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Gene Information
Gene symbol: TNF
Gene name: tumor necrosis factor
HGNC ID: 11892
Synonyms: TNFSF2, DIF, TNF-alpha
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 21885868 | Transfer experiments determined the role of hepatic tumor necrosis factor (TNF)/inducible nitric oxide synthase-producing dendritic cells (Tip-DCs) and adipose tissue macrophages (ATMs) in inflammation-induced insulin resistance, determined by homeostatic assessment of insulin resistance. |
| 2 | 21885868 | Targeting Tip-DCs and ATMs with curcusomes in ob/ob mice reduced NF-?B/RelA DNA binding activity, reduced TNF, and enhanced interleukin-4 production. |
| 3 | 3102976 | The cytotoxins tumour necrosis factor (TNF) and lymphotoxin (LT) synergize with IFN-gamma in a number of activities. |
| 4 | 3139756 | We have previously reported that the cytokines IFN-gamma and TNF-alpha each upregulate the expression of class I MHC proteins and, in combination, induce the expression of class II MHC proteins on pancreatic islet cells. |
| 5 | 3139756 | At day 6, insulin content of the islets was significantly reduced by exposure to TNF-alpha but not IFN-gamma. |
| 6 | 3069387 | The potentiation of IL-1 effects on beta-cells by tumor necrosis factor alpha (TNF), another macrophage hormone controlled by a gene in the HLA region on chromosome 6, may account for the MHC association of IDDM. |
| 7 | 2491807 | Tumor necrosis factor-alpha (TNF alpha) and interferon-gamma (IFN gamma) have potent effects on bone resorption and collagen synthesis in cultured rat long bones. |
| 8 | 2491807 | This enhanced inhibitory effect was due to the induction of a response to TNF alpha by IFN gamma, since preexposure of cells to IFN gamma for 24 h, followed by incubation with TNF alpha alone for an additional 48 h, also resulted in increased inhibition of DNA synthesis. |
| 9 | 2703526 | These results indicate that the TNF-induced increase in circulating lipid levels can occur in the absence of a TNF-induced inhibition of adipose tissue lipoprotein lipase activity. |
| 10 | 2703526 | In addition, TNF administration to diabetic animals leads to an elevation in serum glucose levels (73% at 17 h) without a change in serum insulin levels. |
| 11 | 2498883 | However, after a 72-hr exposure of islets to interferon gamma (IFN-gamma) and/or tumor necrosis factor alpha (TNF-alpha) (each at 250 units/ml), ICAM-1 was induced on greater than 85% of islet cells. |
| 12 | 2498883 | Class I major histocompatibility complex (MHC) protein expression, detected on control islet cells, was also stimulated by IFN-gamma and/or TNF-alpha. |
| 13 | 2501390 | Because the induction of IL-6 appears to be an important host cell response to injury, we have examined whether IL-6 is produced by murine pancreatic islets or rat insulinoma (RIN-m5F) cells after their exposure to IFN-gamma and TNF-alpha. |
| 14 | 2501390 | A mAb against murine IL-6 abolished (control and IFN-gamma) or significantly reduced (TNF-alpha and TNF-alpha + IFN-gamma) the IL-6 activity in islet supernatants. |
| 15 | 2501390 | The magnitude for the effects of IFN-gamma and TNF-alpha on the production of IL-6 from mouse islets was found to be both time and dose dependent. |
| 16 | 2545735 | To elucidate the possible role of viruses and cytokines in the pathogenesis of IDDM, we have examined the effect of reovirus infection on beta cell major histocompatibility complex (MHC) expression and the effect of interferon-gamma (IFN-gamma) and tumour necrosis factor-alpha (TNF-alpha) on beta cell function in vitro. |
| 17 | 2518361 | When tested as single agents or added together at very low concentrations, interleukin 1 (IL-1), tumor necrosis factor (TNF), and interferon gamma (IFN-gamma) inhibited insulin release from rat islet cell monolayer cultures during 4 day incubations; however, this secretory function improved after the cytokines were removed. |
| 18 | 2577113 | This tight linkage of TNF-alpha alleles with extended haplotypes and the significant increase of heterozygotes in patients could lead to some explanation of the DR3 association with a variety of autoimmune diseases particularly IDDM. |
| 19 | 2105545 | This effect of IFN-gamma was potentiated by TNF-alpha resulting in 27% of the cells expressing class II antigen. |
| 20 | 2179951 | A considerable portion of cells expressing tumor necrosis factor alpha appear to be CD4+ T cells. |
| 21 | 2115042 | Interleukin-1 (IL-1), tumor necrosis factor (TNF), and interferon-gamma (IFN gamma) inhibit insulin release and may be cytotoxic to isolated rodent pancreatic islets. |
| 22 | 2384663 | We previously reported that streptococcal preparation (OK-432), which is a TNF inducer, inhibits insulitis and development of autoimmune diabetes in nonobese diabetic (NOD) mice and Bio-Breeding (BB) rats, as animal models of insulin-dependent diabetes mellitus. |
| 23 | 1698309 | IFN (1000 U/ml) in the presence of LPS significantly potentiated LPS-stimulated Mo TNF-alpha secretion and reduced the levels of IL-1 beta immunoreactivity in Mo lysates. |
| 24 | 1978829 | Previous studies demonstrated that administration of tumor necrosis factor (TNF) to diabetic rats rapidly increases serum triglyceride levels and stimulates hepatic lipogenesis without affecting the activity of adipose tissue lipoprotein lipase or serum insulin levels. |
| 25 | 1996407 | Furthermore, the Mo IL-1 beta and TNF-alpha secretions of IDDM patients were significantly higher than the Mo secretions of TNF-beta genotype-matched healthy controls. |
| 26 | 2016534 | It has been hypothesized that the islets are damaged by the secretion of cytokines such as IL-1 and TNF-alpha and that their function may be altered by IL-6. |
| 27 | 2060425 | Tumor necrosis factor suppresses the endothelial anticoagulant cofactor thrombomodulin and induces expression of the procoagulant cofactor tissue factor. |
| 28 | 1888882 | Human islet insulin secretion was also suppressed during co-culture with recombinant tumor necrosis factor (rTNF) or interferon (rIFN), but not with lymphotoxin (rLT) or rIL-6; rat islet insulin secretion was not suppressed by any of these cytokines. |
| 29 | 1680332 | Flow cytometric analysis showed that HLA expression in this cell line is readily induced by IFN-gamma and modulated by TNF-alpha. |
| 30 | 1893147 | Mononuclear cells from both healthy donors and diabetic patients could inhibit the insulin release with no correlation to TNF content. |
| 31 | 1718801 | Levels of ICAM-1 and LFA-3 expression in normal human islet cells and regulation of their expression by cytokines interferon-gamma (IFN-gamma), tumor necrosis factor alpha (TNF-alpha), interleukin 1 beta (IL-1 beta), and IL-6 have been studied by two-color immunofluorescence staining of pancreatic cryostat sections and fluorescence-activated cell sorter analysis. |
| 32 | 1718801 | IFN-gamma and TNF-alpha alone or in combination strongly enhanced this spontaneous expression of ICAM-1 in a time- and/or dose-dependent and additive manner but had no effect on LFA-3. |
| 33 | 1747949 | Treatment twice a week from 4 weeks of age with OK-432-injected mouse serum, which contained endogenous TNF (75U), but not IL-1, IL-2 and interferon-gamma (IFN-gamma) activity, reduced the intensity of insulitis and significantly inhibited the cumulative incidence of diabetes by 28 weeks of age in NOD mice, as compared with the incidence in non-treated mice (P less than 0.01) and in mice treated with control serum (P less than 0.02). |
| 34 | 1747949 | The results indicate that the inhibition by OK-432 treatment of IDDM in NOD mice was partially mediated by serum factors including endogenous TNF. |
| 35 | 1541051 | We have recently reported that chronic and systemic administration of tumor necrosis factor alpha (TNF) inhibits development of autoimmune diabetes in NOD mice and BB rats, animal models of insulin-dependent diabetes mellitus (IDDM). |
| 36 | 1541051 | The in vivo TNF productivity in the diabetic rats, including the short-term- and long-term-diabetic rats, was correlated positively with the level of fructosamine/albumin (P less than 0.05) and negatively with the level of serum albumin (P less than 0.05), but not with levels of blood glucose. |
| 37 | 1638523 | Injection of tumor necrosis factor elevated serum IL-6 levels and reduced adipose tissue LPL activity by 70%. |
| 38 | 1638523 | Since tumor necrosis factor increases circulating IL-6, some of its effects may be mediated or potentiated by IL-6. |
| 39 | 1526345 | Although in vitro studies showed that TNF decreases adipose tissue lipoprotein lipase activity, recent studies with intact animals demonstrated that TNF increases serum triglyceride levels by stimulating hepatic lipid secretion, not by affecting clearance. |
| 40 | 1395129 | Treatment of BB rats with tumor necrosis factor (TNF) has been reported to prevent the development of IDDM. |
| 41 | 1360342 | Freshly isolated pancreatic beta cells from ob/ob mice did not express ICAM-1, but treatment of the cells with IL-1-beta, TNF-alpha, or INF-gamma strongly induced its expression as measured by immunofluorescence flow cytometry. |
| 42 | 1460428 | Mice bearing a tumor necrosis factor (TNF) alpha transgene controlled by an insulin promoter developed an increasingly severe lymphocytic insulitis, apparently resulting from the induction of endothelial changes with features similar to those observed in other places of intense lymphocytic traffic. |
| 43 | 1341919 | We determined the serum concentrations of tumor necrosis factor (TNF) in 15 nondiabetic healthy subjects and in 36 insulin-dependent (type I) diabetic outpatients. |
| 44 | 8383325 | IL-1 beta and IFN-gamma are sufficient to induce nitric oxide formation by human islets, whereas TNF-alpha potentiates nitrite production. |
| 45 | 8383325 | This combination of cytokines (IL-1 beta, TNF-alpha, and IFN-gamma) also influences insulin secretion by human islets. |
| 46 | 8383325 | Higher concentrations (IL-1 beta at 75 units/ml, 3.5 nM TNF-alpha, and IFN-gamma at 750 units/ml) inhibit insulin secretion from human islets, and the inhibitory effect is prevented by NG-monomethyl-L-arginine. |
| 47 | 8445033 | We investigated the effect of the tumor necrosis factor-alpha (TNF alpha) on the differentiation of human adipocyte precursor cells in primary culture. |
| 48 | 8445033 | Continuous exposure of the cells to TNF alpha completely blocked expression of the adipocyte phenotype and GPDH activity. |
| 49 | 7682590 | The expression of the TNF-alpha transgene was restricted to the pancreas, in contrast to TNF-beta expression from the same promoter, in which the transgene was expressed in the pancreas, kidney, and skin. |
| 50 | 7682590 | The expression of TNF-alpha in the pancreas of transgenic mice resulted in an overwhelming insulitis, composed of CD4+ and CD8+ T cells and B220+ B cells, considerably greater than that of TNF-beta transgenics. |
| 51 | 8333833 | Tumor necrosis factor-alpha (TNF-alpha) mRNA expression by beta TC1 cells was demonstrated 1-3 h after the addition of IL-1 beta. |
| 52 | 8218929 | We argue that IL-1 potentiated by other cytokines (tumor necrosis factor alpha, interferon gamma) is an important effector molecule involved in both early and late events in the immune-mediated process that leads to beta-cell destruction and IDDM. |
| 53 | 8240789 | It is concluded that the gradual increase in IL-1 beta and TNF alpha plasma levels may reflect an ongoing autoimmune inflammatory reaction at the onset of IDDM. |
| 54 | 8242903 | We previously reported that nonspecific immunomodulations with a streptococcal preparation (OK-432), an inducer of tumor necrosis factor (TNF), or with recombinant TNF prevented development of insulin-dependent diabetes mellitus (IDDM) in animal models (NOD mice and BB rats). |
| 55 | 8242903 | These results indicate that treatment with LT, as well as TNF, modulated autoimmunity and prevented development of IDDM in BB/Wor rats which may be low producers of TNF/LT. |
| 56 | 8275942 | This study investigates whether the expression of TNF alpha and its receptors is modulated during drug treatment to reduce insulin resistance. |
| 57 | 8130898 | High doses of IL-1 are cytotoxic to beta cells and strongly inhibit insulin release; high-dose IL-1 plus TNF acts synergically to suppress further the insulin release. |
| 58 | 8130898 | In contrast, we observed that the predominant effect of low-dose IL-1 and TNF when administered separately was the stimulation of insulin release. |
| 59 | 8130898 | We therefore asked whether the combination of low-dose IL-1 plus TNF would act synergistically to stimulate or suppress insulin release. |
| 60 | 8177321 | SAPKs therefore define a new TNF-alpha and stress-activated signalling pathway, possibly initiated by sphingomyelin-based second messengers, which regulates the activity of c-Jun. |
| 61 | 8197147 | Chronic exposure of adipocytes to low concentrations of TNF-alpha strongly inhibits insulin-stimulated glucose uptake. |
| 62 | 8197147 | Concurrently, TNF-alpha treatment causes a moderate decrease in the insulin-stimulated autophosphorylation of the insulin receptor (IR) and a dramatic decrease in the phosphorylation of IR substrate 1, the major substrate of the IR in vivo. |
| 63 | 8197147 | These results show that TNF-alpha directly interferes with the signaling of insulin through its receptor and consequently blocks biological actions of insulin. |
| 64 | 7516691 | The cytokine interleukin-1 (IL-1) turned out to be the ultimate inducer, whereas tumour necrosis factor-alpha (TNF) and unexpectedly the phorbol ester TPA (12-O-tetradecanoylphorbol-13-acetate; 10 nM) synergistically promoted nitrite accumulation. |
| 65 | 7516691 | Besides employing TPA directly, the synergistic effect of TNF could be traced back to protein kinase C activation since protein kinase C inhibitors (IC50 value for staurosporine: 4 nM) potently suppressed nitrite production in the case of IL-1/TNF administration. |
| 66 | 8056188 | Insulin-dependent diabetes mellitus (IDDM) is associated with class II molecules of the MHC on chromosome 6, in particular HLA-DR and -DQ alleles, but a pathogenic role for TNF-alpha in the class III region of the MHC has also been implied. |
| 67 | 7523453 | Since a defective insulin receptor (IR) tyrosine kinase activity has been observed in obesity and NIDDM, we measured the IR tyrosine kinase activity in the Zucker (fa/fa) rat model of obesity and insulin resistance after neutralizing TNF-alpha with a soluble TNF receptor (TNFR)-lgG fusion protein. |
| 68 | 7523453 | These results demonstrate that TNF-alpha participates in obesity-related systemic insulin resistance by inhibiting the IR tyrosine kinase in the two tissues mainly responsible for insulin-stimulated glucose uptake: muscle and fat. |
| 69 | 7926300 | Neutralization of TNF-alpha in one of these models improves insulin sensitivity by increasing the activity of the insulin receptor tyrosine kinase, specifically in muscle and fat tissues. |
| 70 | 7926300 | On a cellular level, TNF-alpha is a potent inhibitor of the insulin-stimulated tyrosine phosphorylations on the beta-chain of the insulin receptor and insulin receptor substrate-1, suggesting a defect at or near the tyrosine kinase activity of the insulin receptor. |
| 71 | 7756973 | Glucose-induced insulin secretion is inhibited by the cytokines interleukin-1 beta (IL-1 beta), interleukin-6 and tumour necrosis factor alpha (TNF) when combined with IL-1 beta in cultured rat islets, by IL-1 beta, TNF and interferon gamma in mouse islets, and by combined treatment of IL-1 beta, TNF and interferon gamma in human islets. |
| 72 | 9098456 | The segregation of these alleles has been associated with levels of TNF alpha or TNF beta production in systemic lupus erythematosis (SLE), insulin-dependent diabetes mellitus (IDDM) and in healthy control individuals. |
| 73 | 7530759 | Treatment of rat islets with a combination of tumor necrosis factor (TNF) and lipopolysaccharide (LPS), conditions known to activate macrophages, stimulate the expression of iNOS and the formation of nitrite. |
| 74 | 7706477 | TNF alpha has been shown to reduce lipoprotein lipase (LPL) activity in adipose tissue. |
| 75 | 7706477 | To elucidate further the transcriptional mechanism of TNF alpha inhibition of LPL gene transcription, transfection analysis was used to locate the site(s) of the LPL promoter that imparts the TNF alpha response. |
| 76 | 7706477 | Electrophoretic mobility shift assays using two 32P-labeled LPL probes spanning the region between -180 and +44 bp revealed the loss of several LPL DNA-protein interactions after TNF alpha treatment, including the binding of NF-Y to the CCAAT box and a protein to the octamer consensus sequence. |
| 77 | 7706477 | These results indicate that TNF alpha regulates at least two DNA-binding proteins on the proximal promoter, thereby inhibiting LPL gene transcription. |
| 78 | 7882592 | The insulin resistance of this disease may be mediated by tumor necrosis factor-alpha (TNF-alpha). |
| 79 | 7895657 | Recent studies indicated a direct role for adipose expression of TNF alpha in obesity-linked insulin resistance and diabetes. |
| 80 | 7895657 | Incubation of 3T3-L1 cells with TNF alpha alone completely inhibited adipocyte conversion and expression of fatty acid-binding protein messenger RNA (mRNA). |
| 81 | 7895657 | Incubation of 3T3-L1 adipocytes with TNF alpha also inhibited insulin-stimulated 2-deoxyglucose uptake as well as expression of GLUT4 protein. |
| 82 | 7540572 | Furthermore, in the presence of tumor necrosis factor (TNF)-alpha, large amounts of NO were produced by IL-1 beta and DNA cleavage occurred more noticeably, although TNF-alpha alone did not generate NO. |
| 83 | 7598712 | Recent evidence suggests that expression of tumor necrosis factor-alpha (TNF-alpha) by adipocytes is a molecular mediator of insulin resistance in obesity. |
| 84 | 7602783 | The expression of the second isozyme, Mn-SOD localized at mitochondrial matrix, is regulated in a complex manner by many stimulants such as interleukin-1, -6, tumor necrosis factor, lipopolysaccharide, and tumor promoters phorbol ester (TPA) and okadaic acid. |
| 85 | 7621993 | FR139317 attenuated the increases in glomerular mRNA levels of alpha 1(I) (P < 0.01), alpha 1(III) (P < 0.01), and alpha 1(IV) (P < 0.01) collagen chains, laminin B1 (P < 0.01) and B2 (P < 0.01) chains, TNF-alpha (P < 0.01), PDGF-B (P < 0.01), TGF-beta (P < 0.001) and basic FGF (P < 0.01) in diabetic rats. |
| 86 | 7560085 | The coding sequences and splicing donor and acceptor sequences of the Tnfa gene, a candidate gene for Idd-16, were identical in the NOD, CTS, and BALB/c alleles, ruling out amino acid changes in the TNF molecule as a determinant of insulin-dependent diabetes mellitus susceptibility. |
| 87 | 7477268 | SAPKs, members of the ERK family, are activated in situ by inflammatory stimuli, including tumour-necrosis factor (TNF) and interleukin-1, and phosphorylate and probably stimulate the transactivation function of c-Jun. |
