLR, and CD36 mRNA. |
| 1318 | 21904540 | SR-BI and CD36 protein levels were decreased. |
| 1319 | 21904540 | During atherosclerosis monocyte-derived macrophages accumulate cholesteryl esters from low-density lipoproteins (LDLs) via lectin-like oxidised LDL receptor-1 (LOX-1) and class AI and AII (SR-AI, SR-AII) and class B (SR-BI, CD36) scavenger receptors. |
| 1320 | 21904540 | High glucose elevated LOX1 mRNA, but decreased SR-AI, SR-BI, LDLR, and CD36 mRNA. |
| 1321 | 21904540 | SR-BI and CD36 protein levels were decreased. |
| 1322 | 21994940 | Protein phosphatase 5 mediates lipid metabolism through reciprocal control of glucocorticoid receptor and peroxisome proliferator-activated receptor-γ (PPARγ). |
| 1323 | 21994940 | In response to adipogenic stimuli, PP5-KO mouse embryonic fibroblast cells showed almost no lipid accumulation with reduced expression of adipogenic markers (aP2, CD36, and perilipin) and low fatty-acid synthase enzymatic activity. |
| 1324 | 22174394 | In untrained individuals, specific transient increases in monocyte expression of PPARγ-regulated genes were observed within 1.5-3 h of exercise (1.7 ± 0.4, 2.6 ± 0.4, and 1.4 ± 0.1 fold for CD36, liver X receptor-α, and ATP-binding cassette subfamily A member 1, respectively, P < 0.05), with expression returning to basal levels within 24 h. |
| 1325 | 22228715 | Adipocyte CD36 and diacylglycerol acyltransferase (DGAT) correlated with LBSQ palmitate storage in the postprandial and walking condition, respectively. |
| 1326 | 22228715 | Transmembrane transport (CD36) and esterification into triglycerides (DGAT) may be rate-limiting steps for LBSQ FFA storage during feeding and exercise. |
| 1327 | 22228715 | Adipocyte CD36 and diacylglycerol acyltransferase (DGAT) correlated with LBSQ palmitate storage in the postprandial and walking condition, respectively. |
| 1328 | 22228715 | Transmembrane transport (CD36) and esterification into triglycerides (DGAT) may be rate-limiting steps for LBSQ FFA storage during feeding and exercise. |
| 1329 | 22327076 | Class B scavenger receptors (SR-Bs), such as SR-BI/II or CD36, bind lipoproteins but also mediate bacterial recognition and phagocytosis. |
| 1330 | 22327076 | In evaluating whether blocking receptors can prevent intracellular bacterial proliferation, phagocyte cytotoxicity, and proinflammatory signaling in bacterial infection/sepsis, we found that SR-BI/II- or CD36-deficient phagocytes are characterized by a reduced intracellular bacterial survival and a lower cytokine response and were protected from bacterial cytotoxicity in the presence of antibiotics. |
| 1331 | 22327076 | Mice deficient in either SR-BI/II or CD36 are protected from antibiotic-treated cecal ligation and puncture (CLP)-induced sepsis, with greatly increased peritoneal granulocytic phagocyte survival (8-fold), a drastic diminution in peritoneal bacteria counts, and a 50-70% reduction in systemic inflammation (serum levels of IL-6, TNF-α, and IL-10) and organ damage relative to CLP in wild-type mice. |
| 1332 | 22327076 | Targeting SR-B receptors with L-37pA, a peptide that functions as an antagonist of SR-BI/II and CD36 receptors, also increased peritoneal granulocyte counts, as well as reduced peritoneal bacteria and bacterium-induced cytokine secretion. |
| 1333 | 22327076 | These results demonstrate that the reduction of both SR-BI/II- and CD36-dependent bacterial invasion and inflammatory response in the presence of antibiotic treatment results in granulocyte survival and local bacterial containment, as well as reduces systemic inflammation and organ damage and improves animal survival during severe infections. |
| 1334 | 22327076 | Class B scavenger receptors (SR-Bs), such as SR-BI/II or CD36, bind lipoproteins but also mediate bacterial recognition and phagocytosis. |
| 1335 | 22327076 | In evaluating whether blocking receptors can prevent intracellular bacterial proliferation, phagocyte cytotoxicity, and proinflammatory signaling in bacterial infection/sepsis, we found that SR-BI/II- or CD36-deficient phagocytes are characterized by a reduced intracellular bacterial survival and a lower cytokine response and were protected from bacterial cytotoxicity in the presence of antibiotics. |
