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PMID |
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1 |
2485397
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Mean urinary excretion of lysozyme, beta 2-microglobulin and N-acetyl-beta-D-glucosaminidase (NAG) in both Albustix-negative and positive patients were significantly elevated above the control range.
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2 |
2485397
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The increased excretion of lysozyme, beta 2-microglobulin and NAG was found in 21, 55 and 62% of the normoalbuminuric patients, and in 40, 57 and 74% of the microalbuminuric patients, respectively.
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3 |
2485397
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The albumin/ASP ratio increased as nephropathy advanced.
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4 |
10674354
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IL4 and IL4Ralpha genes are not linked or associated with type 1 diabetes.
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5 |
10674354
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Here we have evaluated IL4 and the alpha subunit of the IL-4 receptor (IL4Ralpha) genes using the affected sibpair (ASP) and transmission/disequilibrium test (TDT).
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6 |
10982176
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Fine-mapping of the type 1 diabetes locus (IDDM4) on chromosome 11q and evaluation of two candidate genes (FADD and GALN) by affected sibpair and linkage-disequilibrium analyses.
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7 |
10982176
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Previous studies have identified a susceptibility region for insulin-dependent (type 1) diabetes mellitus on chromosome 11q13 (IDDM4).
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8 |
10982176
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We also identified polymorphisms in two candidate genes, Fas-associated death domain protein (FADD) and galanin (GALN).
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9 |
10982176
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However, ETDT did reveal significant association/linkage with the marker D11S987 (P=0.0004) within the IDDM4 interval defined by ASP analyses, suggesting that IDDM4 may be in the close proximity of D11S987.
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10 |
14749280
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This review will address the biology, actions, and regulation of three adipocyte hormones-leptin, acylation stimulating protein (ASP), and adiponectin-with an emphasis on the most recent literature.
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11 |
14749280
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Leptin treatment dramatically improves metabolic abnormalities (insulin resistance and hyperlipidemia) in patients with relative leptin deficiency due to lipoatrophy.
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12 |
14749280
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Leptin production is primarily regulated by insulin-induced changes of adipocyte metabolism.
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13 |
14749280
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Dietary fat and fructose, which do not increase insulin secretion, lead to reduced leptin production, suggesting a mechanism for high-fat/high-sugar diets to increase energy intake and weight gain.
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14 |
14749280
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In mice, ASP deficiency results in reduced body fat, obesity resistance, and improved insulin sensitivity.
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15 |
14749280
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Adiponectin production is stimulated by thiazolidinedione agonists of peroxisome proliferator-activated receptor-gamma and may contribute to increased insulin sensitivity.
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16 |
14749280
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Adiponectin and leptin cotreatment normalizes insulin action in lipoatrophic insulin-resistant animals.
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17 |
14749280
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This review will address the biology, actions, and regulation of three adipocyte hormones-leptin, acylation stimulating protein (ASP), and adiponectin-with an emphasis on the most recent literature.
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18 |
14749280
|
Leptin treatment dramatically improves metabolic abnormalities (insulin resistance and hyperlipidemia) in patients with relative leptin deficiency due to lipoatrophy.
|
19 |
14749280
|
Leptin production is primarily regulated by insulin-induced changes of adipocyte metabolism.
|
20 |
14749280
|
Dietary fat and fructose, which do not increase insulin secretion, lead to reduced leptin production, suggesting a mechanism for high-fat/high-sugar diets to increase energy intake and weight gain.
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21 |
14749280
|
In mice, ASP deficiency results in reduced body fat, obesity resistance, and improved insulin sensitivity.
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22 |
14749280
|
Adiponectin production is stimulated by thiazolidinedione agonists of peroxisome proliferator-activated receptor-gamma and may contribute to increased insulin sensitivity.
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23 |
14749280
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Adiponectin and leptin cotreatment normalizes insulin action in lipoatrophic insulin-resistant animals.
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24 |
15029093
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Several adipokines are increased in the obese state and have been implicated in hypertension (angiotensinogen), impaired fibrinolysis (PAI-1) and insulin resistance (ASP, TNFalpha, IL-6, resistin).