| 88 | 8781713 | Since glutamic acid decarboxylase-65 (GAD-65) is a target autoantigen in IDDM, we investigated whether the cytokines IL-1 beta, TNF alpha IFN gamma altered islet cell expression of GAD-65 and whether the effect of cytokines on GAD-65 expression was similar to their effect on insulin secretion. |
| 89 | 8781713 | We found that: 1) IL-1 beta at low dose (1 U/ml) which stimulated insulin secretion, had no effect on GAD-65 expression, whereas higher doses of IL-1 beta (10, 100, 1000 U/ml) which inhibited insulin secretion, decreased GAD-65 expression. 2) TNF alpha at doses of 10, 100, 1000 U/ml which stimulated insulin secretion had no effect on GAD-65 expression. 3) IFN gamma at doses of 10, 100, 1000 U/ml had no effect on insulin secretion or on GAD-65 expression. 4) In combination, IL-1 beta plus TNF alpha and IFN gamma showed a similar inhibitory effect on GAD-65 expression as IL-1 beta alone. |
| 90 | 8781713 | In summary: 1) IL-1 beta dramatically inhibits GAD-65 expression. 2) TNF alpha and IFN gamma have no effect on GAD-65 expression. |
| 91 | 8662965 | The addition of inhibitors for nuclear factor kappaB (NF-kappaB) to the cells caused a loss of the gamma-GCS mRNA expression in response to TNF-alpha. |
| 92 | 8662965 | In summary, the expression of gamma-GCS is regulated by TNF-alpha or IL-1beta in endothelial cells mediated by NF-kappaB stimulation, and impairment of the regulation of gamma-GCS in hyperglycemic cells may be a cause of medical complications that develop in diabetes mellitus. |
| 93 | 8666137 | Inhibition of tumor necrosis factor (TNF)-alpha action has recently been shown to reverse insulin resistance dramatically and to improve glycemic control in obese rodents. |
| 94 | 8666137 | TNF-alpha neutralization over a period of 4 weeks had no effect on insulin sensitivity in obese NIDDM subjects. |
| 95 | 8779862 | Although IL-1 beta and TNF-alpha are themselves capable of inducing NO synthase (NOS) in glia, the specific factors mediating LPS induction of NOS in brain have not been identified. |
| 96 | 8779862 | To determine whether LPS induction of NOS in brain cells is mediated by IL-1 or TNF-alpha, acting alone or in concert, the effects of IL-1-receptor antagonist (IL-1Ra) and of TNF-soluble receptor (TNFsRp55), presented individually and in combination, on LPS-induced NOS activity were tested. |
| 97 | 8779862 | TNF-alpha alone induced NO production weakly as compared with IL-1, but combined submaximal concentrations of IL-1 beta (1 nM) and TNF-alpha (10 nM) induced NOS synergistically. |
| 98 | 8779862 | The results indicate that LPS induction of NOS activity in brain cells is mediated in part by both IL-1 beta and TNF-alpha. |
| 99 | 8781295 | Therefore, we examined the effect of TNF-alpha on basal and insulin-mediated transport of 2-deoxy[3H]-glucose in L6 rat muscle cells. |
| 100 | 8781295 | Comparative experiments with 3T3-L1 adipocytes showed that in cells cultured with insulin, TNF-alpha decreased basal transport but the insulin-stimulated increase was unaffected. |
| 101 | 8803477 | IGF-I (6.5 nM) maximally stimulated glucose uptake 7-fold after 24 h incubation, while 23 nM TNF-alpha maximally stimulated glucose uptake 3-fold only after 48 h incubation. |
| 102 | 8803477 | In contrast, the treatment with 23 nM TNF-alpha failed to phosphorylate either IGF-I receptor beta-subunit or IRS-1 but did phosphorylate MAP kinase as much as IGF-I did. |
| 103 | 8803477 | Despite a similar extent to which TNF-alpha induced MAP kinase phosphorylation as IGF-I did, TNF-alpha stimulated glucose uptake less compared to IGF-I. |
| 104 | 8910278 | These results indicate that aP2 is central to the pathway that links obesity to insulin resistance, possibly by linking fatty acid metabolism to expression of TNF-alpha. |
| 105 | 8913531 | TNF-alpha (1000 U/ml), on the other hand, affected none of these parameters either alone or in any combination with TGF-alpha or IFN-gamma. |
| 106 | 8920883 | In transgenic mice, TNF alpha expression on the islets resulted in massive insulitis, composed of CD4+ T cells, CD8+ T cells, and B cells. |
| 107 | 8920883 | Despite infiltration of considerable number of lymphoid cells in islets, expression of TNF alpha protected NOD mice from IDDM. |
| 108 | 8932996 | Since the Fas antibody showed no cross-reactive activity of tumour necrosis factor (TNF), the cytotoxic effect was not mediated by TNF receptors. |
| 109 | 9015760 | Tumor necrosis factor-alpha (TNF-alpha) can modulate the signalling capacity of tyrosine kinase receptors; in particular, TNF-alpha has been shown to mediate the insulin resistance associated with animal models of obesity and noninsulin-dependent diabetes mellitus. |
| 110 | 9015760 | In order to determine whether the effects of TNF-alpha might involve alterations in the expression of specific protein-tyrosine phosphatases (PTPases) that have been implicated in the regulation of growth factor receptor signalling, KRC-7 rat hepatoma cells were treated with TNF-alpha, and changes in overall tissue PTPase activity and the abundance of three major hepatic PTPases (LAR, PTP1B, and SH-PTP2) were measured in addition to effects of TNF-alpha on ligand-stimulated autophosphorylation of insulin and epidermal growth factor (EGF) receptors and insulin-stimulated insulin receptor substrate-1 (IRS-1) phosphorylation. |
| 111 | 9015760 | TNF-alpha caused a dose-dependent decrease in insulin-stimulated IRS-1 phosphorylation and EGF-stimulated receptor autophosphorylation to 47-50% of control. |
| 112 | 9015760 | However, immunoblot analysis showed that TNF-alpha treatment resulted in a 2.5-fold increase in the abundance of SH-PTP2, a 49% decrease in the transmembrane PTPase LAR, and no evident change in the expression of PTP1B. |
| 113 | 9015760 | Since SH-PTP2 has been shown to interact directly with both the EGF receptor and IRS-1, increased abundance of this PTPase, may mediate the TNF-alpha effect to inhibit signalling through these proteins. |
| 114 | 9015760 | Furthermore, decreased abundance of the LAR PTPase, which has been implicated in the regulation of insulin receptor phosphorylation, may account for the less marked effect of TNF-alpha on the autophosphorylation state of the insulin receptor while postreceptor actions of insulin are inhibited. |
| 115 | 9174153 | Insulin-dependent diabetes mellitus (IDDM) and Graves' disease (GD) are autoimmune endocrinopathies and associated with distinct HLA-DR and -DQ alleles as well as several tumor necrosis factor alpha (TNF-alpha) and beta (TNF-beta) alleles. |
| 116 | 9174153 | TNF-alpha and TNF-beta interact with TNF receptor (TNF-R), of which two subtypes have been described: TNF-R1 and TNF-R2. |
| 117 | 9392477 | Furthermore, TNF-alpha has distinct effects on adipose tissue including induction of insulin resistance, induction of leptin production, stimulation of lipolysis, suppression of lipogenesis, induction of adipocyte dedifferentiation, and impairment of preadipocyte differentiation in vitro. |
| 118 | 9392477 | Taken together, these effects all tend to decrease adipocyte volume and number and suggest a role for TNF-alpha in limiting increase in fat mass. |
| 119 | 9396242 | Therefore, we designed a study to determine: (1) the effect of TNF-alpha on insulin sensitivity, and (2) the effect of LPD on the TNF-alpha response and the risk factors of atherosclerosis, such as insulin sensitivity and lipid metabolism, in patients with diabetic renal failure. |
| 120 | 9396242 | These results indicate that: (1) TNF-alpha derived from PBMCs might affect insulin sensitivity in patients with diabetic renal failure, and (2) LPD does not have any significant effect on the risk factors of atherosclerosis. |
| 121 | 9550435 | Islet grafts and spleens from TNF-alpha-treated mice at 10 days after islet transplantation contained significantly fewer CD4+ and CD8+ T cells, and significantly decreased mRNA levels of type 1 cytokines (IFN-gamma, IL-2, and TNF-beta) than islet grafts and spleens from control mice. |
| 122 | 9550435 | Regarding type 2 cytokines, IL-4 mRNA levels were not changed significantly in islet grafts or spleens of TNF-alpha-treated mice, whereas IL-10 mRNA levels were decreased significantly in islet grafts of TNF-alpha-treated mice and not significantly changed in spleens. |
| 123 | 9550435 | These results suggest that TNF-alpha partially protects beta cells in syngeneic islet grafts from recurrent autoimmune destruction by reducing CD4+ and CD8+ T cells and down-regulating type 1 cytokines, both systemically and locally in the islet graft. |
| 124 | 9421370 | Incubation for 24 h with tumor necrosis factor-alpha (TNF-alpha) but not C2-ceramide decreased the concentration and insulin-induced tyrosine phosphorylation of IRS-1 in this experimental system. |
| 125 | 10212230 | In addition, in response to tumor necrosis factor-alpha (TNF-alpha) + lipopolysaccharide, activated resident macrophages mediate beta-cell damage via intraislet IL-1 release followed by IL-1-induced iNOS expression by beta-cells. |
| 126 | 10727667 | High glucose or mannitol also enhanced TNFalpha-stimulated NF-kappaB activity. |
| 127 | 10727667 | An antioxidant N-acetyl-L-cysteine and a selective protein kinase C (PKC) inhibitor GF109203X significantly suppressed the TNFalpha-induced NF-kappaB activation, and abrogated potentiation of TNFalpha-induced NF-kappaB activity caused by high glucose (27.5 mmol/l). |
| 128 | 10798271 | This prothrombotic, proinflammatory state is characterised by vaso-constriction, platelet and leukocyte activation and adhesion (externalization, expression and upregulation of von Willebrand factor, platelet activating factor, P-selectin, ICAM-1, IL-8, MCP-1, TNF alpha, etc.), promotion of thrombin formation, coagulation and fibrin deposition at the vascular wall (expression of tissue factor, PAI-1, phosphatidyl serine, etc.) and, in platelet-leukocyte coaggregates, additional inflammatory interactions via attachment of platelet CD40-ligand to endothelial, monocyte and B-cell CD40. |
| 129 | 10814778 | Hsp60 expression was found to be enhanced in response to cytokines as diverse as IL-1beta, TNF-alpha, IL-4, IL-6 and IL-10. |
| 130 | 10814778 | Upregulation of hsp27, however, was primarily induced by immunoregulatory cytokines like IL-4, IL-6 and TGF-beta whereas alphaB-crystallin expression was found to be enhanced by the pro-inflammatory cytokine TNF-alpha only. |
| 131 | 10764814 | Since insulin resistance is a risk factor for vascular disease, we examined the effects of TNFalpha on mitogenic signaling by insulin. |
| 132 | 10764814 | Preincubation (30-120 min) with TNFalpha had no effect on insulin-induced IR phosphorylation. |
| 133 | 10764814 | In contrast, TNFalpha transiently suppressed insulin-induced ERK1/2 activation. |
| 134 | 10764814 | Insulin-induced phosphorylation of Shc was inhibited by TNFalpha in a similar pattern. |
| 135 | 10764814 | Thus, TNFalpha selectively interferes with insulin-induced mitogenic signaling by inhibiting the phosphorylation of Shc and the downstream activation of ERK1/2. |
| 136 | 10969838 | Because it is known that TNF-alpha induces apoptosis of adipocytes and upregulates UCP2 mRNA, a marked increase of TNF-alpha mRNA with an increase of UCP2 in adipocytes caused CLA-induced apoptosis. |
| 137 | 10975477 | Also, a tendency toward increased percentage levels of CD4+ T cells producing IFN-gamma or IL-4 and of CD8+ T cells producing either TNF-alpha or IFN-gamma was seen, but due to the small number of patients investigated, these differences did not attain statistic significance. |
| 138 | 10990075 | Cyclophosphamide treatment decreased IL-12, IL-1beta, IL-2, IFN-gamma and TNF-alpha gene expressions in mononuclear spleen cells but IL-4 gene expression increased. |
| 139 | 11120352 | They produce antithrombotic and thrombotic factors such as t-PA and PAI-1 and respond to TNFalpha, an important factor correlated with the inflammatory process by modifying growth characteristics by producing cytokines such as GM-CSF by expressing ICAM-1 on the surface and by producing large amounts of nitric oxide and endothelin. |
| 140 | 11126235 | Analysis of these animals demonstrated that the genetic absence of TNF signaling in obesity: (i) significantly improves insulin receptor signaling capacity and consequently insulin sensitivity; (ii) prevents brown adipose tissue atrophy and beta3-adrenoreceptor deficiency and improves thermo-adaptive responses, (iii) decreases the elevated PAI-1 and TGFbeta production; and (iv) lowers hyperlipidemia and hyperleptinemia. |
| 141 | 11126408 | The aim of this study was to investigate if TNFalpha and IFNgamma signal through mitogen-activated protein kinases in isolated rat islets of Langerhans and if they potentiate mitogen-activated protein kinase activity induced by IL-1beta. |
| 142 | 11126408 | Exposure to IL-1beta or TNFalpha significantly increased mitogen-activated protein kinase activity, whereas IFNgamma tended to decrease extracellular-signal-regulated kinase activity. |
| 143 | 11126408 | Further, TNFalpha and IFNgamma were found to synergistically increase mitogen-activated protein kinase activity induced by IL-1beta. |
| 144 | 10995595 | TNF-alpha impairs insulin-mediated glucose uptake in adipocytes, but because of lipolytic effects the interpretation of clinical studies and the extent to which TNF-alpha affects muscle insulin sensitivity are unclear. |
| 145 | 10995595 | The present study investigated the effects of TNF-alpha and a PKC inhibitor (RO-318220) on basal and insulin-stimulated 2-[(3)H]deoxyglucose uptake in cultured L6 myoblasts. |
| 146 | 10995595 | Incubation with TNF-alpha at 1 or 10 ng/ml for 24 h had no significant effect on basal glucose uptake, insulin sensitivity or maximal insulin responsiveness. |
| 147 | 10995595 | In conclusion, although increased TNF-alpha expression and plasma concentrations have been implicated in the pathogenesis of insulin resistance in various clinical states, there is no evidence that TNF-alpha impairs insulin-stimulated glucose uptake in a skeletal-muscle-derived cell line. |
| 148 | 10878750 | Importantly, results from knockout mice deficient in TNF-alpha or its receptors have suggested that TNF-alpha has a role in regulating in vivo insulin sensitivity. |
| 149 | 11147775 | The generation of small adipocytes, presumably mediated by increased expression of UCP-1 in addition to increased lipolysis in response to AJ-9677, was associated with decreased TNF-alpha and free fatty acid production and may be the mechanism of amelioration of insulin resistance in KK-Ay/Ta diabetic obese mice. |
| 150 | 11160134 | This antibody revealed that TNF-alpha, IGF-1, or insulin stimulated phosphorylation of IRS-1 at Ser307 in 3T3-L1 preadipocytes and adipocytes. |
| 151 | 11254704 | Fas ligand (FasL), perforin, TNF-alpha, IL-1, and NO have been considered as effector molecule(s) leading to beta cell death in autoimmune diabetes. |
| 152 | 11254704 | IFN-gamma treatment conferred susceptibility to TNF-alpha-induced apoptosis on otherwise resistant insulinoma cells by STAT1 activation followed by IFN regulatory factor (IRF)-1 induction. |
| 153 | 11259621 | In contrast, LG100268 increased TNF-alpha and had no effect or suppressed the expression of GLUT4, MCPT, SCD1, and CD36. |
| 154 | 11287357 | Adipose tissue expresses tumor necrosis factor (TNF) and interleukin (IL)-6, which may cause obesity-related insulin resistance. |
| 155 | 11287357 | Thus the local expression of TNF and plasma IL-6 are higher in subjects with obesity-related insulin resistance. |
| 156 | 11410238 | Tumor necrosis factor-alpha (TNF-alpha) is a key component of obesity-diabetes link, we therefore examined the attenuating effect of VO(opt)(2) on impaired insulin signal transduction induced by TNF-alpha. |
| 157 | 11410238 | Overall, the present study demonstrates that VO(opt)(2) exerts an anti-diabetic effect in ob/ob mice by ameliorating impaired glucose tolerance, and furthermore, attenuates the TNF-alpha-induced decrease in IRS-1 phosphorylation in adipocytes. |
| 158 | 11410238 | These results suggest that the anti-diabetic action of VO(opt)(2) is derived from an attenuation of a TNF-alpha induced impaired insulin signal transduction via inhibition of protein tyrosine phosphatase, providing a potential clinical utility for VO(opt)(2) in the treatment of NIDDM. |
| 159 | 11416024 | However, TNFalpha signaling in the brain and the potential interaction with leptin have not been investigated to date. |
| 160 | 11416024 | Here we studied the tyrosine phosphorylation of STAT (signal transducer and activator of transcription) proteins in the hypothalamus of normal rats after iv injection of recombinant murine leptin or TNFalpha or coinjection of both cytokines. |
| 161 | 11416024 | Immunoblot analysis of hypothalamic lysates with a phospho-specific STAT3 antibody showed a 6- to 7-fold stimulation of STAT3 tyrosine phosphorylation in response to both leptin and TNFalpha. |
| 162 | 11416024 | No other STAT proteins (STAT1, STAT5) were activated by leptin, whereas TNFalpha injection resulted in a dose-dependent phosphorylation of hypothalamic STAT5. |
| 163 | 11416024 | In contrast to its action in the brain, leptin was unable to produce STAT3 phosphorylation in the liver, either alone or in combination with TNFalpha. |
| 164 | 11416024 | These data show that TNFalpha, independently of leptin, activates hypothalamic STAT signaling pathways and enhances leptin action at the level of STAT3. |
| 165 | 11508268 | Although MFP14 reduced anti-CD3 and/or LPS-induced blood levels of IFN-gamma, TNF-alpha and IL-12 it increased IL-4 and IL-10. |
| 166 | 11712393 | Current concept is that, when PPAR-gamma is activated by these drugs, the number of small adipocytes is increased to replace large adipocytes, thereby decreasing the release of TNF-alpha and FFA from adipose tissue. |
| 167 | 11712415 | Moreover, PPAR gamma/RXR inhibitors decrease lipogenesis in WAT, while TZD stimulate adipocyte differentiation and apoptosis, thereby both preventing adipocyte hypertrophy, which is associated with alleviation of insulin resistance presumably due to decreases in FFA, and TNF alpha, and upregulation of adiponectin. |
| 168 | 11887976 | (i) IL-6, through effects on sICAM-1, and TNF-alpha via effects on sVCAM-1, may promote vascular adhesion; (ii) plasma levels of TNF-alpha are associated with dyslipidaemia and increased blood pressure, adding to vascular disease risk; (iii) the actions of both cytokines are probably modified by altered production of soluble receptors in diabetic subjects. |
| 169 | 11707432 | We have found that insulin resistance induced by tumor necrosis factor-alpha (TNF-alpha) in 3T3-L1 adipocytes was accompanied by increased GM3 ganglioside expression caused by elevating GM3 synthase activity and its mRNA. |
| 170 | 11707432 | Pharmacological depletion of GM3 in adipocytes by an inhibitor of glucosylceramide synthase prevented the TNF-alpha-induced defect in insulin-dependent tyrosine phosphorylation of IRS-1 and also counteracted the TNF-alpha-induced serine phosphorylation of IRS-1. |
| 171 | 11812741 | In addition, pretreatment of lipopolysaccharide (LPS)-stimulated peritoneal macrophages with SOD mimic inhibited the LPS-dependent increase in TNF-alpha as well as the NADPH oxidase-dependent release of superoxide. |