| 1336 | 22327076 | Mice deficient in either SR-BI/II or CD36 are protected from antibiotic-treated cecal ligation and puncture (CLP)-induced sepsis, with greatly increased peritoneal granulocytic phagocyte survival (8-fold), a drastic diminution in peritoneal bacteria counts, and a 50-70% reduction in systemic inflammation (serum levels of IL-6, TNF-α, and IL-10) and organ damage relative to CLP in wild-type mice. |
| 1337 | 22327076 | Targeting SR-B receptors with L-37pA, a peptide that functions as an antagonist of SR-BI/II and CD36 receptors, also increased peritoneal granulocyte counts, as well as reduced peritoneal bacteria and bacterium-induced cytokine secretion. |
| 1338 | 22327076 | These results demonstrate that the reduction of both SR-BI/II- and CD36-dependent bacterial invasion and inflammatory response in the presence of antibiotic treatment results in granulocyte survival and local bacterial containment, as well as reduces systemic inflammation and organ damage and improves animal survival during severe infections. |
| 1339 | 22327076 | Class B scavenger receptors (SR-Bs), such as SR-BI/II or CD36, bind lipoproteins but also mediate bacterial recognition and phagocytosis. |
| 1340 | 22327076 | In evaluating whether blocking receptors can prevent intracellular bacterial proliferation, phagocyte cytotoxicity, and proinflammatory signaling in bacterial infection/sepsis, we found that SR-BI/II- or CD36-deficient phagocytes are characterized by a reduced intracellular bacterial survival and a lower cytokine response and were protected from bacterial cytotoxicity in the presence of antibiotics. |
| 1341 | 22327076 | Mice deficient in either SR-BI/II or CD36 are protected from antibiotic-treated cecal ligation and puncture (CLP)-induced sepsis, with greatly increased peritoneal granulocytic phagocyte survival (8-fold), a drastic diminution in peritoneal bacteria counts, and a 50-70% reduction in systemic inflammation (serum levels of IL-6, TNF-α, and IL-10) and organ damage relative to CLP in wild-type mice. |
| 1342 | 22327076 | Targeting SR-B receptors with L-37pA, a peptide that functions as an antagonist of SR-BI/II and CD36 receptors, also increased peritoneal granulocyte counts, as well as reduced peritoneal bacteria and bacterium-induced cytokine secretion. |
| 1343 | 22327076 | These results demonstrate that the reduction of both SR-BI/II- and CD36-dependent bacterial invasion and inflammatory response in the presence of antibiotic treatment results in granulocyte survival and local bacterial containment, as well as reduces systemic inflammation and organ damage and improves animal survival during severe infections. |
| 1344 | 22327076 | Class B scavenger receptors (SR-Bs), such as SR-BI/II or CD36, bind lipoproteins but also mediate bacterial recognition and phagocytosis. |
| 1345 | 22327076 | In evaluating whether blocking receptors can prevent intracellular bacterial proliferation, phagocyte cytotoxicity, and proinflammatory signaling in bacterial infection/sepsis, we found that SR-BI/II- or CD36-deficient phagocytes are characterized by a reduced intracellular bacterial survival and a lower cytokine response and were protected from bacterial cytotoxicity in the presence of antibiotics. |
| 1346 | 22327076 | Mice deficient in either SR-BI/II or CD36 are protected from antibiotic-treated cecal ligation and puncture (CLP)-induced sepsis, with greatly increased peritoneal granulocytic phagocyte survival (8-fold), a drastic diminution in peritoneal bacteria counts, and a 50-70% reduction in systemic inflammation (serum levels of IL-6, TNF-α, and IL-10) and organ damage relative to CLP in wild-type mice. |
| 1347 | 22327076 | Targeting SR-B receptors with L-37pA, a peptide that functions as an antagonist of SR-BI/II and CD36 receptors, also increased peritoneal granulocyte counts, as well as reduced peritoneal bacteria and bacterium-induced cytokine secretion. |