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25 |
15029093
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Conversely, leptin and adiponectin both exert an insulin-sensitizing effect, at least in part, by favoring tIssue fatty-acId oxIdation through activation of AMP-activated kinase.
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26 |
15029093
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In obesity, insulin resistance has been linked to leptin resistance and decreased plasma adiponectin.
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27 |
15029093
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In lipoatrophic mice, where leptin and adiponectin circulating levels are low, administration of the two adipokines synergistically reverses insulin resistance.
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28 |
15029093
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Leptin and adiponectin also have distinct properties: leptin, as a long-term integrative signal of energy store and adiponectin, as a potent anti-atherogenic agent.
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29 |
15029093
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The thiazolIdinedione anti-diabetic drugs increase endogenous adiponectin production in rodents and humans, supporting the Idea that the development of new drugs targeting adipokines might represent a promising therapeutic approach to protect obese patients from insulin resistance and atherosclerosis.
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30 |
18615583
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Acylation stimulating protein (ASP) stimulates triglyceride synthesis and glucose transport via its receptor C5L2.
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31 |
18615583
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In human studies, ASP is increased in insulin resistant states such as obesity, diabetes, polycystic ovary syndrome and late pregnancy (the latter two associated with altered sex hormones).
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32 |
18615583
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The aims were (i) to evaluate ASP response and C5L2 expression following treatment with sex steroid hormones and (ii) to identify mechanisms of ASP resistance using 3T3-L1 adipocytes and preadipocytes.
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33 |
18615583
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ASP increased p-PKCalpha and PKCzeta to 161% (P < 0.0.001) and 160% (P < 0.01), a stimulation effectively blocked by PROG (10(-8) and 10(-6) M) and TEST (10(-6) M).
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34 |
18615583
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Sex steroid hormone-induced ASP resistance via C5L2 may contribute to altered adipose tissue function and insulin resistance phenotype in humans.
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35 |
18615583
|
Acylation stimulating protein (ASP) stimulates triglyceride synthesis and glucose transport via its receptor C5L2.
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36 |
18615583
|
In human studies, ASP is increased in insulin resistant states such as obesity, diabetes, polycystic ovary syndrome and late pregnancy (the latter two associated with altered sex hormones).
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37 |
18615583
|
The aims were (i) to evaluate ASP response and C5L2 expression following treatment with sex steroid hormones and (ii) to identify mechanisms of ASP resistance using 3T3-L1 adipocytes and preadipocytes.
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38 |
18615583
|
ASP increased p-PKCalpha and PKCzeta to 161% (P < 0.0.001) and 160% (P < 0.01), a stimulation effectively blocked by PROG (10(-8) and 10(-6) M) and TEST (10(-6) M).
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39 |
18615583
|
Sex steroid hormone-induced ASP resistance via C5L2 may contribute to altered adipose tissue function and insulin resistance phenotype in humans.
|
40 |
18615583
|
Acylation stimulating protein (ASP) stimulates triglyceride synthesis and glucose transport via its receptor C5L2.
|
41 |
18615583
|
In human studies, ASP is increased in insulin resistant states such as obesity, diabetes, polycystic ovary syndrome and late pregnancy (the latter two associated with altered sex hormones).
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42 |
18615583
|
The aims were (i) to evaluate ASP response and C5L2 expression following treatment with sex steroid hormones and (ii) to identify mechanisms of ASP resistance using 3T3-L1 adipocytes and preadipocytes.
|
43 |
18615583
|
ASP increased p-PKCalpha and PKCzeta to 161% (P < 0.0.001) and 160% (P < 0.01), a stimulation effectively blocked by PROG (10(-8) and 10(-6) M) and TEST (10(-6) M).
|
44 |
18615583
|
Sex steroid hormone-induced ASP resistance via C5L2 may contribute to altered adipose tissue function and insulin resistance phenotype in humans.
|
45 |
18615583
|
Acylation stimulating protein (ASP) stimulates triglyceride synthesis and glucose transport via its receptor C5L2.