| 172 | 11907416 | TNF-alpha and the combination of the three human cytokines caused a transient increase in cumulative insulin levels. |
| 173 | 11907416 | TNF-alpha alone enhanced insulin content on day 3. |
| 174 | 11912559 | Because tumor necrosis factor-alpha (TNF-a ) is proinflammatory and may thus inhibit the action of insulin at the endothelial cell level, we have now investigated whether TNF-a affects (1) insulin receptor content; (2) insulin receptor (IR) autophosphorylation induced by insulin, and (3) e-NOS expression by the endothelial cells. |
| 175 | 11912559 | Although the inhibition of IR autophosphorylation by TNF-alpha is known to occur at the adipocyte level, the data on the inhibitory effect of TNF-alpha on insulin-induced e-NOS expression and IRP contents are novel. |
| 176 | 11914744 | TNFalpha alone did not induce MHC class II expression, but enhanced IFN gamma-induced MHC class II expression. |
| 177 | 11916923 | Exposure of isolated human adipocytes to tumor necrosis factor-alpha (TNF-alpha) produced a marked and specific decrease in the mRNA encoding the SREBP1c isoform and completely blocked the insulin-induced cleavage of SREBP1 protein. |
| 178 | 11970897 | In contrast, treatment with TNF-alpha inhibited basal and insulin-induced LCFA uptake and reduced FATP1 and -4 levels. |
| 179 | 11978627 | Tumor necrosis factor-alpha (TNF-alpha) is a contributing cause of the insulin resistance seen in obesity and obesity-linked type 2 diabetes, but the mechanism(s) by which TNF-alpha induces insulin resistance is not understood. |
| 180 | 11978627 | Importantly, a number of adipocyte-abundant genes, including GLUT4, hormone sensitive lipase, long-chain fatty acyl-CoA synthase, adipocyte complement-related protein of 30 kDa, and transcription factors CCAAT/enhancer binding protein-alpha, receptor retinoid X receptor-alpha, and peroxisome profilerator-activated receptor gamma were significantly downregulated by TNF-alpha treatment. |
| 181 | 11978627 | Nuclear factor-kappaB (NF-kappaB) was activated within 15 min of TNF-alpha addition. 3T3-L1 adipocytes expressing IkappaBalpha-DN, a nondegradable NF-kappaB inhibitor, exhibited normal morphology, global gene expression, and insulin responses. |
| 182 | 11978627 | However, absence of NF-kappaB activation abolished suppression of >98% of the genes normally suppressed by TNF-alpha and induction of 60-70% of the genes normally induced by TNF-alpha. |
| 183 | 11978627 | Thus the changes in adipocyte gene expression induced by TNF-alpha could lead to insulin resistance. |
| 184 | 11978647 | Insulin stimulated TNF-alpha secretion in a dose-dependent manner (P < 0.01); the addition of RSG (10(-8) mol/l) reduced TNF-alpha secretion (P < 0.05). |
| 185 | 12032139 | Tumor necrosis factor (TNF) + interferon-gamma (IFNgamma) was more potent at inducing cell death in SOCS-1-/- islets than in wild type. |
| 186 | 12032139 | The TNF + IFNgamma damage of islets was mediated by inducible nitric-oxide synthase (iNOS), and increased iNOS expression and nitric oxide production were found in SOCS-1-/- islets following cytokine treatment. |
| 187 | 12351658 | In this study, using phosphospecific antibodies against rat IRS-1 phosphorylated at Ser(307) (equivalent to Ser(312) in human IRS-1), we observed serine phosphorylation of IRS-1 in response to TNF-alpha or calyculin A treatment that paralleled surrogate markers for IKK activation. |
| 188 | 12568116 | TNF + IFNgamma did not induce caspase 3 activation in primary mouse islets. |
| 189 | 12581487 | Tumor necrosis factor-alpha (TNF-alpha) and IFN-gamma cytokine secretion in the 10,000 IU group at month 5 showed a significant decrease that corresponded with the effect of ingested IFN-alpha on decreasing gadolinium enhancements. |
| 190 | 12626032 | In conclusion, increased TNF-alpha and leptin levels may contribute to insulin resistance in GDM and in the third trimester of normal pregnancy and may negatively influence the anthropometric parameters of the newborns. |
| 191 | 12653178 | Similarly, the stimulation of the vagus nerve may inhibit TNF synthesis in the liver and acetylecholine, the principal vagal neurotransmitter, significantly attenuates the release of pro-inflammatory cytokines TNF-alpha, interleukin 1,6 and 18, but not the anti-inflammatory cytokine IL-10 in experiments. |
| 192 | 13679655 | TNF pathway and TGFb play an important role in the regulation of PAI-1 synthesis in the adipose tissue and the liver with steatosis. |
| 193 | 14561180 | All the cytokines of the TNF superfamily mediate their effects through the activation of the transcription factor NF-kappaB, c-Jun N-terminal kinase, apoptosis, and proliferation. |
| 194 | 12554784 | TNFalpha, which activates three different MAPKs [ERK, p38, and jun amino terminal kinase (JNK)], also induces insulin resistance. |
| 195 | 12670740 | For example, the thiazolidinediones, a class of oral anti-diabetic agents that reduce insulin resistance and improve beta-cell function, might mediate these effects by regulating adipocyte-derived factors, in particular TNF-alpha and FFAs. |
| 196 | 12690081 | These results are in agreement with the hypothesis that the synthesis of adipose tissue TNFalpha and leptin could induce the production of interleukin-6, CRP, and other acute-phase reactants, thus contributing to the maintenance of chronic low-grade inflammation state involved in the progression of obesity and its associated comorbidities. |
| 197 | 12714437 | TNF-alpha, IL-6, and CRP were significantly correlated with insulin resistance estimated by the homeostatic model assessment (r=0.48, P<0.05; r=0.56, P<0.01; and r=0.35, P<0.05, respectively). |
| 198 | 12714437 | Concentrations of CRP and IL-6 decreased after weight loss (median, 8.6 and interquartile range, 2.7/14.5 vs 2.5 and 1.2/4.1 mg/L; P<0.006, and 5.13 and 2.72/12.15 vs 3.95 and 1.97/5.64 pg/mL, P<0.02, respectively), whereas serum levels of TNF-alpha remained unchanged (8.6 and 6.3/18.8 vs 11.7 and 5.8/17.2 pg/mL; NS.). |
| 199 | 12714600 | Furthermore, other serine kinases including Akt, extracellular regulated kinase, mammalian target of rapamycin, and PKCzeta were also activated by TNF-alpha (as assessed by phospho-specific antibodies). |
| 200 | 12825835 | We recently reported that the activation by UDP of rat P2Y6 nucleotide receptors expressed in 1321N1 astrocytoma cells protected them from TNFalpha-induced apoptosis by suppressing activation of caspase 3 and 8. |
| 201 | 12825835 | Cell death was induced in 1321N1 astrocytoma cells permanently expressing the rat P2Y6 receptor by exposure to TNFalpha in the presence of cycloheximide. |
| 202 | 12825835 | The activation of P2Y6 receptors by UDP both protected the astrocytes from TNF-alpha induced apoptosis and activated protein kinase C (PKC) isotypes. |
| 203 | 12830456 | A stepwise multiple regression analysis showed that UAE was significantly associated with hs-CRP level (P < 0.001), duration of diabetes (P < 0.001), urinary TNF-alpha level (P < 0.01), and glycated hemoglobin level (P < 0.05; adjusted R2 = 0.73; P < 0.001). |
| 204 | 12924619 | The results suggest that the Chinese medicine JTKL, which contains PG as one of its valid components, improves insulin resistance by modulating muscle fiber composition and TNF-alpha in skeletal muscles in hypertensive and insulin-resistant FFR. |
| 205 | 12927809 | Several observations showed that the adiponectin and aP2 genes can be differentially regulated in adipocytes: (1) Topiramate, an anti-epileptic agent with weight-reducing properties, increased adiponectin mRNA levels and secretion, but did not, like the thiazolidinediones, increase aP2 expression; (2) IL-6 reduced adiponectin, but significantly increased, aP2 expression; and (3) TNFalpha inhibited adiponectin, but paradoxically increased, aP2 expression in PPAR gamma 2-infected C/EBP alpha null cells. |
| 206 | 12934668 | Finally, TNF-alpha decreased adipose tissue LPL activity in both control and EFAD animals. |
| 207 | 12941766 | Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) selectively induces apoptosis of tumor cells but not most normal cells. |
| 208 | 12947309 | Interferon (IFN)-gamma acts synergistically with interleukin (IL)-1beta and tumor necrosis factor (TNF)-alpha to activate isoform of nitric oxide synthetase (iNOS) gene expression, induce apoptosis, and impair glucose-stimulated insulin release (GSIR) in pancreatic islets. |
| 209 | 12878589 | Here we demonstrate that LDL(-) increases tumor necrosis factor alpha (TNFalpha)-induced inflammatory responses through NF kappa B and AP-1 activation with corresponding increases in vascular cell adhesion molecule-1 (VCAM1) expression. |
| 210 | 12878589 | In contrast, exposing LDL(-) to the key lipolytic enzyme lipoprotein lipase (LPL) reversed these responses, inhibiting VCAM1 below levels seen with TNFalpha alone. |
| 211 | 14514596 | Leptin and tumor necrosis factor (TNF)-alpha are associated with insulin resistance and cardiovascular disease. |
| 212 | 14514632 | We previously reported that interleukin-1beta (IL-1beta) alone does not cause apoptosis of beta-cells, whereas when combined with gamma-interferon (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha), it exerts a distinct apoptotic effect. |
| 213 | 14514632 | Exposure to IL-1beta for 24 h decreased cellular IB1/JIP-1 content by 66 +/- 17%; this IL-1beta effect was maintained in the presence of TNF-alpha + IFN-gamma, which did not influence IB1/JIP-1 levels by themselves. |
| 214 | 14514632 | A similar increase in TNF-alpha + IFN-gamma-induced apoptosis was produced by adenoviral expression of antisense IB1/JIP-1 and was not further enhanced by addition of IL-1beta, indicating that IL-1beta-mediated suppression of IB1/JIP-1 in beta-cells increases their susceptibility to cytokine-induced apoptosis. |
| 215 | 14527361 | However, PECAM-1 expression was reduced in the cells treated with TNF-alpha, IFN-gamma, TNF-alpha + IFN-gamma and AGEs-BSA + TNF-alpha. |
| 216 | 12952969 | IL-6, in contrast to TNF-alpha, did not increase pS-307 of insulin-receptor substrate (IRS)-1 or JNK activation. |
| 217 | 12952969 | However, IL-6, like TNF-alpha exerted long term inhibitory effects on the gene transcription of IRS-1, GLUT-4, and peroxisome proliferator-activated receptor gamma. |
| 218 | 12952969 | An important interaction with TNF-alpha was found because TNF-alpha markedly increased IL-6 mRNA and protein secretion. |
| 219 | 12952969 | These results show that IL-6, through effects on gene transcription, is capable of impairing insulin signaling and action but, in contrast to TNF-alpha, IL-6 does not increase pS-307 (or pS-612) of IRS-1. |
| 220 | 15033908 | Fas expression is thought to be induced by proinflammatory cytokines, such as IL-1beta, interferon-gamma (IFNgamma), and TNFalpha, released by islet-infiltrating mononuclear cells. |
| 221 | 15059968 | In this model, insulin stimulated Grb14 expression, while TNF-alpha increased ZIP expression. |
| 222 | 15127201 | Activation of the receptor for advanced glycation end products (RAGE) reportedly triggers cellular responses implicated in the pathogenesis of diabetes, such as increasing vascular cell adhesion molecule-1 (VCAM-1) expression on vascular endothelial cells and inducing TNF-alpha secretion by mononuclear cells. |
| 223 | 15127201 | In contrast, the reported RAGE ligand S100b was confirmed to induce VCAM-1 expression on endothelial cells and TNF-alpha secretion by PBMCs after 24 h of treatment. |
| 224 | 15171689 | Administration of pioglitazone to 19 diabetic patients significantly increased the plasma levels of EC-SOD (69.9+/-19.3 ng/ml to 97.4+/-25.9 ng/ml; P < 0.0001) and adiponectin, while it decreased tumor necrosis factor-alpha (TNF-alpha). |
| 225 | 15240650 | The proinflammatory cytokines TNFalpha, IL-6, and IL-8 are released from the placenta at term and have been implicated in and/or associated with various metabolic events, including decreased insulin sensitivity. |
| 226 | 15149950 | When added in combination with IL-6 or leptin (10 microg/ml), the TNF-alpha-induced increase in DAG synthesis was inhibited. |
| 227 | 15465639 | Culture with TNF-alpha increased activity of both SULT 1A1 and 1A3 in the HT-29 cells; TGF-beta also increased activities of both isoforms but to a lesser extent; insulin increased activity of SULT 1A1 only. |
| 228 | 15467196 | Choroidal explants in the early diabetic stage released vascular endothelial growth factor (VEGF) and tended to increase tumor necrosis factor (TNF) alpha and platelet-derived growth factor (PDGF)-B, and concomitantly facilitated growth of sprout and buds, compared to the normal control. |
| 229 | 15472209 | Inverse correlations between indexes of insulin sensitivity and serum markers of inflammation have been observed and, particularly, TNF-alpha has been shown to be associated with the appearance of insulin resistance in pregnancy. |
| 230 | 15258755 | All the PDCL showed resistance to Fas-mediated apoptosis but were significantly sensitive to the pro-apoptotic effect of inflammatory cytokines [interleukin (IL)-1beta, tumor necrosis factor (TNF)alpha and interferon gamma]. |
| 231 | 15319185 | Unstimulated islet endothelium showed constitutive levels of ICAM-1 counter-ligand expression with minimal VCAM-1 expression; however, TNF-alpha stimulation increased cell surface density of both molecules. |
| 232 | 15578112 | Moreover, in patients with type 2 diabetes, serum resistin levels are correlated with levels of soluble tumor necrosis factor alpha receptor, an inflammatory marker linked to obesity, insulin resistance, and atherosclerosis. |
| 233 | 15895517 | The present results thus indicate that CLA feeding promotes insulin resistance in obese/diabetic mice by at least inverse regulation of leptin and adiponectin, and TNFalpha, adipocytokines known to either ameliorate or deteriorate insulin sensitivity, respectively. |
| 234 | 16145910 | Rosiglitazone can decrease the level of serum TNF-alpha significantly and improve insulin resistance. |
| 235 | 15613407 | In obese subjects with type 2 diabetes mellitus, the administration of r-metHuLeptin for 4 or 16 wk, resulting in high pharmacologic leptin levels, did not activate the TNF-alpha system or increase cytokines or inflammatory markers, including IL-10, IL-6, C-reactive protein, monocyte chemoattractant protein-1, and soluble intercellular adhesion molecule-1. |
| 236 | 15690148 | CD40 is expressed by beta cells, and its expression is upregulated by proinflammatory cytokines (IL-1beta, IFN-gamma and TNF-alpha). |
| 237 | 15700135 | Autotaxin expression was up-regulated by treatment with TNFalpha (insulin resistance-promoting cytokine), and down-regulated by rosiglitazone treatment (insulin-sensitising compound) in 3T3F442A adipocytes. |
| 238 | 15700136 | The OPG production into the medium decreased dose- and time-dependently after insulin treatment (maximal effect approximately 60% of control) in HVSMCs, whereas TNF-alpha supplement gave rise to increased OPG synthesis in a time- and dose-dependent manner (maximal effect approximately 200% of control). |
| 239 | 15749853 | We now report that HSP60 in vitro differentially modulates the expression of Th1/Th2 transcription factors in human T cells: HSP60 down-regulates T-bet, NF-kappaB, and NFATp and up-regulates GATA-3, leading to decreased secretion of TNF-alpha and IFN-gamma and enhanced secretion of IL-10. |
| 240 | 15753227 | TNF-alpha and glucose induced a dose- and time-dependent activation of the p38 MAP kinase, the downstream kinase mitogen- and stress-activated kinase 1, and the transcription factor cAMP-responsive element-binding protein (CREB), in EPCs. |
| 241 | 15757867 | SOCS-1, -2 and -3 mRNA expression was strongly increased in human islets after exposure, in vitro, to IFN-gamma, IL-1beta and TNF-alpha. |
| 242 | 15766512 | In addition, adiponectin inhibits the inflammatory process that accompanies atherogenesis, as it reduces the expression of endothelial adhesion molecules, macrophage-to-foam cell transformation, tumor necrosis factor-alpha (TNF-alpha) expression in macrophages and adipocytes, and smooth muscle cell proliferation. |
| 243 | 15772055 | IL-6 stimulates the appearance in the circulation of other anti-inflammatory cytokines such as IL-1ra and IL-10 and inhibits the production of the proinflammatory cytokine TNF-alpha. |
| 244 | 15772055 | We suggest that regular exercise induces suppression of TNF-alpha and thereby offers protection against TNF-alpha-induced insulin resistance. |
| 245 | 15784408 | Fasting blood samples were used to determine concentrations of TNF alpha, soluble TNF receptors 1 (sTNFR1) and 2 (sTNFR2) in the same 13 MA (7 women, 6 men, age=27.0+/-2.0 years, BMI=23.0+/-0.7) and 13 NHW (7 women, 6 men, age=24.8+/-1.5 years, BMI=22.8+/-0.6) previously shown to exhibit differences in insulin sensitivity. |
| 246 | 15784465 | To better understand the cytokine death-signal transduction pathways in human beta cells, we investigated the inhibitory effects of Bcl-2 (protooncogene bcl-2) and X-linked inhibitor of apoptosis (XIAP) on TRAIL (TNF-related apoptosis-inducing ligand)-induced human beta-cell destruction. |
| 247 | 15718275 | Immunohistochemistry displayed a greater amount of TNF-related apoptosis-inducing ligand (TRAIL) and KILLER, a key murine ligand and receptor involved in the extrinsic pathway, expressed in cumulus cells from hyperglycemic mice compared with controls, suggesting that this apoptotic pathway may be up-regulated under diabetic stress. |
| 248 | 15826820 | Using quantitative real-time PCR we could show that basal TGF-beta mRNA expression is about 2-fold decreased in end-stage renal failure patients, while expression of TNF-alpha becomes 2-fold increased, further doubling during hemodialysis. |
| 249 | 15837949 | Tumor necrosis factor-alpha (TNF-alpha), an inducer of angiotensinogen in hepatocytes, is elevated in hyperinsulinemic, obese individuals and may provide a link in mediating insulin upregulation of the RAS in adipose tissue. |
| 250 | 15837949 | Isolated human abdominal subcutaneous adipocytes (n=12) were treated with insulin (1 to 1000 nmol/L), insulin in combination with RSG (10 nmol/L), and RSG (10 nmol/L) alone to determine angiotensinogen expression and angiotensin II, bradykinin, and TNF-alpha secretion. |
| 251 | 15837949 | Subcutaneous adipocytes were also treated with TNF-alpha (10 to 100 ng/mL) to examine the direct effect on angiotensinogen expression and angiotensin II secretion. |
| 252 | 15837949 | Insulin increased TNF-alpha secretion in a concentration-dependent manner (P<0.01), whereas RSG (10 nmol/L) significantly reduced the insulin-mediated rise in TNF-alpha (P<0.001), as well as angiotensin and angiotensin II. |
| 253 | 15837949 | This study also demonstrates a potential TNF-alpha-mediated mechanism through which insulin may stimulate the RAS and may contribute to explain obesity-associated hypertension. |