| 1348 | 22327076 | These results demonstrate that the reduction of both SR-BI/II- and CD36-dependent bacterial invasion and inflammatory response in the presence of antibiotic treatment results in granulocyte survival and local bacterial containment, as well as reduces systemic inflammation and organ damage and improves animal survival during severe infections. |
| 1349 | 22327076 | Class B scavenger receptors (SR-Bs), such as SR-BI/II or CD36, bind lipoproteins but also mediate bacterial recognition and phagocytosis. |
| 1350 | 22327076 | In evaluating whether blocking receptors can prevent intracellular bacterial proliferation, phagocyte cytotoxicity, and proinflammatory signaling in bacterial infection/sepsis, we found that SR-BI/II- or CD36-deficient phagocytes are characterized by a reduced intracellular bacterial survival and a lower cytokine response and were protected from bacterial cytotoxicity in the presence of antibiotics. |
| 1351 | 22327076 | Mice deficient in either SR-BI/II or CD36 are protected from antibiotic-treated cecal ligation and puncture (CLP)-induced sepsis, with greatly increased peritoneal granulocytic phagocyte survival (8-fold), a drastic diminution in peritoneal bacteria counts, and a 50-70% reduction in systemic inflammation (serum levels of IL-6, TNF-α, and IL-10) and organ damage relative to CLP in wild-type mice. |
| 1352 | 22327076 | Targeting SR-B receptors with L-37pA, a peptide that functions as an antagonist of SR-BI/II and CD36 receptors, also increased peritoneal granulocyte counts, as well as reduced peritoneal bacteria and bacterium-induced cytokine secretion. |
| 1353 | 22327076 | These results demonstrate that the reduction of both SR-BI/II- and CD36-dependent bacterial invasion and inflammatory response in the presence of antibiotic treatment results in granulocyte survival and local bacterial containment, as well as reduces systemic inflammation and organ damage and improves animal survival during severe infections. |
| 1354 | 22378540 | Impact of carbamylation and glycation of collagen type I on migration of HT1080 human fibrosarcoma cells. |
| 1355 | 22378540 | In this in vitro study, we investigated the impact of carbamylated and glycated collagen type I on the migratory behavior of the highly invasive HT1080 human fibrosarcoma cells. |
| 1356 | 22378540 | In addition, the influence of these collagen modifications on actin and vinculin organization was studied. |
| 1357 | 22378540 | Impact of carbamylation and glycation of collagen type I on migration of HT1080 human fibrosarcoma cells. |
| 1358 | 22378540 | In this in vitro study, we investigated the impact of carbamylated and glycated collagen type I on the migratory behavior of the highly invasive HT1080 human fibrosarcoma cells. |
| 1359 | 22378540 | In addition, the influence of these collagen modifications on actin and vinculin organization was studied. |
| 1360 | 22431576 | Mechanistic studies revealed that CD36-dependent JNK2 activation is involved in this prothrombotic pathway. |
| 1361 | 22456541 | Metabolic syndrome is linked to chromosome 7q21 and associated with genetic variants in CD36 and GNAT3 in Mexican Americans. |
| 1362 | 22456541 | Furthermore, we examined 29 single-nucleotide polymorphisms (SNPs) from the fatty acid translocase (FAT or CD36, 18 SNPs) gene and guanine nucleotide binding protein, α transducing 3 (GNAT3, 11 SNPs) gene, located within the 1-LOD support interval region for their association with MS and its related traits. |
| 1363 | 22456541 | Remarkably, rs11760281 in GNAT3 and rs1194197 near CD36 exhibited the strongest associations with MS (P = 0.0003, relative risk (RR) = 1.6 and P = 0.004, RR = 1.7, respectively) and several other related traits. |
| 1364 | 22456541 | Metabolic syndrome is linked to chromosome 7q21 and associated with genetic variants in CD36 and GNAT3 in Mexican Americans. |
| 1365 | 22456541 | Furthermore, we examined 29 single-nucleotide polymorphisms (SNPs) from the fatty acid translocase (FAT or CD36, 18 SNPs) gene and guanine nucleotide binding protein, α transducing 3 (GNAT3, 11 SNPs) gene, located within the 1-LOD support interval region for their association with MS and its related traits. |