|
46 |
18615583
|
In human studies, ASP is increased in insulin resistant states such as obesity, diabetes, polycystic ovary syndrome and late pregnancy (the latter two associated with altered sex hormones).
|
47 |
18615583
|
The aims were (i) to evaluate ASP response and C5L2 expression following treatment with sex steroid hormones and (ii) to identify mechanisms of ASP resistance using 3T3-L1 adipocytes and preadipocytes.
|
48 |
18615583
|
ASP increased p-PKCalpha and PKCzeta to 161% (P < 0.0.001) and 160% (P < 0.01), a stimulation effectively blocked by PROG (10(-8) and 10(-6) M) and TEST (10(-6) M).
|
49 |
18615583
|
Sex steroid hormone-induced ASP resistance via C5L2 may contribute to altered adipose tissue function and insulin resistance phenotype in humans.
|
50 |
18615583
|
Acylation stimulating protein (ASP) stimulates triglyceride synthesis and glucose transport via its receptor C5L2.
|
51 |
18615583
|
In human studies, ASP is increased in insulin resistant states such as obesity, diabetes, polycystic ovary syndrome and late pregnancy (the latter two associated with altered sex hormones).
|
52 |
18615583
|
The aims were (i) to evaluate ASP response and C5L2 expression following treatment with sex steroid hormones and (ii) to identify mechanisms of ASP resistance using 3T3-L1 adipocytes and preadipocytes.
|
53 |
18615583
|
ASP increased p-PKCalpha and PKCzeta to 161% (P < 0.0.001) and 160% (P < 0.01), a stimulation effectively blocked by PROG (10(-8) and 10(-6) M) and TEST (10(-6) M).
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54 |
18615583
|
Sex steroid hormone-induced ASP resistance via C5L2 may contribute to altered adipose tissue function and insulin resistance phenotype in humans.
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55 |
19622482
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The values of ASP and SSA increased significantly in HT and DBT patients compared to the control group.
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56 |
19622482
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In this work, abnormalities in the erythrocyte aggregation could be detected by the values of ASP, EAC and SSA, which might be involved in vascular disorders of diseases such as hypertension and diabetes.
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57 |
19622482
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The values of ASP and SSA increased significantly in HT and DBT patients compared to the control group.
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58 |
19622482
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In this work, abnormalities in the erythrocyte aggregation could be detected by the values of ASP, EAC and SSA, which might be involved in vascular disorders of diseases such as hypertension and diabetes.
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59 |
19956096
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To assess whether this, or other specific variants, are responsible for T1D risk, the Type I Diabetes Genetics Consortium analyzed 28 PTPN22 SNPs in 2295 affected sib-pair (ASP) families.
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60 |
19956096
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When considering rs2476601 'C' founder chromosomes, a second haplotype (AGGGGC) centromeric of PTPN22 in the C1orf178 region was associated with protection from T1D (odds ratio=0.81, P=0.0005).
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61 |
22180093
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This gene has been demonstrated to encode a functional receptor of acylation-stimulating protein (ASP), a G-protein-coupled receptor (GPCR), that has been shown to influence insulin secretion in cultured pancreatic islet cells in vitro and is a stimulator of triglyceride synthesis and glucose transport in vivo.
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62 |
23831465
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DIO mice exhibited higher basal levels of plasma ASP and, after 30weeks of diet, showed lower ASP receptor (C5L2) expression in adipose tissue compared to chow-fed mice.
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63 |
23831465
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Additionally, ex vivo ASP stimulation failed to induce normal Ser(473)AKT phosphorylation in adipose tissue from DIO mice VS chow-fed controls.
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64 |
23831465
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DIO mice exhibited higher basal levels of plasma ASP and, after 30weeks of diet, showed lower ASP receptor (C5L2) expression in adipose tissue compared to chow-fed mice.
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65 |
23831465
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Additionally, ex vivo ASP stimulation failed to induce normal Ser(473)AKT phosphorylation in adipose tissue from DIO mice VS chow-fed controls.
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