| 254 | 15850715 | Long chain polyunsaturated fatty acids (LCPUFAs) increase cell membrane fluidity and enhance the number of insulin receptors and the affinity of insulin to its receptors; suppress TNF-alpha, IL-6, macrophage migration inhibitory factor (MIF) and leptin synthesis; increase the number of GLUT-4 receptors, serve as endogenous ligands of PPARs, modify lipolysis, and regulate the balance between pro- and anti-oxidants, and thus, play a critical role in the pathogenesis of insulin resistance. |
| 255 | 15850785 | The aims of the present study were: (1) to identify the promoter region responsible for basal transcription of the human adiponectin gene, and (2) to investigate the mechanism by which adiponectin was regulated by TNF-alpha. |
| 256 | 15850785 | The present data indicate that the putative response elements for SREBP and C/EBP are required for human adiponectin promoter activity, and that suppression by TNF-alpha may, at least in part, be associated with inactivation of C/EBP-beta. |
| 257 | 15790730 | Neutralization of MIF also down-regulated the ex vivo secretion of the proinflammatory mediators, TNF-alpha, interferon-gamma, and nitric oxide, while augmenting that of the antiinflammatory cytokine, IL-10. |
| 258 | 15849359 | In addition, using a phospho-specific antibody against IRS-1 phosphorylated at Ser(24), we found that interleukin-1 or TNF-alpha treatment of Fao cells stimulated increased phosphorylation of endogenous IRS-1 at Ser(24). |
| 259 | 15849359 | TNF-alpha-regulated phosphorylation at Ser(24) in the pleckstrin homology domain of IRS-1 by mPLK/IRAK represents an additional mechanism for cross-talk between inflammatory signaling and insulin signaling that may contribute to metabolic insulin resistance. |
| 260 | 15935983 | Anti-sense IGFBP-3 oligo at 10 microg/mL significantly inhibited apoptosis induced by 100 ng/mL TNF-alpha, serum-free conditions, or high (25 mM) glucose. |
| 261 | 15935983 | Increased IGFBP-3 release associated with high ambient glucose or TNF-alpha was inhibited by pre-treatment with anti-sense oligo. |
| 262 | 15935983 | In summary, these data support a novel mechanism for TNF-alpha-induced mesangial cell apoptosis mediated by IGFBP-3 and present regulation of pThr308 activity as a novel mechanism underlying IGFBP-3 action. |
| 263 | 15952917 | Among those, adiponectin, visfatin and omentin appear as insulin-sensitising adipocytokines, whereas TNF-alpha, IL-6 and resistin induce insulin resistance. |
| 264 | 15917841 | Gene expression and/or medium concentrations of interleukin (IL)-1beta, IL-1 receptor antagonist (IL-1 RA), TNFalpha, IL-6, IL-8, resistin, PAI-1 and leptin were analysed. |
| 265 | 15917841 | Thus, human adipose tissue from nonobese individuals releases substantial amounts of IL-6, IL-8 and IL-1 RA and the gene expression of these cytokines, like that of IL-1beta and PAI-1, is regulated by TNFalpha. |
| 266 | 16039994 | Induction of TNF-alpha in U937 cells by hResistin was markedly reduced in the presence of either dominant negative IkappaBalpha plasmid or PDTC, a pharmacological inhibitor of NF-kappaB. |
| 267 | 16093575 | Troglitazone improved insulin sensitivity (mean increase in whole body glucose uptake 23.1 +/- 10.5% (p = 0.047)) and normalised plasma concentrations of hsCRP, tPA and TNF-alpha, whereas it did not significantly change IL-6, leptin and PAI-1. |
| 268 | 16043194 | On the other hand, it has been suggested that TNFalpha may facilitate glucose uptake through GLUT 1 expression. |
| 269 | 16114068 | Similarly, in type 2 diabetes, the adipocyte-derived cytokines including TNF-alpha are elevated in the circulation, causing inflammation and insulin resistance. |
| 270 | 16114068 | We used RINr1046-38 (RIN) insulin-producing beta-cells, which constitutively express calbindin-D(28k), to characterize the effect of TNF-alpha on apoptosis, replication, insulin release, and gene and protein expression. |
| 271 | 16114068 | The subcellular localizations of Bcl-2, an antiapoptotic protein, and Bax, a proapoptotic protein, within RIN cells were altered with TNF-alpha treatment such that the two were colocalized with mitochondria in the perinuclear region. |
| 272 | 16154537 | Here, we found that: (i) XIAP level was inversely correlated with tumor necrosis factor (TNF)-alpha-induced apoptosis in MIN6N8 insulinoma cells; (ii) adenoviral XIAP overexpression abrogated the TNF-alpha-induced apoptosis through inhibition of caspase activity; (iii) downregulation of XIAP by antisense oligonucleotide or Smac peptide sensitized MIN6N8 cells to TNF-alpha-induced apoptosis; (iv) XIAP expression was induced by TNF-alpha through a nuclear factor-kappaB (NF-kappaB)-dependent pathway, and interferon (IFN)-gamma prevented such an induction in a manner independent of NF-kappaB, which presents a potential mechanism underlying cytotoxic IFN-gamma/TNF-alpha synergism. |
| 273 | 16157299 | To understand the role of adipocytokines in improving insulin sensitivity via activation of the nuclear receptor peroxisome proliferator-activated receptor-alpha (PPAR-alpha) and -gamma (PPAR-gamma), we examined the expression of visfatin, adiponectin, and TNF-alpha in visceral fat depots of Otsuka Long-Evans Tokushima fatty (OLETF) rats from early to advanced diabetic stage (from 28 to 40 weeks of age). |
| 274 | 16157299 | Rosiglitazone significantly increased serum adiponectin concentration from 20 to 40 weeks of age (P<0.05), whereas fenofibrate reduced TNF-alpha concentration. |
| 275 | 16175602 | In conclusion, forced overfeeding with a high-fat diet in mice induces obesity, insulin resistance, and SH in the absence of TNF signaling or Cyp2e1 induction. |
| 276 | 16180338 | While TNFalpha produced a decrease on VAP-1/SSAO membrane form content, isoproterenol did not modify it. |
| 277 | 16186396 | TNF-alpha infusion increases phosphorylation of p70 S6 kinase, extracellular signal-regulated kinase-1/2, and c-Jun NH(2)-terminal kinase, concomitant with increased serine and reduced tyrosine phosphorylation of insulin receptor substrate-1. |
| 278 | 16186410 | We hypothesize that CIDEA alleles regulate human obesity through impact on basal metabolic rate and adipocyte TNF-alpha signaling. |
| 279 | 16143422 | TNFalpha pathway activity was correlated with LDL cholesterol, steatosis, and insulin resistance, which, in turn, was correlated with the severity of liver damage. |
| 280 | 16143422 | TNFalpha genotype modulates the activity of the TNFalpha pathway, influences insulin sensitivity and the severity of HCV chronic hepatitis. |
| 281 | 16306347 | IL-1beta and/or TNF-alpha plus IFN-gamma induce beta-cell apoptosis via the activation of beta-cell gene networks under the control of the transcription factors NF-kappaB and STAT-1. |
| 282 | 16307975 | Markers of 8-hydroxydeoxy-guanosine (8-OHdG), endothelin-1 (ET-1), and [nitrate+nitrite], an indicator of nitric oxide (NO) production, in addition to C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) in peripheral blood were also determined. |
| 283 | 16129698 | Six weeks after STZ injection, impairment of left ventricular (LV) function parameters measured by a Millar-tip catheter (peak LV systolic pressure; dP/dtmax; dP/dtmin) was accompanied by a significant increment of ICAM-1 and VCAM-1 (CAMs) expression, as well as of beta2-leukocyte-integrins+ (CD18+, CD11a+, CD11b+) and cytokine (TNF-alpha and IL-1beta)-expressing infiltrates in male Sprague-Dawley (SD-STZ) rats compared with normoglycemic littermates. |
| 284 | 16263129 | This was accompanied by increased medium levels of TNFalpha, IFNgamma and IL-10, which suggest that either CD4(+)CD25(+) cells, macrophages, or both, down-regulate production of both Th1 and certain Th2 cytokines. |
| 285 | 16219717 | We found that adiponectin was negatively correlated with body mass index, waist to hip ratio, insulin, and fasting triglyceride, and positively with high-density lipoprotein, low-density lipoprotein, and total cholesterol, TNF-alpha, and sVCAM-1, but was not related to C-reactive protein, IL-6, and sE-selectin. |
| 286 | 16331857 | In most cells, TNF mediates its effects through activation of caspases, NF-kappaB, AP-1, c-jun N-terminal kinase, p38 MAPK, and p44/p42 MAPK. |
| 287 | 16358360 | Ten daily injections of 400 ng IL-23, starting on the first day of MLD-STZ administration led to significant and sustained hyperglycemia along with weight loss compared with controls (no IL-23), and a significant increase in the number of infiltrating cells, a lower insulin content, enhanced apoptosis, expression of IFN-gamma and IL-17 (not seen in the controls) and a significant increase in the expression of TNF-alpha and IL-18 in the pancreatic islets. |
| 288 | 16367949 | IL-10 and IL-15 increased significantly from phases 2 to 3, whereas that of TNF-alpha decreased significantly and progressively from phases 1 to 3 in the spleens. |
| 289 | 16367949 | IL-15 is known to up-regulate the production of proinflammatory cytokines, IL-1beta, IL-8, IL-12, IL-17, IFN-gamma and TNF-alpha and has an inhibitory effect on activation-induced cell death. |
| 290 | 16277639 | NIT-1 cells are highly susceptible to caspase-dependent apoptosis induced by TNF-alpha alone. |
| 291 | 16277639 | TNF-alpha also did not induce phosphorylation of c-Jun N-terminal kinase in NIT-1 cells. |
| 292 | 16328103 | Insulin modulates TNF-alpha-induced ICAM-1 expression on microvascular endothelium controlling, therefore, leukocyte adhesion and migration. |
| 293 | 16368716 | In cultured retinal capillary endothelial cells, PEDF significantly decreased TNF-alpha and ICAM-1 expression under hypoxia. |
| 294 | 16430720 | TNF-alpha and ICAM-1 levels in atherosclerotic plaques appear to progressively increase whereas adiponectin levels progressively decrease with smoking status. |
| 295 | 16433757 | Pro-inflammatory cytokines, IL-1beta and IL-6, were significantly increased 3 h after IPIT, while TNF-alpha was elevated for up to 5 days post-IPIT. |
| 296 | 16170833 | TNFalpha correlated inversely with insulin secretion in pregnancy (r = -0.35, p = 0.03) and was significantly higher in the GDM group (2.62 +/- 0.3 vs 1.88 +/- 0.3 pg/mL, p = 0.01) in pregnancy. |
| 297 | 16468038 | However, LTA is in linkage disequilibrium with both the HLA gene cluster and the gene encoding TNF-alpha, making inferences about causality difficult. |
| 298 | 16492207 | In summary, pioglitazone caused an immediate increase in circulating adiponectin levels, followed by a reduction of TNF-alpha. |
| 299 | 16505224 | Compared with nondiabetic plaques, diabetic plaques had more macrophages, T-cells, and HLA-DR+ cells (P < 0.001); more ubiquitin, proteasome 20S activity (TNF-alpha), and NF-kappaB (P < 0.001); and more markers of oxidative stress (nitrotyrosine and O2(-) production) and MMP-9 (P < 0.01), along with a lesser collagen content and IkappaB-beta levels (P < 0.001). |
| 300 | 16507891 | At 21 hours, TNF-alpha inhibition significantly reduced fibroblast apoptosis and caspase-3 activity in both diabetic and normoglycemic mice (P < 0.05). |
| 301 | 16555056 | By trend analyses, group L had reduced levels of PAI-1 (p=0.002), hs-CRP (p<0.0001) and TNF-alpha (p=0.006), while no significant changes were observed in the levels of leptin or adiponectin. |
| 302 | 16634986 | Furthermore, adiponectin secretion from adipocytes is enhanced by thiazolidinediones (which also act to antagonize TNF-alpha effects). |
| 303 | 16634986 | Thus, adiponectin may be the common mechanism by which TNF-alpha promotes, and the thiazolidinediones suppress, insulin resistance and inflammation. |
| 304 | 16437243 | Results showed that: (1) IL-10 production was lower; (2) IL-10 ICC was reduced; (3) B7-H1-expressing CD19(+) cells were diminished; and (4) TNFalpha production and ICC by CD4(+) T cells was augmented in DM patients. |
| 305 | 16556731 | NF-kappaB activation was induced in INS-1E cells and in 208F cells after exposure to cytokines, but apoptosis was induced only in INS-1E cells, with a more pronounced proapoptotic effect of IL-1beta than of TNF-alpha. |
| 306 | 16814613 | Adiponectin levels increased from 3.7 to 10.3 mug/mL at week 48 (P < .01); the levels of the other cytokines were unchanged: TNF-alpha, 9.1 vs 8.8 pg/mL; IL-1a, 3.9 vs 3.4 pg/mL; IL-6, 19.4 vs 13.4 pg/mL; and leptin, 24.8 vs 29.6 ng/mL (P > .05 for all). |
| 307 | 16870142 | In addition, insulin failed to decrease angptl4 mRNA expression in an insulin-resistant state induced by TNF-alpha in 3T3-L1 adipocytes. |
| 308 | 16880599 | TNFalpha induces insulin resistance in type 2 diabetes, but its mechanism of action is not fully understood. |
| 309 | 16696964 | Levels of TNF-alpha, IL10 and total NAG enzyme activity with its A and B isoforms were measured in serum and urine of all participants. |
| 310 | 16983055 | In addition, sleep loss induced a more than 3-fold increase in transcription of interleukin 6 messenger RNA and a 2-fold increase in tumor necrosis factor alpha messenger RNA. |
| 311 | 17001213 | We analysed the relationship of these risk factors with the following five gene polymorphisms potentially involved in cardiovascular risk: ATP-binding cassette transporter A1-R219K, Peroxisome proliferator-activated receptor (PPAR)-alpha-L162V, Lipoprotein lipase (LPL)-HindIII, Paraoxonase (PON)1-Q192R, and Tumour necrosis factor (TNF)-alpha-G-308A. |
| 312 | 17002473 | We also showed that dietary CLA significantly decreased the level of tumor necrosis factor-alpha (TNF-alpha), associated with the development of insulin resistance, in the skeletal muscle of Zucker rats. |
| 313 | 16857181 | Serum EC-SOD concentrations may be a sensitive biochemical marker of insulin resistance in patients with type 2 diabetes and hypertension and that losartan improves insulin sensitivity by increasing EC-SOD and adiponectin production and decreasing TNF-alpha production. |
| 314 | 17026986 | TNF-alpha-induced endothelial cell apoptosis was associated with increased inducible NO synthase but reduced endothelial NO synthase (eNOS) protein expression. |
| 315 | 17026986 | N-acetylcysteine attenuation of TNF-alpha-induced human vascular endothelial cell apoptosis is associated with the restoration of eNOS expression. |
| 316 | 17046548 | Incubation of THLE-5b cells with TNF-alpha stimulated PAI-1 production via protein kinase C-, mitogen-activated protein kinase-, protein tyrosine kinase-, and nuclear factor-kappaB-dependent pathways. |
| 317 | 17046548 | A thiazolidinedione, pioglitazone, reduced TNF-alpha-induced PAI-1 production by 32%, via protein kinase C- and nuclear factor-kappaB-dependent pathways. |
| 318 | 17062893 | Leptin levels were decreased, while TNF-alpha and IL-6 were increased at diagnosis and normalized at 1 month. |
| 319 | 17065523 | In addition, SK inhibitors were shown to block TNFalpha-induced expression of adhesion proteins, suppress VEGF-induced vascular leakage in an in vivo mouse model, and reduce retinal vascular leakage in the rat diabetic retinopathy model. |
| 320 | 16737350 | SAA treatment of vascular endothelial cells and monocytes markedly increased the production of inflammatory cytokines, e.g., interleukin (IL)-6, IL-8, tumor necrosis factor alpha, and monocyte chemoattractant protein-1. |
| 321 | 16895955 | We measured serum concentrations and sc and epicardial adipose tissue mRNA expression of IL-6, monocyte chemoattractant protein-1 (MCP-1), TNF-alpha, leptin, resistin, and adiponectin and sc and epicardial adipose tissue mRNA expression of CD14, CD45, and CD68. |
| 322 | 17072583 | TNFalpha has been described as a link between obesity and the development of insulin resistance, an important contributor to the pathogenesis of type 2 diabetes. |
| 323 | 17072583 | NR1HR agonists ameliorate TNFalpha-induced insulin resistance restoring completely insulin-stimulated glucose uptake and SLC2A4 translocation to plasma membrane. |
| 324 | 17072583 | This effect is parallel to the recovery of the insulin cascade insulin receptor/IRS-2/phosphatidylinositol 3-kinase/protein kinase B, and could be due to the fact that T0901317 prevents the increase of PTPN1 production and phosphatase activity produced by TNFalpha. |
| 325 | 17083157 | Tumor necrosis factor-alpha (TNF-alpha) system is potentially involved in the development of insulin resistance during pregnancy. |
| 326 | 17087783 | The decrease in TNF-alpha concentrations during oGTT and the inverse correlation between endogenous hyperinsulinaemia and serum TNF-alpha concentrations suggested an anti-inflammatory effect of moderately-high insulin concentrations. |
| 327 | 17181562 | In case of obesity, FFAs and TNF-alpha are produced in abundance by adipocytes, whereas the production of adiponectin, an anti-inflammatory adipokine, is reduced. |
| 328 | 17189873 | We compared the number of circulating monocyte and dendritic cell (DC) subsets as well as their capacity to produce inflammatory cytokines IL-1beta, IL-6, and tumor necrosis factor-alpha (TNF-alpha) in type 2 diabetic men with (n=11) and without (n=44) chronic atherosclerotic complications. |
| 329 | 17189875 | Proinflammatory cytokines such as interleukin-1 and tumor necrosis factor-alpha (TNF-alpha) also stimulated NF-kappaB-dependent transcription and showed an additive effect with high glucose. |
| 330 | 16770837 | ADMA (30 microM) significantly increased the activity of NF-kappaB and elevated the levels of ICAM-1 and TNF-alpha, and pre-treatment with rosiglitazone (10 or 30 microM) markedly inhibited the increased activity of NF-kappaB and reduced the elevated levels of TNF-alpha and ICAM-1 induced by ADMA in cultured endothelial cells. |
| 331 | 16943230 | The ability of VEGF-C to prevent apoptosis induced by TNFalpha or hyperglycaemia in endothelial cells was assessed by flow cytometry. |
| 332 | 16943230 | TNFalpha up regulated both VEGF-C and vascular endothelial growth factor receptor-2 (VEGFR)-2 expression in endothelial cells in a dose-dependent manner, but had no effect on VEGFR-3. |
| 333 | 16943230 | Flow cytometry results showed that VEGF-C prevented endothelial cell apoptosis induced by TNFalpha and hyperglycaemia and that the antiapoptotic effect was mainly via VEGFR-2. |
| 334 | 16943230 | In pericytes, the expression of VEGF-C mRNA remained stable on exogenous TNFalpha treatment. |
| 335 | 16943230 | In retinal endothelial cells, TNFalpha stimulates the expression of VEGF-C, which in turn protects endothelial cells from apoptosis induced by TNFalpha or hyperglycaemia via VEGFR-2 and thus helps sustain retinal neovascularisation. |
| 336 | 17079333 | SIMPL (signaling molecule that associates with mouse Pelle-like kinase) is a component of a signaling pathway through which tumor necrosis factor-alpha (TNF-alpha) induces NF-kappaB-controlled gene transcription. |
| 337 | 17079333 | SIMPL interacts with the nuclear pool of the NF-kappaB subunit, p65, in a TNF-alpha-dependent manner to enhance p65-dependent gene transcription. |
| 338 | 17079333 | SIMPL mutants lacking sites of TNF-alpha-enhanced phosphorylation impaired nuclear localization and prevented TNF-alpha-induced p65 transactivation activity. |