| 1366 | 22456541 | Remarkably, rs11760281 in GNAT3 and rs1194197 near CD36 exhibited the strongest associations with MS (P = 0.0003, relative risk (RR) = 1.6 and P = 0.004, RR = 1.7, respectively) and several other related traits. |
| 1367 | 22456541 | Metabolic syndrome is linked to chromosome 7q21 and associated with genetic variants in CD36 and GNAT3 in Mexican Americans. |
| 1368 | 22456541 | Furthermore, we examined 29 single-nucleotide polymorphisms (SNPs) from the fatty acid translocase (FAT or CD36, 18 SNPs) gene and guanine nucleotide binding protein, α transducing 3 (GNAT3, 11 SNPs) gene, located within the 1-LOD support interval region for their association with MS and its related traits. |
| 1369 | 22456541 | Remarkably, rs11760281 in GNAT3 and rs1194197 near CD36 exhibited the strongest associations with MS (P = 0.0003, relative risk (RR) = 1.6 and P = 0.004, RR = 1.7, respectively) and several other related traits. |
| 1370 | 22564615 | Cholesterol transporters, such as scavenger receptor (SR)-A1, CD36, and ATP binding cassette (ABC) A1 and G1 (ABCG1), coordinate to regulate cellular lipid status. |
| 1371 | 22564615 | Protein and mRNA expression of cholesterol influx (SR-A1 and CD36) and efflux (ABCA1 and ABCG1) transporters were evaluated using Western blot analysis and real-time quantitative polymerase chain reaction, respectively. |
| 1372 | 22564615 | SR-A1 and CD36 mRNA expression levels were 1.5-fold and 3.5-fold higher, respectively, in high glucose-stimulated than control mesangial cell, whereas ABCG1 mRNA expression decreased to 60% of controls; however, there was no decrease in ABCA1 mRNA. |
| 1373 | 22564615 | Cholesterol transporters, such as scavenger receptor (SR)-A1, CD36, and ATP binding cassette (ABC) A1 and G1 (ABCG1), coordinate to regulate cellular lipid status. |
| 1374 | 22564615 | Protein and mRNA expression of cholesterol influx (SR-A1 and CD36) and efflux (ABCA1 and ABCG1) transporters were evaluated using Western blot analysis and real-time quantitative polymerase chain reaction, respectively. |
| 1375 | 22564615 | SR-A1 and CD36 mRNA expression levels were 1.5-fold and 3.5-fold higher, respectively, in high glucose-stimulated than control mesangial cell, whereas ABCG1 mRNA expression decreased to 60% of controls; however, there was no decrease in ABCA1 mRNA. |
| 1376 | 22564615 | Cholesterol transporters, such as scavenger receptor (SR)-A1, CD36, and ATP binding cassette (ABC) A1 and G1 (ABCG1), coordinate to regulate cellular lipid status. |
| 1377 | 22564615 | Protein and mRNA expression of cholesterol influx (SR-A1 and CD36) and efflux (ABCA1 and ABCG1) transporters were evaluated using Western blot analysis and real-time quantitative polymerase chain reaction, respectively. |
| 1378 | 22564615 | SR-A1 and CD36 mRNA expression levels were 1.5-fold and 3.5-fold higher, respectively, in high glucose-stimulated than control mesangial cell, whereas ABCG1 mRNA expression decreased to 60% of controls; however, there was no decrease in ABCA1 mRNA. |
| 1379 | 22580174 | CD36 as a target to prevent cardiac lipotoxicity and insulin resistance. |
| 1380 | 22580174 | The fatty acid transporter and scavenger receptor CD36 is increasingly being implicated in the pathogenesis of insulin resistance and its progression towards type 2 diabetes and associated cardiovascular complications. |
| 1381 | 22580174 | The redistribution of CD36 from intracellular stores to the plasma membrane is one of the earliest changes occurring in the heart during diet induced obesity and insulin resistance. |
| 1382 | 22580174 | This elicits an increased rate of fatty acid uptake and enhanced incorporation into triacylglycerol stores and lipid intermediates to subsequently interfere with insulin-induced GLUT4 recruitment (i.e., insulin resistance). |
| 1383 | 22580174 | Using in vitro model systems of high-fat diet induced insulin resistance, the results indicate the feasibility of using CD36 as a target for adaptation of cardiac metabolic substrate utilization. |