| 339 | 17438370 | The factors contributing to defects in fatty acid metabolism are not understood but new data demonstrates that increased TNFalpha in obesity increases protein phosphatase 2C (PP2C), which in turn suppresses the activity of AMP-activated protein kinase (AMPK), a critical regulator of energy metabolism.(1) These data identify a novel mechanism by which inflammation in obesity is a precursor to defects in skeletal muscle fatty acid oxidation that generates a vicious cycle exacerbating the development of insulin resistance. |
| 340 | 17440992 | SEC treatments dose-dependently decreased IL-6 and TNF-alpha levels, increased IL-4 and IL-10 levels, as well as upregulated IL-10 mRNA expression (P < 0.05). |
| 341 | 17442272 | Cytokines like TNFalpha and IL-6 are secreted by the inflammatory cells and have been shown to impair normal adipocyte differentiation. |
| 342 | 17454170 | TNF-alpha levels were correlated with glycated hemoglobin in GDM. |
| 343 | 16787648 | Using logistic regression analysis we demonstrated that IL-6 levels (III versus I tertile, OR: 2.10; 1.10-3.75), TG (III versus I tertile OR: 27.45; 8.47-88.93), fasting insulin (III versus I tertile OR: 2.84; 1.50-5.42), and age (OR: 1.038; 1.002-1.075) were associated with low HDL-C independent of smoking, BMI, waist circumference, hypertension, diabetes, physical activity, alcohol intake, oral hypoglycaemics, CRP, IL-18, and TNF-alpha levels. |
| 344 | 17347312 | Our results suggest that decreased plasma adiponectin, increased plasma resistin and cholesterol, and elevated levels of TNF-alpha and IL-6 in adipocytes may all contribute to the insulin resistance observed in GH-Tg mice. |
| 345 | 17498265 | The TNF-alpha-308 G allele was in linkage disequilibrium (LD) with the human leukocyte antigen (HLA)-B*0801-DRB1*0301 haplotype, while TNF-alpha-308 A allele was in LD with the HLA-B*5001-DRB1*0301 and B*5801-DRB1*0301 haplotypes, suggesting that the effect of TNF-alpha -308 A allele is not because of its being in LD with any HLA alleles, but because of its functional role and its integrated effect with other cytokines. |
| 346 | 17505154 | TNF-alpha, IL-6 and hs-CRP levels were positively, adiponectin negatively correlated with adipocyte size. |
| 347 | 17592243 | In addition, IL-1alpha and TNF-alpha stimulating the insulin, TGF-beta, and Toll-like receptor signaling pathways may have different effects in diabetic keratocytes. |
| 348 | 17617381 | In this study, we show that methylglyoxal inhibits TNF-induced NF-kappaB activation and NF-kappaB-dependent reporter gene expression by inhibiting the DNA binding capacity of NF-kappaB p65. |
| 349 | 17617381 | The TNF-induced nuclear translocation of NF-kappaB p65 was also delayed, but not inhibited, in the presence of methylglyoxal. |
| 350 | 17627577 | Despite accumulating evidence showing that TNF-related apoptosis inducing ligand (TRAIL) plays a role in vascular biology and that its decoy receptor osteoprotegerin (OPG) is expressed in the vessel wall, modulation of these TNF and TNF-R family members in the early phases of diabetes mellitus has not been investigated. |
| 351 | 17647141 | We determined the prevalence of Tregs by Foxp3 expression of CD4 (+) cells; prevalence of myeloid and plasmacytoid dendritic cells (DCs); prevalence of tumor necrosis factor (TNF)-alpha and interleukin(IL)-12 producing monocytes; and prevalence of IL-2, IL-4 and IFN-gamma producing CD4 (+) cells. |
| 352 | 17595249 | Changes in bone-specific ALP levels showed a moderate negative correlation with the changes in the TNF-alpha levels after rosiglitazone treatment and after diet in the diabetic control group. |
| 353 | 17676307 | Both purified and recombinant hCG prevented development of diabetes in NOD mice. hCG decreased the proportion and number of CD4(+) and CD8(+) T cells and inhibited T cell proliferative responses against beta cell antigens. hCG treatment suppressed IFN-gamma production, but increased IL-10 and TGF-beta production in splenocytes stimulated with anti-CD3 antibody. hCG treatment also suppressed TNF-alpha production in splenocytes stimulated with lipopolysaccharide. |
| 354 | 17716860 | Our data indicate that NOD derived FTOC produce a smaller percentage of double negative (CD4(-)/CD8(-)) thymocytes expressing TNF receptors compared to non-diabetic C57BL/6 (B6) derived FTOC. |
| 355 | 17719095 | Adipose tissue macrophages (ATMs) are suspected to be the major source of inflammatory mediators such as TNF-alpha and IL-6 that interfere with adipocyte function by inhibiting insulin action. |
| 356 | 17785827 | This phenotype correlates with a diminished proliferation capacity of both CD4+CD25- effector and CD4+CD25+ regulatory T cells upon in vitro stimulation of the TLR1/TLR2 pathway by the ligand palmitoyl-3-cysteine-serine-lysine 4, and with the constitutive down-regulation of Tnf-alpha and IL-6 in macrophages of Idd6- congenic mice. |
| 357 | 17620422 | The induction of X-linked inhibitor of apoptosis protein by TNF-alpha was inhibited by IFN-gamma in STAT1(+/-) islet cells but not in STAT1(-/-) islet cells. |
| 358 | 17646208 | Tumor necrosis factor (TNF)-alpha is known to affect insulin sensitivity, glucose, and lipid metabolism through alternative and redundant mechanisms at both translational and post-translational levels. |
| 359 | 17664271 | We found that beta-arrestin-1 is associated with TRAF2 (TNF receptor-associated factor 2), an adaptor protein of TNF receptors, and that TNFalpha acutely stimulates tyrosine phosphorylation of G alpha(q/11) with an increase in G alpha(q/11) activity. |
| 360 | 17664271 | TNFalpha also led to activation of JNK with increased expression of the proinflammatory gene, monocyte chemoattractant protein-1 and matrix metalloproteinase 3, and beta-arrestin-1 knockdown inhibited both of these effects. |
| 361 | 17893259 | Recently, we have determined the transcriptome of omental adipose tissue, leading to the identification of a new candidate gene for obesity-related metabolic complications, zinc finger protein 36 (ZFP36), which is known to down-regulate tumor necrosis factor-alpha TNF-alpha) expression. |
| 362 | 17141246 | The objectives of this study were to examine the influence of PPAR gamma and its agonist (rosiglitazone) on the TNFalpha, IL-6, IL-8 and IL-10 gene expression in monocytes of patients with diabetic macroangiopathy and to analyse obtained results in context of selected atherogenic factors ant direct indicators of endothelial lesion. |
| 363 | 17883332 | We examined, in vascular endothelial cells, whether the selective expression of heme oxygenase-1 (HO-1) offers cytoprotection against glucose- and TNF-mediated cell death. |
| 364 | 17883332 | The effects of HO-1 transduction (Ad-VECAD-HO-1 gene) on HO-1 expression, HO activity, and the response to TNF and hyperglycemia were studied. |
| 365 | 17883332 | Selective expression of HO-1 prevented TNF- and hyperglycemia-mediated superoxide (O2-) formation, DNA degeneration, and upregulation of caspase, but increased the expression of pAkt and Bcl-xL, proteins responsible for endothelial dysfunction in diabetes. |
| 366 | 17950103 | Real-time polymerase chain reaction was used to measure gene expression of LPIN1 and adipogenic (PPARgamma, SREBP1c) and inflammatory markers (IL6, TNFalpha, TNFR1, and TNFR2). |
| 367 | 17952840 | By contrast, circulating visfatin, TNF-alpha, and IL-6 levels showed no difference between DM2 and control women, while adiponectin plasma levels were significantly decreased in the DM2 women (p<0.001). |
| 368 | 17956334 | Finally, IL-6 mediates anti-inflammatory effects by stimulating the production of anti-inflammatory cytokines and by suppressing TNFalpha (tumour necrosis factor alpha) production. |
| 369 | 17962866 | Tumor necrosis factor affects insulin receptor substrate phosphorylation, resulting in decreased glucose uptake and compensatory hyperinsulinemia. |
| 370 | 17966038 | HLA-DQ8 transgenic mice expressing the costimulatory molecule, B7.1 (RIP.B7.1), or the proinflammatory cytokine, TNF-alpha (RIP.TNF) or both (RIP.B7.RIP.TNF) under the control of rat insulin promoter (RIP) were used. |
| 371 | 17936398 | Treatments with insulin and TNFalpha as well as stearic acid, a saturated free fatty acid, upregulated RELMbeta expression, while d-glucose downregulated RELMbeta. |
| 372 | 17936398 | These results suggest RELMbeta expression to be regulated directly by nutrients such as glucose and saturated free fatty acids including stearic acid, as well as by hormones including insulin and TNFalpha. |
| 373 | 18064475 | TNF-alpha expression was seen in Schwann cells and some macrophages of DLRPN and LRPN nerves, whereas IL-6 expression was minimal. |
| 374 | 18064475 | NF-kappaB expression correlated with the number of empty nerve strands (P < 0.01) and the frequency of axonal degeneration (P < 0.05), whereas TNF-alpha expression correlated inversely with the number of empty nerve strands of teased fibers (P < 0.05). |
| 375 | 18078928 | Tumor necrosis factor (TNF)-alpha and local activation of the renin-angiotensin system may contribute to insulin resistance and atherosclerosis. |
| 376 | 18078928 | ACE, angiotensinogen, and angiotensin AT(1) receptor mRNA expression were upregulated time-dependently by TNF-alpha. |
| 377 | 18078928 | These results suggest that TNF-alpha and the local renin-angiotensin system coordinately stimulate PAI-1 production in hepatocytes. |
| 378 | 18171433 | MAP4k4 depletion in adipocytes increases many of the RIP140-sensitive genes, increases adipogenesis and mediates some actions of tumour necrosis factor-alpha (TNF-alpha). |
| 379 | 18180317 | In a spontaneously transformed human umbilical vein endothelial cell (HUVEC) line, C11-spontaneously transformed HUVEC (STH) and primary HUVEC cells, GLP-1 treatment, in the presence of a dipeptidyl peptidase IV inhibitor, attenuated induction of PAI-1 protein and mRNA expression by tumour necrosis factor-alpha (TNF-alpha). |
| 380 | 18180317 | GLP-1 also inhibited the effect of TNF-alpha on a reporter gene construct harbouring the proximal PAI-1 promoter. |
| 381 | 18180317 | In addition, GLP-1 attenuated TNF-alpha-mediated induction of Nur77 mRNA and TNF-alpha-mediated binding of nuclear proteins (NPs) to the PAI-1, Nur77, cis-acting response element nerve growth factor induced clone B response element (NBRE). |
| 382 | 18180317 | Taken together, these observations suggest that GLP-1 inhibits TNF-alpha-mediated PAI-1 induction in vascular endothelial cells, and this effect may involve Akt-mediated signalling events and the modulation of Nur77 expression and NP binding to the PAI-1 NBRE. |
| 383 | 17895880 | The release of adiponectin was enhanced by insulin and by inhibition of endogenous tumor necrosis factor (TNFalpha) using etancercept. |
| 384 | 18296638 | MKP-4 also reversed the effect of TNF-alpha to inhibit insulin signaling; alter IL-6, Glut1 and Glut4 expression; and inhibit insulin-stimulated glucose uptake in 3T3-L1 adipocytes. |
| 385 | 17940160 | In this regard, the Ser(307) residue in IRS-1 has been identified as a site for the inhibitory effects of TNF-alpha in myotubes, with p38 mitogen-activated protein kinase and inhibitor kB kinase being involved in the phosphorylation of this residue. |
| 386 | 17940160 | Conversely, Ser phosphorylation of IRS-2 mediated by TNF-alpha activation of mitogen-activated protein kinase was the mechanism found in brown adipocytes. |
| 387 | 17940160 | Moreover, up-regulation of PTP1B expression was recently found in cells treated with TNF-alpha Accordingly, myocytes and primary brown adipocytes deficient in PTP1B are protected against insulin resistance induced by this cytokine. |
| 388 | 17940160 | Furthermore, down-regulation of PTP1B activity is possible by the use of pharmacological agonists of nuclear receptors that restore insulin sensitivity in the presence of TNF-alpha. |
| 389 | 18081694 | TNFalpha neither induced beta-cell death nor did it potentiate the effects of IL-1beta, IFNgamma or IL-1beta/IFNgamma . |
| 390 | 18187553 | Exogenous TNF-alpha infusion increased c-Jun N-terminal kinase phosphorylation and insulin receptor substrate-1 serine 307 phosphorylation, and inhibited insulin-induced signaling in liver. |
| 391 | 18252892 | We isolated islets from mice lacking Bid, Bax, or Bak and those overexpressing Bcl-2 and exposed them to Fas ligand, tumor necrosis factor (TNF)-alpha, and proinflammatory cytokines or cytotoxic stimuli that activate the mitochondrial apoptotic pathway (staurosporine, etoposide, gamma-radiation, tunicamycin, and thapsigargin). |
| 392 | 18433704 | TNF-alpha induces the osteogenic bone morphogenetic protein-2 (BMP-2), Msx2, Wnt3a, and Wnt7a mRNAs and leads to increased aortic calcium accumulation. |
| 393 | 18433704 | Treatment with the TNF-alpha neutralizing antibody infliximab abrogates aortic BMP-2-Msx2-Wnt3a and Wnt7a signaling and attenuates aortic calcium accumulation significantly. |
| 394 | 18436850 | In pericytes undergoing apoptosis induced by either TNF-alpha or high glucose Ang-1 increased survival (P < 0.05 for TNF-alpha; P < 0.01 for high glucose), whereas Ang-2 increased apoptosis. |
| 395 | 18437085 | Although various members of the tumor necrosis factor (TNF) family, such as Fas ligand or TNF, have recently been implicated in the development of T1D, the lack of TNF-related apoptosis-inducing ligand (TRAIL) expression or function facilitates the onset of T1D. |
| 396 | 18281274 | We find that adipose tissue inflammation and the pro-inflammatory cytokine tumor necrosis factor alpha (TNFalpha) regulate PTP1B expression in vivo. |
| 397 | 18281274 | PTP1B overexpression in high fat-fed mice coincided with increased adipose tissue expression of the macrophage marker CD68 and TNFalpha, which is implicated in causing obesity-induced insulin resistance. |
| 398 | 18281274 | TNFalpha increased PTP1B mRNA and protein levels by 2- to 5-fold in a dose- and time-dependent manner in adipocyte and hepatocyte cell lines. |
| 399 | 18281274 | TNFalpha administration in mice increased PTP1B mRNA 1.4- to 4-fold in adipose tissue, liver, skeletal muscle, and hypothalamic arcuate nucleus and PTP1B protein 2-fold in liver. |
| 400 | 18281274 | Actinomycin D treatment blocked, and high dose salicylate treatment inhibited by 80%, TNFalpha-induced PTP1B expression in adipocyte cell lines, suggesting TNFalpha may induce PTP1B transcription via nuclear factor kappaB (NFkappaB) activation. |
| 401 | 18281274 | Chromatin immunoprecipitation from adipocyte cell lines and liver of mice demonstrated TNFalpha-induced recruitment of NFkappaB subunit p65 to the PTP1B promoter in vitro and in vivo. |
| 402 | 18329387 | A20 negatively regulates NFkappaB (nuclear factor kappaB) signaling induced by TNF receptor family and Toll-like receptors, but the mechanism of A20 action is poorly defined. |
| 403 | 18334666 | ZF rats displayed a decrease in both HO activity and HO-1 and HO-2 protein levels and an increase in tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 compared with Zucker lean (ZL) rats. |
| 404 | 18334666 | In summary, this study demonstrates that the antiobesity effect of HO-1 induction results in an increase in adiponectin secretion, in vivo and in vitro, a decrease in TNF-alpha and IL-6, and a reduction in weight gain. |
| 405 | 18385532 | In this study we tested this hypothesis by investigating the effects of dehydroxymethylepoxyquinomicin (DHMEQ), a novel NF-kappaB inhibitor, on tumor necrosis factor-alpha (TNF-alpha)-induced beta cell dysfunction. |
| 406 | 18385532 | DHMEQ suppressed TNF-alpha-induced NF-kappaB activation and partially ameliorated glucose-stimulated insulin secretion in a dose-dependent manner. |
| 407 | 18385532 | DHMEQ also partially ameliorated decreased cell viability and insulin mRNA level induced by TNF-alpha. |
| 408 | 18475052 | These results suggest that GLP-1 inhibits IFN-gamma-induced NO production by suppression of TNF-alpha production. |
| 409 | 18481952 | IL-1beta and TNFalpha mediate activation of the transcription factor NF-kappaB (nuclear factor kappaB) pathway. |
| 410 | 17614271 | After 12 weeks, weight, body mass index, waist circumference, hip circumference, waist-to-hip ratio, total body fat, total cholesterol, triglyceride, tumor necrosis factor alpha (TNF-alpha), IL-6, resistin and leptin had significantly decreased, while adiponectin and IL-10 had significantly increased. |
| 411 | 17614271 | A bivariate correlation analysis found that increment in IL-10 and baseline IL-10 levels significantly correlated with decrement in TNF-alpha (P<.01) and baseline adiponectin (r=.52, P<.001), respectively. |
| 412 | 18593820 | The present study was undertaken to determine how tumour necrosis factor-alpha (TNF-alpha) elicits the inhibition of glucose-stimulated insulin secretion (GSIS) in rat insulinoma cells (INS)-1 beta-cells. |
| 413 | 18593820 | TNF-alpha pretreatment did not change the expression levels of insulin, PDX-1, glucose transporter 2, glucokinase, K(ATP) channels, Ca(2)(+) channels, and exocytotic molecules and, furthermore, did not reduce the glucose-stimulated ATP level. |
| 414 | 18593820 | The TNF-alpha treatment was thought to activate c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein kinase (MAPK), and NF-kappaB inflammatory signals, since TNF-alpha increased phospho-JNK and phospho-p38 and reduced I kappaB levels. |
| 415 | 18593820 | These data demonstrate that TNF-alpha inhibits GSIS by reducing the glucose-stimulated Ca(2)(+) influx, possibly through the activation of JNK and p38 MAPK and NF-kappaB inflammatory signals. |
| 416 | 18661119 | In addition to previously reported IL-8, MIP-1beta and MCP-1, CD40 stimulation in ductal cells produced IL-1beta, IFN-gamma, TNF-alpha, granulocyte colony-stimulating factor and granulocyte-macrophage colony-stimulating factor. |
| 417 | 18680073 | We show that the levels of IL-8 and IL-17 were unchanged, IL-1 beta, IL-6 and TNFalpha were elevated and the level of IL-7 was decreased in PCOS patients compared to obese controls. |
| 418 | 18755353 | Pioglitazone repressed endothelial TNFalpha-induced VCAM-1 messenger ribonucleic acid expression and promoter activity, and induced hepatic IkappaBalpha in a manner dependent on both pioglitazone exposure and PPARalpha expression. |
| 419 | 18650421 | Microarray profiling revealed that, in TNF-alpha-stimulated monocytes, the induction of 25% NF-kappaB downstream genes, including the histone H3-lysine 27 demethylase JMJD3, was attenuated by SET7/9 depletion. |
| 420 | 18787467 | Irrespective of IR, DM is generally characterized by overproduction of the proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha), whereas action of the latter is modulated by the anti-inflammatory cytokine interleukin-10 (IL-10). |
| 421 | 18792875 | TNF-alpha induces production of IL-6 and it has been suggested that a causal relationship exists between endothelial dysfunction and these cytokines. |
| 422 | 18641283 | CBD inhibited adenosine uptake via equilibrative nucleoside transporter 1 and synergistically enhanced adenosine's TNF-alpha suppression after treatment with LPS. |
| 423 | 18849088 | Cell cultures were stimulated with LPS to evaluate TNF-alpha and IL-6 or with PMA and Ionomycin to evaluate IFN-gamma, IL-8 and IL-10 intracellular staining. |