| 1384 | 22580174 | CD36 as a target to prevent cardiac lipotoxicity and insulin resistance. |
| 1385 | 22580174 | The fatty acid transporter and scavenger receptor CD36 is increasingly being implicated in the pathogenesis of insulin resistance and its progression towards type 2 diabetes and associated cardiovascular complications. |
| 1386 | 22580174 | The redistribution of CD36 from intracellular stores to the plasma membrane is one of the earliest changes occurring in the heart during diet induced obesity and insulin resistance. |
| 1387 | 22580174 | This elicits an increased rate of fatty acid uptake and enhanced incorporation into triacylglycerol stores and lipid intermediates to subsequently interfere with insulin-induced GLUT4 recruitment (i.e., insulin resistance). |
| 1388 | 22580174 | Using in vitro model systems of high-fat diet induced insulin resistance, the results indicate the feasibility of using CD36 as a target for adaptation of cardiac metabolic substrate utilization. |
| 1389 | 22580174 | CD36 as a target to prevent cardiac lipotoxicity and insulin resistance. |
| 1390 | 22580174 | The fatty acid transporter and scavenger receptor CD36 is increasingly being implicated in the pathogenesis of insulin resistance and its progression towards type 2 diabetes and associated cardiovascular complications. |
| 1391 | 22580174 | The redistribution of CD36 from intracellular stores to the plasma membrane is one of the earliest changes occurring in the heart during diet induced obesity and insulin resistance. |
| 1392 | 22580174 | This elicits an increased rate of fatty acid uptake and enhanced incorporation into triacylglycerol stores and lipid intermediates to subsequently interfere with insulin-induced GLUT4 recruitment (i.e., insulin resistance). |
| 1393 | 22580174 | Using in vitro model systems of high-fat diet induced insulin resistance, the results indicate the feasibility of using CD36 as a target for adaptation of cardiac metabolic substrate utilization. |
| 1394 | 22580174 | CD36 as a target to prevent cardiac lipotoxicity and insulin resistance. |
| 1395 | 22580174 | The fatty acid transporter and scavenger receptor CD36 is increasingly being implicated in the pathogenesis of insulin resistance and its progression towards type 2 diabetes and associated cardiovascular complications. |
| 1396 | 22580174 | The redistribution of CD36 from intracellular stores to the plasma membrane is one of the earliest changes occurring in the heart during diet induced obesity and insulin resistance. |
| 1397 | 22580174 | This elicits an increased rate of fatty acid uptake and enhanced incorporation into triacylglycerol stores and lipid intermediates to subsequently interfere with insulin-induced GLUT4 recruitment (i.e., insulin resistance). |
| 1398 | 22580174 | Using in vitro model systems of high-fat diet induced insulin resistance, the results indicate the feasibility of using CD36 as a target for adaptation of cardiac metabolic substrate utilization. |
| 1399 | 22662869 | Advanced oxidation protein products activate intrarenal renin-angiotensin system via a CD36-mediated, redox-dependent pathway. |
| 1400 | 22665120 | In diabetic mice, we observed an increase in EGFRtk phosphorylation and ER stress marker expression (CHOP, ATF4, ATF6, and phosphorylated-eIF2α) in heart and mesenteric resistance arteries, which were reduced with AG1478, Tudca, and insulin. |
| 1401 | 22665120 | Cardiac fibrosis, enhanced collagen type I, and plasminogen activator inhibitor 1 were decreased with AG1478, Tudca, and insulin treatments. |
| 1402 | 22665120 | Moreover, in mesenteric resistance arteries, the mRNA levels of Nox2 and Nox4 and the NADPH oxidase activity were augmented in streptozotocin mice and reduced with treatments. |
| 1403 | 22678998 | Postprandial inhibition of gastric ghrelin secretion by long-chain fatty acid through GPR120 in isolated gastric ghrelin cells and mice. |