| 424 | 18979174 | Tumor necrosis factor alpha (TNFalpha)-stimulated gene 6 (TSG-6) is involved in inflammation, extracellular matrix formation, cell migration, and development. |
| 425 | 18997420 | Gene expression study revealed that the diet up-regulated expression of adiponectin and down-regulated tumor necrosis factor-alpha (TNF-alpha). |
| 426 | 19011089 | DsbA-L expression in 3T3-L1 adipocytes is stimulated by the insulin sensitizer rosiglitazone and inhibited by the inflammatory cytokine TNFalpha. |
| 427 | 19022947 | In contrast to CRP and TNFalpha, adiponectin increases during weight loss and insulin sensitivity. |
| 428 | 18476983 | TNF-alpha (3.8-3.4 vs. 5.2-4.5 pg/ml) decreased (p < 0.05) and adiponectin (6.3-17.8 vs. 7.1-16.4 microg/ml) increased (p < 0.01), while leptin did not change following either treatment. |
| 429 | 19120317 | Multiple studies have shown that thymus-derived naturally occurring Tregs constitutively express the forkhead/winged helix transcription factor FoxP3 in addition to high levels of CD25, the negative co-stimulatory molecule CTLA-4, and the glucocorticoid-induced TNF receptor-related protein GITR. |
| 430 | 19125180 | Resistin mRNA expression is increased in PBMC from DM2 women, together with increased expression of the inflammatory cytokines IL-1beta, TNF-alpha, and IL-6, independent of obesity. |
| 431 | 19144262 | Moreover, TCTP transgenic Tregs inhibit the development of autoimmune diabetes due to increased survival of suppressive Tregs and decreased expression of pancreatic TNF-alpha. |
| 432 | 19159557 | In the DM rats the IkappaBalpha protein expression in the skeletal muscle was significantly lower (P < 0.05) and the NF-kappaB P65 DNA binding activity increased, and TNF-alpha, IL-1B, and IL-6 expression levels were up-regulated in comparison with the normal control group. |
| 433 | 19159557 | Early treatment of insulin and gliclazide increased the IkappaBalpha protein expression, decreased the NF-kappaB P65 DNA binding activity and the TNF-alpha expression in the skeletal muscle. |
| 434 | 19227810 | Adiponectin secretion is inhibited by TNF-alpha and by catecholamines, and is stimulated by PPAR gamma activation. |
| 435 | 19227907 | Immunological control included determination of the subpopulation composition of lymphocytes, immunoglobulins, circulating immune complexes (CIC), antibodies to cardiolipin (CL), proinflammatory cytokines: IL-1alpha, IL-2, IL-6, IL-8, alpha-interferon, tumor necrosis factor alpha (TNFalpha). |
| 436 | 19284081 | Leptin, adiponectin, TNF alfa, the hepatic expression of suppressor of cytokine signalling 3 (SOCS3), and hyperinsulinemia have been considered as heavily influencing fibrosis extension and nonresponsiveness to the IFN-alpha. |
| 437 | 19356108 | Increased adiponectin levels were associated with a decrease in TNF-alpha-induced ICAM-1 and VCAM-1 and caspase 3 activity in endothelial cells while phosphorylation of eNOS at Ser-1179 increased. |
| 438 | 19378424 | To examine the hypothesis that serum concentration of C-reactive protein (CRP) is inversely associated with insulin sensitivity and obesity, and that this may by mediated by tumor necrosis factor-alpha (TNFalpha) and interleukin-6 (IL-6). |
| 439 | 19013780 | Although the adiponectin secretion was reduced in the presence of lipopolysaccharide plus TNF-alpha and IFN-gamma, only gamma-oryzanol supported the activity of adiponectin secretion under NF-kappaB activated condition. |
| 440 | 19074983 | In endothelial cells, downregulation of LASY aggravated the inflammatory response that manifested as an increase in both basal and TNF-alpha-induced expression of the proinflammatory cytokine, monocyte chemoattractant protein-1 (MCP-1). |
| 441 | 19122171 | IGF1R downregulation uncovered an insulin-induced reduction in activation of NF-kappaB and inhibition of MCP-1 upregulation in response to TNF-alpha. |
| 442 | 19138703 | Cytoplasmic and nuclear fractions of cerebral cortex and hippocampus were prepared for the quantification of acetylcholinesterase activity, oxidative-nitrosative stress, tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), NFkappabeta and caspase-3. |
| 443 | 19138703 | After 10 weeks of streptozotocin injection, the rats produced significant increase in transfer latency which was coupled with enhanced acetylcholinesterase activity, increased oxidative-nitrosative stress, TNF-alpha, IL-1beta, caspase-3 activity and active p65 subunit of NFkappabeta in different regions of diabetic rat brain. |
| 444 | 19240767 | TNF-related apoptosisinducing ligand (TRAIL) and osteoprotegerin had the highest level of expression. |
| 445 | 19095738 | Because NF-kappaB is known to associate with acute phase inflammatory cytokines, we examined whether TNFalpha or IL-1beta could regulate GPB5. |
| 446 | 19188427 | The differences in endothelial cell and skeletal muscle signaling were mediated by the cell-specific, additive effects of IL-6 and insulin because this treatment markedly increased tumor necrosis factor (TNF)-alpha protein expression in HAECs without any effect on TNF-alpha in skeletal muscle. |
| 447 | 19188427 | In the presence of insulin, IL-6 contributes to aberrant endothelial cell signaling because of increased TNF-alpha expression. |
| 448 | 19208906 | Improvements to muscle and liver insulin sensitivity (approximately 200-400%) correlated with 50-75% decreased tumor necrosis factor (TNF)alpha production and coincided with severe Mstn deficiency. |
| 449 | 19208906 | Short-term treatment of Mstn(Ln/Ln) mice with recombinant Mstn led to increased plasma TNFalpha and insulin resistance. |
| 450 | 19228796 | Serum insulin and pancreatic insulin content were reduced in LP-fed NOD offspring at 8 weeks, as were serum interferon gamma and pancreatic tumor necrosis factor alpha, while the number of pancreatic islets demonstrating peri-insulitis, and the degree of invasiveness were reduced. |
| 451 | 19324019 | The present study demonstrates that IGFBP-3, the hypoxia-mimetic agent cobalt chloride, and TNF-alpha inhibit rosiglitazone-induced adiponectin transcription in mouse embryo fibroblasts that stably express PPAR-gamma2. |
| 452 | 19324019 | These results suggest that IGFBP-3 may mediate the inhibition of adiponectin transcription by hypoxia and TNF-alpha, and that IGFBP-3 binding to RXR-alpha may be required for the observed inhibition. |
| 453 | 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. |
| 454 | 19422086 | These genes were largely associated with activated neutrophils and macrophages, including chemokine ligands, CXCL1, CXCL2, CCL3, CCL4; chemokine receptors, CXCR1 or CXCR2, CCR1, CCR2; and regulatory cytokines tumor necrosis factor alpha and interleukin-6. |
| 455 | 19351711 | TNF-alpha, but not IL-6 or resistin, increased Wnt10b, completely inhibited the normal differentiation of the preadipocytes, and instead induced a proinflammatory and macrophage-like phenotype of the cells. |
| 456 | 19454585 | Exposure of human AT and liver tissue in culture to LPS did not alter resistin concentration; however, concentrations of IL-1beta, IL-6, and TNFalpha were significantly increased in these tissues. |
| 457 | 19394939 | By contrast, when compared with baseline values, subjects treated with n-3 PUFA had significant improvement in FMD (9.1+/-5.8% vs. 11.7+/-4.4%, p=0.02) that was accompanied by decreased plasma triglycerides (117+/-73mg/dl vs. 86+/-44mg/dl, p=0.001) and TNF-alpha levels (8.9+/-2.3pg/ml vs. 6.8+/-2.7pg/ml, p=0.001), and a trend towards increased plasma adiponectin levels (7.8+/-4.5microg/ml vs. 9.5+/-5.1microg/ml, p=0.09). |
| 458 | 19666844 | These findings demonstrate that the endothelial dysfunction occurring in type 2 diabetes is the result of the effects of the inflammatory cytokine TNF-alpha and TNF-alpha-related signaling, including the expression of MCP-1 and adhesion molecules, which further exacerbates vessel inflammation and oxidative stress. |
| 459 | 19690174 | Human and rat primary beta cells were sorted by FACS and cultured for 24 h +/- 20 ng/ml TNF-alpha to explore the impact on apoptosis, proliferation, and short-term insulin secretion (1 h, 2.8 mm glucose followed by 1 h, 16.7 mm glucose at the end of the 24-h culture period) as well as key signaling protein phosphorylation and expression. |
| 460 | 19769745 | Preincubation of cells with TNFalpha, followed by insulin, significantly prevented insulin-mediated nuclear exclusion of Foxa2 and substantially increased its nuclear concentration. |
| 461 | 19769745 | TNFalpha alone, however, did not alter the status of cellular Foxa2 or its occupancy on the PEPCK promoter. |
| 462 | 19769745 | Insulin inhibition of PEPCK expression and the preventive effect of TNFalpha could be partially but significantly restored in the presence of Foxa2 siRNA. |
| 463 | 19769745 | Our results indicate that another transcription factor, Foxa2, is at least partly responsible for the attenuating effect of TNFalpha on insulin action on PEPCK expression and glucose production in HepG2 cells. |
| 464 | 19674864 | Concurrent decreases in TNF-alpha and adipose tissue mass suggest that in dogs, as in humans, this adipokine may be implicated in the insulin resistance of obesity. |
| 465 | 19745063 | The transcription factor forkhead box 01 (FOXO1) was tested for mediating TNF stimulation of osteoclastogenic and inflammatory factors in bone morphogenetic protein 2 pretreated ATDC5 and C3H10T1/2 chondrogenic cells. |
| 466 | 19745063 | FOXO1 knockdown by small-interfering RNA significantly reduced TNF-alpha, receptor activator for nuclear factor kB ligand, macrophage colony-stimulating factor, interleukin-1alpha, and interleukin-6 mRNA compared with scrambled small-interfering RNA. |
| 467 | 19745063 | These results suggest that diabetes-enhanced TNF-alpha increases the expression of resorptive factors in chondrocytes through a process that involves activation of FOXO1 and that TNF-alpha dysregulation leads to enhanced osteoclast formation and accelerated loss of cartilage. |
| 468 | 19144543 | Because the ubiquitin-proteasome pathway (UPS) is required for activation of nuclear factor kappa beta (NFkB), a transcription factor that regulates inflammatory genes, we evaluated the UPS activity, NFkB activation, and tumor necrosis factor-alpha (TNF-alpha), a proinflammatory cytokine, in ischemic specimens of diabetic myocardium and relate them to the glycemic control (HbA(1c)), oxidative stress (nitrotyrosine, a modified amino acid produced by reactive O(2)), and cardiac outcome (echocardiographic parameters). |
| 469 | 19356801 | RT-PCR analysis of mRNA transcripts of diabetogenic cytokines revealed that the expression of TNF-alpha, and IFN-gamma was significantly enhanced in pancreatic lymph nodes by day 10 after diabetes induction in ST2-deficient mice in comparison with wild type BALB/c mice while IL-17 was detected only in ST2(-/-) mice by day 21. |
| 470 | 19474523 | In this study, we used two cellular models of insulin resistance, one induced by treatment with tumor necrosis factor-alpha (TNF-alpha) and the other with the glucocorticoid dexamethasone. |
| 471 | 19700629 | Because the engagement of intercellular adhesion molecule-1 (ICAM-1), B7.1, B7.2, and CD40 on monocytes with their ligands on T cells plays roles in cytokine production, we investigated the effects of AGE-2 and AGE-3 on the expressions of ICAM-1, B7.1, B7.2, and CD40 on monocytes, the production of interferon gamma and tumor necrosis factor alpha, and the lymphocyte proliferation in human peripheral blood mononuclear cells and their modulation by prostaglandin E(2) (PGE(2)). |
| 472 | 19740750 | We demonstrate that tumor necrosis factor alpha and free fatty acids, key inflammatory stimuli involved in obesity-associated autocrine/paracrine inflammatory signaling, stimulate adipocyte expression and secretion of macrophage chemoattractants. |
| 473 | 19741020 | These cytokines all increased adhesion and differentiation of THP1 cells (P < 0.05), but only TNF-alpha and IL-6 increased MMP-9 expression (50- and 60-fold, respectively; P < 0.05). |
| 474 | 19819972 | Results showed that short-term TNF-alpha treatment significantly increased lipolysis, iNOS expression, and NO production in a time- and dose-dependent manner. |
| 475 | 19819972 | Moreover, pretreatment with inhibitors of iNOS and guanylate cyclase, but not an adenylate cyclase inhibitor, abolished TNF-alpha-induced lipolysis and HSL phosphorylation. |
| 476 | 19819972 | In conclusion, short-term TNF-alpha treatment induces lipolysis in 3T3-L1 adipocytes by increasing iNOS expression and NO production, which activates the guanylyl cyclase/cGMP-dependent pathway and induces phosphorylation of HSL. |
| 477 | 19845893 | There were no associations between AMPD1 C34T or ADA G22A genotypes and TNF-alpha or its receptors. |
| 478 | 19376168 | There was dose and time dependent expression of hVEGF and hIL-1Ra or hHGF and hIL-1Ra by islets, which led to decrease in caspase-3 activity and apoptosis induced by a cocktail of TNF-alpha, IL-1beta and IFN-gamma. |
| 479 | 19696185 | PD153035 treatment for 1 day decreased the protein expression of inducible nitric oxide synthase, tumor necrosis factor (TNF)-alpha, and interleukin (IL)-6 in the stroma vascular fraction, suggesting that this drug reduces the M1 proinflammatory state in ATMs, as an initial effect, in turn reducing the circulating levels of TNF-alpha and IL-6, and initiating an improvement in insulin signaling and sensitivity. |
| 480 | 19929783 | Furthermore, tumor necrosis factor-alpha (TNF-alpha) and/or triglyceride accumulation-induced nuclear factor-kappaB (NF-kappaB) activation in the liver is shown to play a role in insulin resistance in patients with HCV-related chronic liver disease as well. |
| 481 | 20061825 | MAb E4 potently antagonized the cytolytic activity of NKL cells against BaF/3-MICA cells expressing NKG2D ligand, and blocked the NKG2D ligand-induced secretion of TNFalpha, IFNgamma and GM-CSF, as well as surface expression of CRTAM by NK cells cultured on immobilized MICA or ULBP-1 ligands. |
| 482 | 19056300 | Six months of good glycemic control that followed 6 months of poor glycemic control failed to reverse the elevations in IL-1beta, TNF receptor type I, and intercellular cell adhesion molecule 1 but had some beneficial effects on TNF-alpha, inducible nitric oxide synthase, and vascular cell adhesion molecule 1, however these mediators remained significantly elevated. |
| 483 | 19902175 | In vitro, TNF-alpha enhanced mRNA levels of gene sets related to apoptosis and Akt and p53 but not mitochondrial or cell-cycle pathways. |
| 484 | 19902175 | TNF-alpha also increased genes involved in inflammation, cytokine, Toll-like receptor and nuclear factor-kB pathways, which were significantly reduced by FOXO1 knockdown. |
| 485 | 19934001 | Only neutralizing antibodies against tumor necrosis factor-alpha (TNFalpha) attenuated KC-induced alterations in hepatocyte fatty acid oxidation, triglyceride accumulation, and insulin responsiveness. |
| 486 | 19955001 | Serum cholesterol concentration affects the pro-inflammatory potential of LPS to induce TNF release from T2D monocytes in the presence or absence of CTRP-3. |
| 487 | 20004646 | TNF-alpha increased the expression of osteogenic marker genes including RUNX2, osterix, alkaline phosphatase (ALP), and bone sialoprotein, and it also promoted matrix mineralization in VSMCs. |
| 488 | 20004646 | In addition, TNF-alpha enhanced MSX2 expression in a dose- and time-dependent manner. |
| 489 | 20004646 | New protein synthesis was dispensable for MSX2 induction by TNF-alpha, and the inhibition of NF-kappaB by BAY-11-7082 or by dominant negative IkappaBalpha abolished the TNF-alpha-directed induction of MSX2 expression. |
| 490 | 20004646 | In conclusion, our study suggests that TNF-alpha directly induces MSX2 expression through the NF-kappaB pathway, which in turn induces expression of ALP, a key molecule in mineralization, in VSMCs. |
| 491 | 20007364 | The levels of expression of TNF-alpha, MCP-1, IFN-gamma, and IL-1beta were decreased; and the level of IL-10 increased in early responders. |
| 492 | 19195861 | HG and TNFalpha induced the expression of cell adhesion molecules and reduced that of occludin in EC. |
| 493 | 20134099 | The aim of this study was to test the effect of atorvastatin therapy on CD36 scavenger receptor expression, nuclear factor-kappaB (NFkappaB) levels and markers of inflammation (C-reactive protein, CRP, Tumor Necrosis Factor-alpha, TNF-alpha) in circulating monocytes from diabetic patients. |
| 494 | 20188786 | Exposing differentiated 3T3-L1 cells to RAW264.7 CM resulted in gene over-expressions of TNF-alpha, IL-6 and resistin, however, mRNA expression of adiponectin and PPARgamma were down-regulated. |
| 495 | 20378819 | In a subset analysis of 362 women who also had measurements of inflammatory and endothelial biomarkers, plasma resistin levels significantly correlated with IL-6, soluble TNF receptor 2, intercellular adhesion molecule 1, vascular adhesion molecule 1, and E-selectin after controlling for age and body mass index. |
| 496 | 20406798 | The following measures were assessed in the left ventricle: size of MI, systolic and diastolic function by echocardiography, cytokines by ELISA (TNF-alpha, IL-1beta, IL-6, and IL-10), gene expression by real-time PCR (Bax, Fas, p53, Bcl-2, HIF1-alpha, VEGF, and IL8r), caspase-3 activity by spectrofluorometric assay, glucose transporter type 1 and 4 (GLUT-1 and GLUT-4) protein expression by western blotting, and capillary density and fibrosis by histological analysis. |
| 497 | 20594413 | These pathways are classifiable into several categories: reactive oxygen species (ROS) metabolism and antioxidant defenses, p53 pathway signaling, nitric oxide (NO) signaling pathway, hypoxia signaling, transforming growth factor (TGF)-beta bone morphogenetic protein (BMP) signaling, tumor necrosis factor (TNF) ligand-receptor signaling, and mitochondrial function. |
| 498 | 20594416 | From these results, it is possible that TNF-alpha is a key regulator of the reduction of EC-SOD and adiponectin in CoCl(2)-treated 3T3-L1 adipocytes, and we speculated that the reduction of EC-SOD and adiponectin would lead to and/or promote metabolic disorders. |
| 499 | 20547979 | When expressed in cultured mouse islets, IRS-2(5A) was better than IRS-2(WT) in protecting beta-cells from apoptosis induced by a combination of IL-1beta, IFN-gamma, TNF-alpha, and Fas ligand. |
| 500 | 20558773 | In previous work, we found that toxic AGEs, AGE-2 and AGE-3, induced the expression of intracellular adhesion molecule-1, B7.1, B7.2, and CD40 on monocytes, production of interferon-gamma and tumor necrosis factor alpha, and lymphocyte proliferation during human mixed lymphocyte reaction. |
| 501 | 20679400 | Low-dose IL-2 increases the number of T reg cells in the pancreas and induces expression of T reg cell-associated proteins including Foxp3, CD25, CTLA-4, ICOS (inducible T cell costimulator), and GITR (glucocorticoid-induced TNF receptor) in these cells. |
| 502 | 20839494 | Total Akt was negatively correlated with IL-1beta (r = -0.45, p = 0.046), IL-6 (r = -0.44, p = 0.052) and TNF-alpha (r = -0.51, p = 0.025). |
| 503 | 18446810 | Porcine aortic endothelial cells were cultured in 5 and 30 mM glucose and stimulated with TNFalpha, together with FGF-2 or a neutralizing FGF-2 antibody. |
| 504 | 18446810 | TNFalpha-induced endothelial cell death increased for cells in high glucose, and cell death was enhanced with increasing FGF-2 exposure and negated by a neutralizing FGF-2 antibody. |
| 505 | 18446810 | Endothelial cells were most susceptible to TNFalpha-induced cell death when stimulated with FGF-2 18 h prior to TNFalpha, corresponding to cell entry into S phase of the proliferative cycle. |
| 506 | 18475668 | Other cytokines such as IL-1alpha and beta, and TNF-alpha induce a smaller increase in MHC class II antigens on RIN cells, and appear to activate both the G-protein and the PKC signal transduction pathways to varying degrees. |
| 507 | 18549505 | TNF-alpha treatment activated NF-kappaB signaling in differentiated adipocytes by inducing IkappaB degradation and NF-kappaB translocation to the nucleus, and as a result increased IL-6 (6-fold) and COX-2 (2.5-fold) mRNA levels. |
| 508 | 18549505 | TNF-alpha also activated IL-1beta gene expression in differentiated adipocytes, but had no effect on endogenous TNF-alpha mRNA levels. |
| 509 | 18579779 | Furthermore, db/db VSMC were hypersensitive to TNF-alpha inflammatory stimulus, which induced dramatic and sustained decreases in promoter H3K9me3 and Suv39h1 occupancy. |
| 510 | 18653783 | Ex vivo expanded CD34(+) human UCB cells have the capacity to generate multiple hematopoietic lineages and a functional human immune system upon transplantation into TNFalpha-treated NOD-scid IL2rgamma(null) mice. |
| 511 | 19234337 | Apocynin also blocked CCL2 production in endothelial cells (ECs), retinal microglia, and Müller cells stimulated with TNF-alpha, VEGF, or LPS. |
| 512 | 19234337 | Analysis of downstream signals showed that inhibition of NAD(P)H oxidase partially inhibited NF-kappaB activation but did not reduce CCL2 mRNA stability or prevent TNF-alpha-induced phosphorylation of p38MAPK. |
| 513 | 19234337 | However, TNF-alpha-induced Akt phosphorylation was blocked, and inhibiting Akt dramatically decreased CCL2 production. |
| 514 | 19917698 | Some cytokines (IL-1beta and IL-10) are predominantly regulated by TLR4, but others (IL-8 and TNF-alpha) are predominantly regulated by TLR2, due in part to TLR-dictated changes in transcription factor/promoter association. |
| 515 | 19769609 | The urine albumin : creatinine ratio (UACR), renal interstitial fluid (RIF) levels of AngII, TNF-alpha and IL-1beta and renal expression of TNF-alpha and IL-1beta were evaluated in control, untreated diabetic and diabetic rats treated with either a PRR blocker (PRRB; 0.2 mg/kg per day NH3-RILLKKMPSV-COOH), the AT(1) receptor antagonist valsartan (2 mg/kg per day) or combined therapy, administered directly into the renal cortical interstitium for 14 days via osmotic minipumps. 3. |
| 516 | 20454933 | IL-10 correlated with homeostatic model assessment index (P = 0.000) and other variables of glucose homeostasis in diabetes, thus representing a major marker of the disease. (1) Generally inconsistent changes in pro- and anti-inflammatory cytokines occurred when NASH was globally compared to steatosis. (2) In contrast, downregulation of IL-6 and IL-10 was perceived in diabetics with NASH. (3) Arterial hypertension did not play a role in these circumstances. (4) IL-10 maintained strong correlations with glucose metabolism indices. (5) TNF-alpha could not be incriminated for progressive liver damage, as values failed to increase in NASH. (6) Investigations of IL-10 and other counterregulatory cytokines are lacking in this context and deserve further studies. |
| 517 | 20452384 | The effect of TNF-alpha was abated by etanercept, the IKK2 inhibitor TPCA-1, or a p38 inhibitor while that of PMA was reduced by inhibitors of PKC isoforms sensitive to phorbol esters and calcium. |
| 518 | 19538479 | Loss of IL-10 and IFN-gamma was confirmed by RT-PCR analysis of mRNA, while TNF-alpha message was raised. |
| 519 | 20541824 | The expression of iNOS and the promoting apoptosis gene Bax and Fas were significantly up-regulated by the induction of IL-1beta and TNF-alpha. |
| 520 | 20200974 | In vitro studies investigated the proapoptotic transcription factor FOXO1 in regulating TNF-induced apoptosis of chondrogenic ATDC5 and C3H10T1/2 cells as representative of differentiated chondrocytes, which are important during endochondral ossification. mRNA profiling revealed an upregulation of gene sets related to apoptosis in the diabetic group on day 16 when cartilage resorption is active but not day 12 or day 22. |
| 521 | 20200974 | Silencing FOXO1 using siRNA in vitro significantly reduced TNF-induced apoptosis and caspase activity in differentiated chondrocytes. |
| 522 | 20200974 | Inhibiting caspase-8 and caspase-9 significantly reduced TNF-induced apoptosis in chondrogenic cells. |
| 523 | 20718752 | In addition, CIP inhibited AGE-2- and AGE-3-induced expressions of ICAM-1, B7.1, B7.2 and CD40 in monocytes, the production of TNF-alpha and IFN-gamma and lymphocyte proliferation in PBMC. |
| 524 | 20621376 | Moreover, BeWo cells were treated with tumor necrosis factor-alpha (TNF-alpha) and then the intra- and extra-cellular changes of visfatin expression were measured. |
| 525 | 20621376 | We demonstrated that visfatin secretion from BeWo cells was significantly increased but the intracellular expression was decreased at 48h incubation with TNF-alpha in a dose-depended way. |
| 526 | 20621376 | The oversecretion of visfatin from placenta, probably induced by the elevated TNF-alpha level, contributes to the increased serum visfatin concentrations in women with GDM. |
| 527 | 20630610 | NF-kappaB DNA-binding activity, p65 and IkappaBalpha protein levels, and expression of IL-6, TNFalpha and MMP-9 were significantly higher in PBMCs from T2DM patients, than from non-diabetic controls. |
| 528 | 20819535 | To evaluate the association between the four adipokines, adiponectin, leptin, resistin and tumor necrosis factor-alpha (TNF-alpha) with insulin sensitivity, we used a hyperinsulinemic euglycemic clamp to test insulin sensitivity in Chinese patients with obesity and type 1 or type 2 diabetes mellitus versus controls. |
| 529 | 20713153 | CD44 stimulation activates the protein kinase C (PKC) family which in turn activates the transcriptional nuclear factor kappa B (NF-?B) responsible for the expression of the inflammation mediators such as tumor necrosis factor alpha (TNF-?), interleukin-6 (IL-6), interleukin-18 (IL-18), inducible nitric oxide synthase (iNOS), and matrix metalloproteinases (MMPs). |
| 530 | 20703212 | The expression of TNF-related apoptosis-inducing ligand (TRAIL), its decoy receptor osteoprotegerin, and receptors Fas (a Fas ligand receptor) and CD74 (a migration inhibitory factor (MIF) receptor) were induced in human diabetic nephropathy. |
| 531 | 20840785 | Our findings showed that higher HBV DNA levels are associated with lower HDL and adiponectin but induced TNF-alpha values. |
| 532 | 20953353 | Tumor necrosis factor (TNF) and Fas ligand regulate renal cell survival and inflammation, and therapeutic targeting improves the outcome of experimental renal injury. |
| 533 | 20953353 | TNF-related apoptosis-inducing ligand (TRAIL and its potential decoy receptor osteoprotegerin are the two most upregulated death-related genes in human diabetic nephropathy. |
| 534 | 20953353 | While TNF only activates canonical NF-kappaB signaling, TWEAK promotes both canonical and noncanonical NF-kappaB activation in tubular cells, regulating different inflammatory responses. |
| 535 | 20854863 | Samples were typed for 38 tumor necrosis factor (TNF) block single nucleotide polymorphisms (SNP), human leukocyte antigen (HLA)-B and HLA-DRB1 alleles. |
| 536 | 21054880 | We have examined whether saturated nonesterified fatty acids (NEFA) and insulin, which increase in concentration with developing insulin resistance, can trigger the production of interleukin (IL)-6 and tumor necrosis factor (TNF)-? in human monocytes. |
| 537 | 20801512 | Decoy receptor 3 (DcR3), a member of the tumor necrosis factor receptor superfamily, regulates immune responses through competing with receptors of Fas ligand (FasL), LIGHT and TNF-like molecule 1A (TL1A). |
| 538 | 20813470 | After menopause, there is an increase in pro-inflammatory serum markers (IL1, IL6, TNF-alpha), an increase in response of the immune blood cells to these cytokines, a decrease in CD4 T and B lymphocytes and a decrease in the cytotoxic activity of NK cells. |
| 539 | 21151899 | High glucose and hyperglycemia reduced upregulation of the NF-?B inhibitory and atheroprotective protein A20 in human coronary endothelial (EC) and smooth muscle cell (SMC) cultures challenged with Tumor Necrosis Factor alpha (TNF), aortae of diabetic mice following Lipopolysaccharide (LPS) injection used as an inflammatory insult and in failed vein-grafts of diabetic patients. |
| 540 | 19463916 | Twenty-three retinal genes, mainly from TNF ligand and receptor, caspase, Bcl-2 and death domain subfamilies that were upregulated by least a two-fold in PC rats remain upregulated after reversal of hyperglycemia. |
| 541 | 20972877 | Although vasodilation to the endothelium-independent vasodilator sodium nitroprusside (SNP) was not different among WT, db/db, db/db+FSLLRY-NH? and db(TNF-)/db(TNF-), endothelium-dependent acetylcholine (ACh)- and flow-mediated vasodilation were impaired in db/db mice but were enhanced in db(TNF-)/db(TNF-) mice and db/db mice treated with PAR2 antagonist. |
| 542 | 20972877 | PAR2-activating peptide (PAR2-AP, 2-Furoyl-LIGRLO-am)-induced dilation was higher in db/db mice than that in WT, db(TNF-)/db(TNF-) and db/db mice treated with PAR2 antagonist. |
| 543 | 20972877 | Protein expression of gp91(phox) and p47(phox) was lower in db(TNF-)/db(TNF-) compared to db/db mice. |
| 544 | 19633828 | The regulation of TNF-alpha converting enzyme (TACE) and its inhibitor, tissue inhibitor of metalloproteinase 3 (TIMP3), in human type 2 diabetes is unknown. |
| 545 | 16567828 | The results indicate that the risk of CD in children with type 1 diabetes is significantly modified both by the presence of HLA-DQB1*02-DQA1*05 and by a variant of another gene within the major histocompatibility complex, the TNF -308A. |
| 546 | 17259397 | A20 or tumor necrosis factor (TNF)-induced protein 3 (TNFAIP3) is a negative regulator of nuclear factor-kappaB (NF-kappaB). |
| 547 | 21298620 | There was also a significant association between EPO dosage and homeostasis model assessment for insulin resistance (HOMA-IR), hs-CRP, IL-6, tumor necrosis factor a, leptin, and HMW adiponectin levels in DM patients with MIA syndrome. |
| 548 | 21130166 | We found that transgene expression of SOCS-1 rendered the islets significantly more resistant to cytokine-induced cell death after treatment with TNF-alpha alone and in combination with IFN-gamma. |
| 549 | 19996381 | Here, we show that knockdown of SIRT1 in the mouse macrophage RAW264.7 cell line and in intraperitoneal macrophages broadly activates the JNK and IKK inflammatory pathways and increases LPS-stimulated TNFalpha secretion. |
| 550 | 19996381 | We also demonstrate that SIRT1 activators inhibit LPS-stimulated inflammatory pathways, as well as secretion of TNFalpha, in a SIRT1-dependent manner in RAW264.7 cells and in primary intraperitoneal macrophages. |
| 551 | 19883376 | Brd2 knockdown protects 3T3-L1 adipocytes from TNF-alpha (tumour necrosis factor-alpha)-induced insulin resistance, thereby decoupling inflammation from insulin resistance. |
| 552 | 20308528 | Herein, we report that inhibition of the polyol pathway enzyme aldose reductase (AR) prevents high glucose (HG)- and/or TNF-alpha-induced VSMC proliferation by accumulating cells at the G1 phase of the cell cycle. |
| 553 | 20308528 | Collectively, these results show that AR could regulate HG- and TNF-alpha-induced VSMC proliferation by altering the activation of G1/S-phase proteins such as E2F-1, cdks, and cyclins. |
| 554 | 20489161 | SM-caPTH1R downregulated aortic Col1A1, Runx2, and Nox1 expression without altering TNF, Msx2, Wnt7a/b, or Nox4. |
| 555 | 21164077 | High glucose pretreatment (48 hours) enhanced thrombin or PAR-4-activating peptide but not PAR-1-activating peptide evoked intracellular calcium mobilization, migration, and tumor necrosis factor ? gene expression. |
| 556 | 17932314 | HFD promoted obesity, hyperglycemia, and hyperlipidemia, and upregulated serum TNF-alpha in Ldlr(-/-) mice. |
| 557 | 17932314 | Dosing with the TNF-alpha neutralizing antibody infliximab did not reduce obesity, hypercholesterolemia, or hyperglycemia; however, haptoglobin, aortic BMP2, Msx2, Wnt3a, and Wnt7a and aortic calcium accumulation were downregulated by infliximab. |
| 558 | 17932314 | Mice with vascular TNF-alpha augmented by a transgene (SM22-TNFalphaTg) driven from the SM22 promoter upregulated aortic Msx2, Wnt3a, and Wnt7a. |
| 559 | 17932314 | In aortic myofibroblast cultures, TNF-alpha upregulated Msx2, Wnt3a, Wnt7a, and ALP. |
| 560 | 20380652 | The effects of TSN on Akt and NF-kappaB phosphorylation and the expression of tumour necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) in cardiac tissues were examined. |
| 561 | 20380652 | Moreover, pretreatment with wortmannin abolished the beneficial effects of TSN: a reduction of infarct size, a decrease in LVEF, inhibition of myocardial apoptosis and Akt phosphorylation, enhancement of NF-kappaB phosphorylation and an increase of cytokine production including TNF-alpha and IL-6 after I/R injury in diabetic rats. |
| 562 | 21378173 | Human skeletal muscle cells were cultured for up to 24 h with tumor necrosis factor (TNF)-? to induce insulin resistance, and mRNA expression for cytokines was analyzed and compared with controls (without TNF-?). |
| 563 | 21386087 | Stress stimuli such as tumor necrosis factor (TNF) have been shown to induce insulin receptor substrate (IRS)-1 serine phosphorylation and insulin resistance by transactivation of ErbB receptors. |
| 564 | 21386087 | Fao or HepG2 cells exposed to TNF, anisomycin, or sphingomyelinase demonstrated rapid transactivation of ErbB receptors leading to PI3-kinase/Akt activation and IRS-1 serine phosphorylation. p38MAPK inhibition either by SB203580, by small interfering RNA, or by DN-p38MAPK? decreased ErbB receptors transactivation and IRS-1 serine phosphorylation and partially restored insulin-stimulated IRS-1 tyrosine phosphorylation. |
| 565 | 21386087 | When cells were incubated with specific ErbB receptors antagonists or in cells lacking ErbB receptors, anisomycin- and TNF-induced IRS-1 serine phosphorylation was attenuated, despite intact p38MAPK activation. |
| 566 | 20043993 | Moreover, we observe a correlation between preadipocyte phenotype and Fstl1 expression in that TNFalpha-mediated de-differentiation of 3T3-L1 adipocytes is accompanied by re-expression of Fstl1 transcript and protein. |
| 567 | 20068130 | On the other hand, the expression and activity of 12-lipoxygenase, an enzyme responsible for metabolizing arachidonic acid, and the production of tumor necrosis factor-alpha (TNF-alpha), a critical insulin resistance-inducing factor, are largely inhibited by lipocalin-2 deficiency. |
| 568 | 20068130 | Lipocalin-2 stimulates the expression and activity of 12-lipoxygenase and TNF-alpha production in fat tissues. |
| 569 | 20068130 | Cinnamyl-3,4-dihydroxy-alpha-cyanocinnamate (CDC), an arachidonate lipoxygenase inhibitor, prevents TNF-alpha expression induced by lipocalin-2. |
| 570 | 20068130 | Moreover, treatment with TNF-alpha neutralization antibody or CDC significantly attenuated the differences of insulin sensitivity between wild-type and Lcn2-KO mice. |
| 571 | 20068130 | Lipocalin-2 deficiency protects mice from developing aging- and obesity-induced insulin resistance largely by modulating 12-lipoxygenase and TNF-alpha levels in adipose tissue. |
| 572 | 21038470 | The CD8(+) Treg express CD25, glucocorticoid-induced TNF receptor family, CTLA-4, Foxp3, and TNFR2, and the combined expression of TNFR2 and CD25 identifies a potent subpopulation of CD8(+) Treg. |
| 573 | 21227528 | Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) was originally isolated as an inducer of apoptosis. |
| 574 | 21510113 | Proposed biological mechanisms in experimental animals included up regulation of inflammatory signals like cytokines and TNF-alpha, oxidative stress, hypomethylation, decreased DNA repair and apoptosis, cell proliferation, angiogenesis, activation of several enzymes like methyl transferase which converts inorganic arsenic to MMA and DMA, and GSH in in-vivo and in-vitro in experimental rat liver slices. |
| 575 | 20067961 | Indexes of inflammation including nuclear factor-kappaB (NF-kappaB) binding, and the expression of SOCS3, tumor necrosis factor-alpha (TNF-alpha), and interleukin (IL)-1beta in MNCs, increased significantly after glucose and cream intake, but TLR-4 expression and plasma LPS concentrations increased only after cream intake. |
| 576 | 20067961 | Although both glucose and cream induce NF-kappaB binding and an increase in the expression of SOCS3, TNF-alpha, and IL-1beta in MNCs, only cream caused an increase in LPS concentration and TLR-4 expression. |
| 577 | 19846171 | Tumor necrosis factor alpha (TNFalpha) is a proinflammatory adipokine hypothesized to link obesity with insulin resistance. |
| 578 | 19846171 | Functional studies suggest that TNFalpha acts through pathways involving adipokines and fatty acids to induce insulin resistance. |
| 579 | 19846171 | We tested the hypothesis that the association of measures of TNFalpha activity with insulin resistance is independent of obesity and adipose tissue biomarkers. |
| 580 | 19846171 | Tumor necrosis factor alpha receptor 2 was still associated to HOMA-IR after adding adiponectin, resistin, and triglycerides (individually and simultaneously). |
| 581 | 19846171 | We conclude that, in a representative community sample, measures of TNFalpha activity are associated with insulin resistance, even after accounting for central adiposity and other adipose tissue biomarkers. |
| 582 | 15585763 | After adjustment for age, sex, body mass index, diabetes, smoking, ejection fraction, New York Heart Association class, ischemic etiology, statin use, and serum glucose, TFA levels were positively associated with interleukin (IL) 1beta (difference from mean: 0.38 pg/mL; percentage difference from mean: 66%; P=0.04), IL-1 receptor antagonist (4033 pg/mL; 297%; P=0.006), IL-6 (9.5 pg/mL; 123%; P=0.006), IL-10 (241 pg/mL; 183%; P=0.02), tumor necrosis factor (TNF) alpha (256 pg/mL; 249%; P=0.02), TNF receptor 1 (537 pg/mL; 41%; P=0.03), TNF receptor 2 (39 242 pg/mL; 247%; P=0.001), monocyte chemoattractant protein 1 (117 pg/mL; 119%; P=0.004), and brain natriuretic peptide (40 pg/mL; 57%; P=0.04). |
| 583 | 21480818 | TNFA -308A allele was associated with reduced basal TNF? mRNA levels in NG and DM2 and reduced alkaline phosphatase (tALP) after treatment (p<0.05). |