| 1404 | 22678998 | Using quantitative RT-PCR and immunofluorescence staining, we detected a high level of expression of the long-chain fatty acid (LCFA) receptor GPR120, while the other LCFA receptor, GPR40, was undetectable. |
| 1405 | 22678998 | Meal-induced increase in gastric mucosal LCFA was assessed by measuring the transcripts of markers for tissue uptake of LCFA, lipoprotein lipase (LPL), fatty acid translocase (CD36), glycosylphosphatidylinositol-anchored HDL-binding protein 1, and nuclear fatty acid receptor peroxisome proliferator-activated receptor-γ. |
| 1406 | 22678998 | Quantitative RT-PCR studies indicate significantly increased mRNA levels of lipoprotein lipase, glycosylphosphatidylinositol-anchored HDL-binding protein 1, and peroxisome proliferator-activated receptor-γ in postprandial gastric mucosa. |
| 1407 | 22678998 | These results suggest that meal-related increases in gastric mucosal LCFA interact with GPR120 on ghrelin cells to inhibit ghrelin secretion. |
| 1408 | 22730524 | This interaction can trigger CD36-dependent JNK2 activation, enhance platelet aggregation, and accelerate thrombus formation. |
| 1409 | 22890211 | Paraoxonases protect against atherogenesis, as serum PON1 exerts a protective role against DM development by stimulating insulin secretion from β cells, and its unique antioxidant properties. |
| 1410 | 22890211 | Insulin may directly inhibit lipid peroxidation via inhibition of NADPH oxidase expression. |
| 1411 | 22890211 | Insulin has additional protective effects against DM-induced macrophage cholesterol accumulation by inhibiting CD36 expression (an oxidized LDL receptor), and by inhibiting HMGCoA reductase expression (the rate limiting enzyme in cholesterol biosynthesis), through inhibition of the formation of active SREBP-1 (the transcription factor that activates HMGCoA reductase). |
| 1412 | 22960064 | The following parameters were analyzed: feeding behavior, visceral adipose tissue mass, plasma lipids, cardiac CD36 expression, localization and insulin regulation, as well as the profile of cardiac lipids. |
| 1413 | 22960064 | The fructose diet increased cardiac plasma membrane content of CD36 in the basal and insulin-stimulated states, and decreased its low density microsomes content. |
| 1414 | 22960064 | The following parameters were analyzed: feeding behavior, visceral adipose tissue mass, plasma lipids, cardiac CD36 expression, localization and insulin regulation, as well as the profile of cardiac lipids. |
| 1415 | 22960064 | The fructose diet increased cardiac plasma membrane content of CD36 in the basal and insulin-stimulated states, and decreased its low density microsomes content. |
| 1416 | 23160140 | Rapamycin, down-regulated the gene expression of perilipin, sterol regulatory element-binding protein 1 (SREBP1) and lipin 1, while tacrolimus down-regulated CD36 and aP2 gene expression. |
| 1417 | 23160140 | All three IAs increased IL-6 gene expression and secretion, but not expression and secretion of TNF-α or adiponectin. |
| 1418 | 23197723 | PPARγ/RXRα-induced and CD36-mediated microglial amyloid-β phagocytosis results in cognitive improvement in amyloid precursor protein/presenilin 1 mice. |
| 1419 | 23197723 | Evaluation of DSP-8658 in the amyloid precursor protein/presenilin 1 mouse model confirmed an increased microglial Aβ phagocytosis in vivo, which subsequently resulted in a reduction of cortical and hippocampal Aβ levels. |
| 1420 | 23223942 | This cross-sectional study evaluated the distribution of serum cross-linked C-telopeptides of collagen type I (βCTXs) in postmenopausal women, the characteristics of bone remodeling, and the factors influencing this bone marker, especially the use of anti-osteoporotic drugs. |
| 1421 | 23447133 | Endothelium-specific expression of DN PPARγ on the ApoE(-/-) background unmasked significant impairment of endothelium-dependent relaxation in aortic rings, increased systolic blood pressure, altered expression of atherogenic markers (e.g., Cd36, Mcp1, Catalase), and enhanced diet-induced atherosclerotic lesion formation in aorta. |
| 1422 | 23447133 | Smooth muscle-specific expression of DN PPARγ, which induces aortic dysfunction and increased systolic blood pressure at baseline, also resulted in enhanced diet-induced atherosclerotic lesion formation in aorta on the ApoE(-/-) background that was associated with altered expression of a shared, yet distinct, set of atherogenic markers (e.g., Cd36, Mcp1, Osteopontin, Vcam1). |
| 1423 | 23447133 | Endothelium-specific expression of DN PPARγ on the ApoE(-/-) background unmasked significant impairment of endothelium-dependent relaxation in aortic rings, increased systolic blood pressure, altered expression of atherogenic markers (e.g., Cd36, Mcp1, Catalase), and enhanced diet-induced atherosclerotic lesion formation in aorta. |
| 1424 | 23447133 | Smooth muscle-specific expression of DN PPARγ, which induces aortic dysfunction and increased systolic blood pressure at baseline, also resulted in enhanced diet-induced atherosclerotic lesion formation in aorta on the ApoE(-/-) background that was associated with altered expression of a shared, yet distinct, set of atherogenic markers (e.g., Cd36, Mcp1, Osteopontin, Vcam1). |
| 1425 | 23557700 | For further elucidation of the role of CD36 in neuronal FA sensing, ventromedial hypothalamus (VMH) CD36 was depleted using adeno-associated viral (AAV) vector expressing CD36 short hairpin RNA (shRNA) in rats. |
| 1426 | 23557700 | Next, weanling rats were injected in the VMH with CD36 AAV shRNA. |
| 1427 | 23557700 | However, VMH CD36-depleted rats did have increased plasma leptin and subcutaneous fat deposition and markedly abnormal glucose tolerance. |
| 1428 | 23557700 | For further elucidation of the role of CD36 in neuronal FA sensing, ventromedial hypothalamus (VMH) CD36 was depleted using adeno-associated viral (AAV) vector expressing CD36 short hairpin RNA (shRNA) in rats. |
| 1429 | 23557700 | Next, weanling rats were injected in the VMH with CD36 AAV shRNA. |
| 1430 | 23557700 | However, VMH CD36-depleted rats did have increased plasma leptin and subcutaneous fat deposition and markedly abnormal glucose tolerance. |
| 1431 | 23557700 | For further elucidation of the role of CD36 in neuronal FA sensing, ventromedial hypothalamus (VMH) CD36 was depleted using adeno-associated viral (AAV) vector expressing CD36 short hairpin RNA (shRNA) in rats. |
| 1432 | 23557700 | Next, weanling rats were injected in the VMH with CD36 AAV shRNA. |
| 1433 | 23557700 | However, VMH CD36-depleted rats did have increased plasma leptin and subcutaneous fat deposition and markedly abnormal glucose tolerance. |
| 1434 | 23796502 | Angiotensin II regulates collagen metabolism through modulating tissue inhibitor of metalloproteinase-1 in diabetic skin tissues. |
| 1435 | 23796502 | We investigated the effect of angiotensin II (Ang II) on matrix metalloproteinase-1 (MMP-1)/tissue inhibitor of metalloproteinase-1 (TIMP-1) balance in regulating collagen metabolism of diabetic skin. |
| 1436 | 23796502 | The collagen type I (Coll I) and collagen type III (Coll III) were measured by histochemistry. |
| 1437 | 23796502 | The expressions of transforming growth factor-β (TGF-β), MMP-1, TIMP-1 and propeptides of types I and III procollagens in skin tissues and fibroblasts were quantified using polymerase chain reaction (PCR), Western blot or enzyme-linked immunosorbent assay (ELISA). |
| 1438 | 23796502 | Collagen dysfunction was documented by changed collagen I/III ratio in streptozotocin (STZ)-injected mice compared with controls. |
| 1439 | 23796502 | In primary cultured fibroblasts, Ang II prompted collagen synthesis accompanied by increases in the expressions of TGF-β, TIMP-1 and types I and III procollagens, and these increases were inhibited by losartan, an Ang II type 1 (AT1) receptor blocker, but not affected by PD123319, an Ang II type 2 (AT2) receptor antagonist. |
| 1440 | 23796502 | These findings present evidence that Ang-II-mediated changes in the productions of MMP-1 and TIMP-1 occur via AT1 receptors and a TGF-β-dependent mechanism. |
| 1441 | 23812099 | CD36 coordinates NLRP3 inflammasome activation by facilitating intracellular nucleation of soluble ligands into particulate ligands in sterile inflammation. |