| 584 | 20354158 | In both hypothalamic cell lines, inflammation was induced by prototypical inflammatory mediators LPS and TNFalpha, as judged by induction of IkappaBalpha (3- to 5-fold) and IL-6 (3- to 7-fold) mRNA and p-IkappaBalpha protein, and TNFalpha pretreatment reduced insulin-mediated p-Akt activation by 30% (P < 0.05). |
| 585 | 20357221 | This study evaluated poly(ADP-ribose) polymerase (PARP) inhibition as a new therapeutic approach for peripheral diabetic neuropathy using clinically relevant animal model and endpoints, and nitrotyrosine (NT), TNF-alpha, and nitrite/nitrate as potential biomarkers of the disease. |
| 586 | 21196299 | The elevated TNF-alpha and IL-1beta, but not IL-6 and VEGF, were decreased by 2 U/ml EPO as detected by real-time PCR and ELISA. |
| 587 | 21196299 | Intravitreal injection of EPO performed 24 h prior to sacrifice significantly reduced TNF-alpha and IL-1beta production while moderately attenuating IL-6 and VEGF in the retinas of streptozotocin-induced diabetic rats. |
| 588 | 17854708 | This study examined the effect of chromium niacinate (Cr-N) or chromium picolinate (Cr-P) supplementation on lipid peroxidation (LP), TNF-alpha, IL-6, C-reactive protein (CRP), glycosylated hemoglobin (HbA(1)), cholesterol, and triglycerides (TG) in diabetic rats. |
| 589 | 18457011 | In this regard, expression of apelin gene in adipose tissue is increased by insulin and TNFalpha. |
| 590 | 21693293 | Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) was originally identified as the third member of the TNF superfamily to induce apoptosis. |
| 591 | 21593200 | Nuclear factor (NF)-?B activation was assessed by treating human embryonic kidney (HEK) 293 and HK-2 cells with tumor necrosis factor (TNF)-? in the presence or absence of Klotho, followed by immunoblot analysis to evaluate inhibitor of ?B (I?B)? degradation, I?B kinase (IKK) and p38 activation, RelA nuclear translocation, and phosphorylation. |
| 592 | 21321581 | Activation of splenic T lymphocytes derived from protected mice in vitro with pharmacological agents that bypass the antigen receptor or immobilized anti-CD3 antibody resulted in enhanced expression of Ifng mRNA and protein without altering the expression of Il4, Il17, Il18, Inos and Tnfa genes nor the secretion of IL-2, IL-4, IL-17 and TNF-? proteins. |
| 593 | 20420526 | There, it suppresses the proinflammatory transcription factors nuclear factor-kappa B, signal transducer and activators of transcription-3, and Wnt/beta-catenin, and it activates peroxisome proliferator-activated receptor-gamma and Nrf2 cell-signaling pathways, thus leading to the downregulation of adipokines, including tumor necrosis factor, interleukin-6, resistin, leptin, and monocyte chemotactic protein-1, and the upregulation of adiponectin and other gene products. |
| 594 | 9930944 | A combination of methylprednisolone, pentoxifylline, cyclosporin A, and nicotinamide (concentrations for each substance as described above) inhibited TNFalpha generation by 74+/-6% (mean value+/-SEM, mononuclear blood cells from seven diabetic patients) without affecting IL-1beta or superoxide generation. |
| 595 | 12436346 | It has been suggested that several agents, such as tumor necrosis factor alpha, could mediate their effects on insulin metabolism through modulating adiponectin secretion from adipocytes. |
| 596 | 18803820 | TNFalpha treatment of 3T3-L1 adipocytes resulted in a ~90% decrease in Tmem182 transcript level. |
| 597 | 19709445 | The level of IL-8 in the medium and the IL-8 mRNA expression after stimulation with either TNF-alpha, IL-1beta, or CRP was significantly enhanced in human adipocytes. |
| 598 | 21633715 | Eleven inflammation- and microvascular-related genes previously demonstrated to be upregulated in young diabetic rats (complement component 1 s subcomponent [C1s], chitinase 3-like 1 [Chi3L1], endothelin 2 [Edn2], guanylate nucleotide binding protein 2 [Gbp2], glial fibrillary acidic protein [Gfap], intracellular adhesion molecule 1 [Icam1], janus kinase 3 [Jak3], lipopolysaccharide-induced TNF factor [Litaf], complement 1-inhibitor [Serping1], signal transducer and activator of transcription 3 [Stat3], tumor necrosis factor receptor subfamily member 12a [Tnfrsf12a]) demonstrated progressively increasing retinal expression in aged normoglycemic rats. |
| 599 | 10199130 | Regarding mechanism of obesity-induced insulin resistance, the increased expression of Tumor necrosis factor alpha and abnormality in PTPase are postulated. |
| 600 | 19202909 | Increasing evidence indicates that altered secretion of adipocytokines such as adiponectin, tumor necrosis factor alpha, monocyte chemoattractant protein-1 and free fatty acids are contributing factors to insulin resistance in obese states. |
| 601 | 20086228 | We found that IL-1beta and TNF-alpha induce the expression of miR-21, miR-34a, and miR-146a both in MIN6 cells and human pancreatic islets. |
| 602 | 20350970 | Moreover, these macrophage Ad-TG mice exhibit enhanced whole-body glucose tolerance and insulin sensitivity with reduced proinflammatory cytokines, MCP-1 and TNF-a (both in the serum and in the metabolic active macrophage), adipose tissue, and skeletal muscle under the high-fat diet condition. |
| 603 | 20646763 | Interestingly, CD40 stimulation induces some CD40 receptor constellations that contain TNF-receptors 1 and 2 and targeting of those alters CD40 signaling outcomes in NOD Th40 cells. |
| 604 | 16130407 | IP-10 correlated IL-18, IL-6, TNF-alpha and MCP-1. |
| 605 | 19477937 | TNF-alpha signals through two receptors, TNFR1 and TNFR2. |
| 606 | 20501675 | To determine whether signaling through TNF and/or nuclear factor-kappaB contributes to bacterial lipopolysaccharide (LPS)-induced activation of type 2 iodothyronine deiodinase (D2) in tanycytes lining the floor and infralateral walls of the third ventricle, the effect of a TNF antagonist on D2 gene expression and LPS-induced Ikappa-Balpha expression in tanycytes were studied. |
| 607 | 20504897 | The plasma Gas6 value was inversely correlated with fasting glucose, tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, and vascular cell adhesion molecule (VCAM)-1. |
| 608 | 21797106 | The group 2 patients had statistically significantly higher levels of IL-1beta (p = 0.01) and IL-6 (p = 0.029) and elevated TNF-alpha and VEGF levels in comparison with group 1 patients. |
| 609 | 21797106 | The cytokine serum levels did not correlate with the duration of DM, the duration of DR (except for IL-1beta, p = 0.045), and hyperlipidemia (except for TNF-alpha, p = 0.05). |
| 610 | 21740847 | Metformin also increased phosphorylation of AMPK and eNOS, and reduced the expression of TGF-?1, basic fibroblast growth factor (bFGF), and tumor necrosis factor (TNF)-?. |
| 611 | 21756351 | We conducted a cross-sectional study in 6,720 subjects from the Twins UK Registry to evaluate the association between 18 single nucleotide polymorphisms (SNPs) in five genes (TLR4, IL1A, IL6, TNFA, and CRP) along the innate immunity-related inflammatory pathway and biomarkers of predisposition to T2DM [fasting insulin and glucose, HDL- and LDL- cholesterols, triglycerides (TGs), amyloid-A, sensitive C-reactive protein (sCRP) and vitamin D binding protein (VDBP) and body mass index (BMI)]. |
| 612 | 16797387 | A death hazard ratio for each 1,000-pmol/L increase in serum MPO level was 1.14 (95% confidence interval [CI], 1.03 to 1.26; P = 0.01) after controlling for age, race (black), diabetes mellitus, dialysis vintage, Charlson comorbidity score, history of previous cardiovascular disease, blood hemoglobin level, and serum concentrations of albumin, CRP, IL-6, and TNF-alpha. |
| 613 | 19521344 | When 3T3-L1 adipocytes were treated with the 12/15-LO products, 12-hydroxyeicosatetranoic acid (12(S)-HETE) and 12-hydroperoxyeicosatetraenoic acid (12(S)-HPETE), expression of proinflammatory cytokine genes, including tumor necrosis factor-alpha (TNF-alpha), monocyte chemoattractant protein 1 (MCP-1), interleukin 6 (IL-6), and IL-12p40, was upregulated whereas anti-inflammatory adiponectin gene expression was downregulated. 12/15-LO products also augmented c-Jun N-terminal kinase 1 (JNK-1) phosphorylation, a known negative regulator of insulin signaling. |
| 614 | 18539754 | We also observed in diabetic mice that augmented RAGE signaling augmented expression of TNF-alpha, because this increase was attenuated by sRAGE or NF-kappaB inhibitor MG132. |
| 615 | 19029992 | In the myocardium, adiponectin-mediated protection from ischemia-reperfusion injury is linked to cyclo-oxygenase-2-mediated suppression of tumor necrosis factor signaling, inhibition of apoptosis by AMP-activated protein kinase, and inhibition of excess peroxynitrite-induced oxidative and nitrative stress. |
| 616 | 19067524 | Coexpression of hVEGF and hIL-1Ra by islets showed decrease in caspase-3 activity and apoptosis induced by a cocktail of inflammatory cytokines such as TNF-alpha, IL-1beta and IFN-gamma. |
| 617 | 19478208 | We hypothesized that resveratrol protects against oxidative stress-induced endothelial dysfunction in aortas of diabetic mice by inhibiting tumor necrosis factor alpha (TNFalpha)-induced activation of NAD(P)H oxidase and preserving phosphorylation of endothelial nitric oxide synthase (eNOS). |
| 618 | 19478208 | Genetic deletion of TNFalpha in diabetic mice (db(TNF-)/db(TNF-)) was associated with a reduced NAD(P)H oxidase activity and vascular O(2)(.-) production and an increased eNOS (Ser1177) phosphorylation, suggesting that TNFalpha plays a pivotal role in aortic dysfunction in diabetes by inducing oxidative stress and reducing NO bioavailability. |
| 619 | 19478208 | Resveratrol restored endothelial function in type 2 diabetes by inhibiting TNFalpha-induced activation of NAD(P)H oxidase and preserving eNOS phosphorylation, suggesting the potential for new treatment approaches to promote vascular health in metabolic diseases. |
| 620 | 18952128 | The zinc finger-containing protein A20 is a negative regulator of TNF-induced JNK (c-Jun-N-terminal kinase) and NFkappaB (nuclear factor kappaB) signaling. |
| 621 | 9568706 | Prolonged treatment (5 days) with either BRL 49653 or another PPAR-gamma2 agonist, 15-d delta-12,14-prostaglandin J2 (15-d deltaPGJ2), blocked TNF-alpha-induced glycerol release by approximately 100%. |
| 622 | 9568706 | BRL 49653 partially blocked the TNF-alpha-mediated reduction in protein levels of hormone-sensitive lipase and perilipin A, two proteins involved in adipocyte lipolysis. |
| 623 | 12351429 | We demonstrate that TNF-alpha increases lipolysis in differentiated human adipocytes by activation of mitogen-activated protein kinase kinase (MEK), extracellular signal-related kinase (ERK), and elevation of intracellular cAMP. |
| 624 | 12351429 | TNF-alpha activated ERK and increased lipolysis; these effects were inhibited by two specific MEK inhibitors, PD98059 and U0126. |
| 625 | 12351429 | TNF-alpha treatment caused an electrophoretic shift of perilipin from 65 to 67 kDa, consistent with perilipin hyperphosphorylation by activated cAMP-dependent protein kinase A (PKA). |
| 626 | 12351429 | Consistent with the hypothesis that TNF-alpha induces perilipin hyperphosphorylation by activating PKA, TNF-alpha increased intracellular cAMP approximately 1.7-fold, and the increase was abrogated by PD98059. |
| 627 | 12351429 | Finally, TNF-alpha decreased the expression of cyclic-nucleotide phosphodiesterase 3B (PDE3B) by approximately 50%, delineating a mechanism by which TNF-alpha could increase intracellular cAMP. |
| 628 | 14693700 | The ability of TNF-alpha to phosphorylate extracellular signal-regulated kinase 1 (ERK1) and ERK2 and to downregulate perilipin (which has been implicated in the lipolytic effect of TNF-alpha) was not affected by glucose. |
| 629 | 15523649 | The region spanning the tumor necrosis factor (TNF) cluster in the human major histocompatibility complex (MHC) has been implicated in susceptibility to numerous immunopathological diseases, including type 1 diabetes mellitus and rheumatoid arthritis. |
| 630 | 18972582 | The purpose of the present study was to examine the effects of AS-IV on the lipolysis and insulin resistance induced by tumor necrosis factor-alpha (TNFalpha) in cultured 3T3-L1 adipocytes. |
| 631 | 18972582 | TNFalpha promotes lipolysis in mammal adipocytes via the mitogen activated protein kinase (MAPK) family resulting in reduced expression/function of perilipin. |
| 632 | 18972582 | Moreover, TNFalpha induced downregulation of key enzymes in lipogenesis, including LPL, FAS and GPAT, were also attenuated by AS-IV. |
| 633 | 9691088 | The IL-1 receptor antagonist protein (IRAP) prevents TNF + LPS + IFN-gamma-induced iNOS expression and nitrite production, and attenuates the inhibitory effects on glucose-stimulated insulin secretion by human islets. |
| 634 | 9691088 | These results indicate that the inhibitory effects of TNF + LPS + IFN-gamma are mediated by nitric oxide, produced by the actions of IL-1 released endogenously within human islets. |
| 635 | 9691088 | Two forms of evidence indicate that resident macrophages are the human islet cellular source of IL-1: culture conditions that deplete islet lymphoid cells prevent TNF + LPS + IFN-gamma-induced iNOS expression, nitric oxide production, and IL-1 mRNA expression by human islets; and IL-1 and the macrophage surface marker CD69 colocalize in human islets treated with TNF + LPS + IFN-gamma as determined by immunohistochemical analysis. |
| 636 | 10690898 | ICE messenger RNA (mRNA) expression was highly up-regulated after 6-, 24-, and 72-h exposure of human islets to interferon (IFN)gamma, tumor necrosis factor (TNF)alpha + IFNgamma or IL-1beta + TNFalpha + IFNgamma, paralleled by increased iNOS (the inducible form of NO synthase) expression and NO production after exposure to the combined cytokines but not to IFNgamma or TNFalpha + IFNgamma. |
| 637 | 11593036 | IL-1beta and IFN-gamma alone, or potentiated by TNF-alpha, are cytotoxic to the insulin producing pancreatic beta-cells and beta-cell lines in vitro and suggested to contribute to the specific beta-cell destruction in Type-1 diabetes mellitus (T1DM). |
| 638 | 12031968 | The presence of cFLIP prevented the weak TNF-alpha-induced reduction in cellular insulin content and secretion; however, it did not prevent the decrease in glucose-stimulated insulin secretion induced by the combined cytokines, in agreement with our previous data demonstrating that interferon-gamma alone could induce these beta-cell dysfunctions. |
| 639 | 12207816 | Diabetic ketosis is associated with increased nitrate levels and the activation of iNOS expression in circulating lymphomonocytes, but it does not affect either the proinflammatory cytokine TNF-alpha or a marker of endothelial dysfunction such as thrombomodulin. |
| 640 | 11784851 | Recombinant forms of MAP3K MEK kinase 1 (MEKK1) interact in vivo and in vitro with the STE20 protein homologue germinal center kinase (GCK), and both GCK and MEKK1 associate in vivo with the adapter protein tumor necrosis factor (TNF) receptor-associated factor 2 (TRAF2). |
| 641 | 12504894 | Levels of the dicarbonyl methylglyoxal (MGO) are elevated in diabetic plasma and MGO-modified bovine serum albumin (MGO-BSA) can trigger cellular uptake of TNF. |
| 642 | 12504894 | Our findings suggest that the presence of chronically elevated levels of MGO-modified bovine serum albumin may contribute to elevated levels of TNFalpha in diabetes. |
| 643 | 16543409 | We show here that SOCS-3 inhibits NFkappaB-dependent transcription induced by overexpression of the upstream IL-1 signaling molecules MyD88, IL-1R-activated kinase 1, TNF receptor-associated factor (TRAF)6, and TGFbeta-activated kinase (TAK)1, but not when the MAP3K MAPK/ERK kinase kinase-1 is used instead of TAK1, indicating that the target for SOCS-3 is the TRAF6/TAK1 signaling complex. |
| 644 | 16936197 | Activation of NF-kappaB by TNF receptor-associated factor (TRAF) 2, TRAF6, NF-kappaB-inducing kinase, or protein kinase D, which transduce signals downstream of Toll-like receptors, TNF receptors, and free radicals, respectively, were all potent activators of the A20 promoter. |
| 645 | 16936197 | Finally, A20 expression was sufficient to protect beta-cells from TNF-induced apoptosis. |
| 646 | 16960890 | In parental HepG2 cells, TNF-alpha treatment for 24 h reduced the phosphorylation of Akt1/PKB-alpha and GSK-3beta and under these conditions cells also showed reduced insulin responsiveness in terms of Akt1/PKB-alpha and GSK-3beta phosphorylation. |
| 647 | 16960890 | TNF-alpha pre-incubated HepG2-CA-Akt/PKB cells showed lower reduction in Akt1/PKB-alpha and GSK-3beta phosphorylation and insulin responsiveness after 24 h as compared to parental HepG2 cells. |
| 648 | 16960890 | We report that the long-term TNF-alpha pre-incubation in both parental HepG2 and HepG2-CA-Akt/PKB-alpha cells leads to the reduction in the levels of IRS-1 without altering the levels of IRS-2. |
| 649 | 16960890 | In order to understand the reason for the differential insulin resistance in both the cell types, the effect of long-term TNF-alpha treatment on the proteins upstream to Akt/PKB was investigated. |
| 650 | 16960890 | As hyperphosphorylation of IRS-1 at Ser 312 can induce its degradation, it is possible that reduced insulin responsiveness after long-term TNF-alpha pre-incubation observed in this study is due to the decrease in IRS-1 levels. |
| 651 | 19324938 | Correspondingly, cardiac glycogen synthase phosphorylation, hexokinase II, PPARalpha, and PGC-1alpha expression, which mediate glucose and lipid metabolisms, were significantly changed along with cardiac lipid accumulation, inflammation (TNF-alpha, plasminogen activator inhibitor 1 [PAI-1], and intracellular adhesion molecule 1 [ICAM-1]), nitrosative damage (3-nitrotyrosin accumulation), and fibrosis in the wild-type diabetic mice. |
| 652 | 19808894 | IkappaB kinase-(IKK)-beta inhibition prevented mitogen-activated protein (MAP) kinase kinase (MEK)/ERK1/2 activation in response to interleukin (IL)-1beta and tumor necrosis factor (TNF)-alpha but not insulin in 3T3-L1 and human adipocytes, suggesting that IKKbeta regulated a MAP kinase kinase kinase (MAP3K) involved in ERK1/2 activation induced by inflammatory cytokines. |
| 653 | 19808894 | We show that the MAP3K8 called Tpl2 was expressed in adipocytes and that IL-1beta and TNF-alpha activated Tpl2 and regulated its expression through an IKKbeta pathway. |
| 654 | 19808894 | Tpl2 mRNA expression was upregulated in adipose tissue of obese mice and patients and correlated with TNF-alpha expression. |
| 655 | 22069270 | Here, we assessed the role in T1D of variants previously reported to be associated with atopic diseases and epithelial barrier function, profilaggrin (), and those that affect the expression levels of the proinflammatory cytokines tumour necrosis factor (TNF)-?, interleukin (IL)-1?, interferon (IFN)? and IL-18. |
| 656 | 18221086 | In 1997, a Glaxo patent described that Troglitazone (first PPAR-gamma ligand to reach market) reduced TNF-induced VCAM1 expression in HUVECs indicating the potential benefit in atherosclerosis. |