| 1442 | 23812099 | Particulate ligands, including cholesterol crystals and amyloid fibrils, induce production of interleukin 1β (IL-1β) dependent on the cytoplasmic sensor NLRP3 in atherosclerosis, Alzheimer's disease and diabetes. |
| 1443 | 23812099 | Consequently, macrophages that lacked CD36 failed to elicit IL-1β production in response to those ligands, and targeting CD36 in atherosclerotic mice resulted in lower serum concentrations of IL-1β and accumulation of cholesterol crystals in plaques. |
| 1444 | 23812099 | CD36 coordinates NLRP3 inflammasome activation by facilitating intracellular nucleation of soluble ligands into particulate ligands in sterile inflammation. |
| 1445 | 23812099 | Particulate ligands, including cholesterol crystals and amyloid fibrils, induce production of interleukin 1β (IL-1β) dependent on the cytoplasmic sensor NLRP3 in atherosclerosis, Alzheimer's disease and diabetes. |
| 1446 | 23812099 | Consequently, macrophages that lacked CD36 failed to elicit IL-1β production in response to those ligands, and targeting CD36 in atherosclerotic mice resulted in lower serum concentrations of IL-1β and accumulation of cholesterol crystals in plaques. |
| 1447 | 23841102 | In this study, we used a nonhuman primate model of Type 1 diabetes to measure early downstream signalling events following engagement of the major platelet collagen receptor, glycoprotein (GP)VI. |
| 1448 | 23841102 | Treatment of platelets with the specific Syk inhibitor BAY61-3606 inhibited GPVI-dependent ROS and, importantly, reduced ROS generation in the poorly controlled diabetes group to that observed in healthy monkeys. |
| 1449 | 23860646 | For instance, deficiency in tissue-nonspecific alkaline phosphatase (TNAP) in mice (Alpl (-/-) mice) and humans leads to hypophosphatasia (HPP), an inborn error of metabolism characterized by epileptic seizures in the most severe cases, caused by abnormal metabolism of pyridoxal-5'-phosphate (the predominant form of vitamin B6) and by hypomineralization of the skeleton and teeth featuring rickets and early loss of teeth in children or osteomalacia and dental problems in adults caused by accumulation of inorganic pyrophosphate (PPi). |
| 1450 | 23860646 | These changes are accompanied by upregulation in the jejunal-ileal expression of the Akp6 IAP isozyme (global IAP, or gIAP) and concomitant upregulation of FAT/CD36, a phosphorylated fatty acid translocase thought to play a role in facilitating the transport of long-chain fatty acids into cells. gIAP, but not dIAP, is able to modulate the phosphorylation status of FAT/CD36. dIAP, even though it is expressed in the duodenum, is shed into the gut lumen and is active in LPS dephosphorylation throughout the gut lumen and in the feces. |
| 1451 | 23860646 | Analogous to the role of IAP in the gut, TNAP expression in the liver may have a proactive role from bacterial endotoxin insult. |
| 1452 | 23860646 | This review recounts the established roles of TNAP and IAP and briefly discusses new areas of investigation related to multisystemic functions of these isozymes. |
| 1453 | 23991091 | This was associated with increased liver weight and serum VLDL/LDL cholesterol and alanine transaminase (ALT) levels, as well as increased hepatic expression of genes involved in glucose regulation (Pck1, Cebpa), fatty acid uptake (Cd36) and lipid metabolism (Fasn, Fabp4, Lpl, Abcd2, Pla2g7). |
| 1454 | 24018334 | NOD1 and NOD2 mRNA expression were significantly up-regulated in monocytes from patients with type 2 diabetes (T2DM) and positively correlated with HOMA-IR and poor glycemic control. |
| 1455 | 24018334 | Patients with T2DM also exhibited increased monocyte activation markers (CD11b and CD36) and proinflammatory signals downstream of NOD (RIPK2 and NFκB) along with the increased circulatory levels of TNF-α and IL-6. |
| 1456 | 24018334 | In vitro stimulation of monocytes with NOD specific ligands-i-EDAP and MDP significantly up regulated the mRNA expression of NOD1 and NOD2 respectively in T2DM. |