Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Genes for adiponectin and resistin are candidate genes of insulin resistance and type 2 diabetes mellitus. The aim of our study was to determine the frequency of single nucleotide polymorphisms (SNP) 45T>G and 276G>T of the adiponectin gene and 62G>A and -180C>G of the resistin gene in patients with obesity (OB), anorexia nervosa (AN) and in control healthy normal-weight women (NW) and to study the influence of particular genotypes on serum concentrations of these hormones and on insulin sensitivity. Serum adiponectin, resistin, tumor necrosis factor alpha (TNF-alpha), insulin, cholesterol, glycated hemoglobin (HbA1c) and blood glucose levels were measured in 77 patients with OB, 28 with AN and 38 NW. DNA analysis was carried out by polymerase chain reaction with restriction analysis of PCR product. The presence of SNP ADP+276 G>T allele was accompanied by higher cholesterol levels in AN patients, higher adiponectin concentrations in OB patients and lower HbA1c levels in NW. SNP of the resistin gene 62G>A was associated with lower HbA1c in NW and higher cholesterol concentrations in OB group. The carriers of the minor G allele in the position -180 of the resistin gene within AN group had significantly higher BMI relative to non-carriers. We conclude that polymorphisms in adiponectin and resistin genes can contribute to metabolic phenotype of patients with obesity and anorexia nervosa.
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PMID:Adiponectin and resistin gene polymorphisms in patients with anorexia nervosa and obesity and its influence on metabolic phenotype. 2086 4

The fact that fat issue is an endocrine gland secreting several hormones participating in the pathogenesis of type 2 diabetes mellitus (DM2) is universally recognized. Fat issue secretes leptin, tumor necrosis factor alpha, resistin, adiponectin, interleukin-6, free fatty acids, visfatin, omentin, perilipin, and other substances that influence the condition of insulinoresistance, one of the main factors responsible for DM2. Subcutaneous fat and visceral depot fat tissue differ in the spectrum of hormones they produce; the list of these hormones is presented in the article. The presence of abdominal or visceral obesity is combined with significant insulinoresistance, which, in its turn, increases the risk of vascular complications of diabetes. The article also cover the participation of other mechanisms - insulin secretion defect, oxidation stress, low secretion of glucagon-like peptide 1, apoptosis, an increased quantity of amyloid and the fl-cell pull in the pancreatic island--in DM2 pathogenesis. The authors present data on the secretion of leptin, resistin, adiponectin, and tumor necrosis factor a, as well as the condition of the functional activity of beta-cells and the degree of insulinoresistance in 30 DM2 patients receiving dietotherapy.
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PMID:[The role of the fat tissue and its hormones in the mechanisms of insulin resistance and the development of type 2 diabetes mellitus]. 1788 4

Low adiponectin expression is common in obesity and is tightly linked to insulin resistance and fat mass expansion. Whereas normal adipocytes offer effective metabolic buffering through well-controlled release and uptake of free fatty acids on demand, adipocyte expansion induced by caloric excess and modulated by genetic, regional, and systemic factors elicits major unfavorable changes in fat cell phenotypes. Large, dysfunctional adipocytes show increased lipolysis and enhanced expression and secretion of proinflammatory and pro-oxidative cytokines. Low adiponectin secretion is a hallmark of impaired adipocyte function; its secretion is inhibited by cytokines such as tumor necrosis factor alpha, interleukin 6 and plasminogen activator inhibitor 1 and by high oxidative stress induced by increased fatty acids that activate nicotinamide adenine dinucleotide phosphate-oxidase. The ensuing hypoadiponectinemia may aggravate insulin resistance and facilitate the evolution of type 2 diabetes. Only massive weight loss allows true and sustained recovery of normal fat cell function as reflected by adiponectin secretion.
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PMID:Hypoadiponectinemia as a marker of adipocyte dysfunction--part II: the functional significance of low adiponectin secretion. 1805 13

Chronic inflammation has been linked with an increased risk of type 2 diabetes and cardiovascular disease. As an endocrine and inflammatory organ, adipose tissue is an important source of circulating pro-inflammatory cytokines. Current evidence strongly supports that chronic inflammation is associated with enlarged body fat mass. Moreover, inflammation is independently linked with abdominal, especially visceral fat mass, possibly due to the regional variation in adipose tissue cytokine production. In addition to pharmacological approaches, lifestyle modifications have been advocated for the treatment of chronic inflammation. A number of studies have indicated that either weight loss via energy restriction, or energy restriction plus other strategies (aerobic exercise, behavioral counseling, and liposuction), could reduce chronic inflammation. While the amount of weight loss tends to be important, exercise and other strategies may have additional effects. A few studies have reported weight loss effects on adipose tissue cytokine production. Weight loss reduces subcutaneous adipose tissue production of pro-inflammatory cytokines (i.e. interleukin 6, tumor necrosis factor alpha) and increases adipose expression of anti-inflammatory cytokines (i.e. interleukin 10, interleukin 1 receptor antagonist). More studies are needed to investigate the role of regional adipose tissue cytokine production in regulation of inflammation and the modulating effects of weight loss.
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PMID:Chronic inflammation: role of adipose tissue and modulation by weight loss. 1822 Jun 15

We reported previously that sera from patients with type 2 diabetes and neuropathy induce autophagy in human neuroblastoma (SH-SY5Y) cells. Here we report that enriched immunoglobulin fractions from a subpopulation of these patients induce autophagy and colocalization with Fas-activated death domain (FADD), a component of the Fas-activated death domain receptor signaling pathway. These effects were replicated by treatment of SY5Y cells with Fas ligand, tumor necrosis factor alpha and an agonist anti-Fas antibody. Preincubation of these sera with a soluble Fas receptor chimera (extracellular domain) markedly decreased the stimulation of autophagy. The results suggest that sera from subset of individuals with type 2 diabetes and neuropathy contain autoantibodies that activate the Fas cascade.
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PMID:Type 2 diabetes with neuropathy: autoantibody stimulation of autophagy via Fas. 1830 64

Obesity and type 2 diabetes course with chronic low-grade inflammation, where adiponectin is down-regulated and pro-inflammatory markers, like interleukin (IL)-6, tumor necrosis factor alpha (TNF-alpha), and C-reactive protein (CRP), are up-regulated. A treatment option to improve the micro- and macro-complications in type 2 diabetes is the use of glycine, which has been demonstrated previously to increase the expression of anti-inflammatory cytokine IL-10 in monocytes and down-regulate the expression of TNF-alpha in monocytes and Kupffer cells. Recently, our group demonstrated that glycine decreases the pro-inflammatory plasmatic cytokines in type 2 diabetes. The aim of this study was to test the effect of glycine on adipokines expression in 3T3-L1 cells. Cells were grown and differentiated in the presence of 10 mM glycine. After 2 days of confluence, cells were differentiated to adipocytes in the same medium supplemented with insulin, dexamethasone, and 3-isobutyl-1-methylxanthine. The RNA was extracted at days 0 and 8 of differentiation (fibroblasts and mature adipocyte phenotypes, respectively). The expression of PPAR-gamma (peroxisome proliferator-activated receptor-gamma), adiponectin, resistin, IL-6 and TNF-alpha were analyzed by real-time PCR. We demonstrated that when 3T3-L1 cells were treated with glycine, IL-6, resistin and TNF-alpha mRNA expression was decreased, but surprisingly adiponectin and PPAR-gamma were up-regulated. In all cases the values were statistically significant (P<0.05) between glycine treatment and controls. These results show that glycine improves the pro-inflammatory profile and up-regulates adiponectin gene expression. Therefore, glycine could be useful as a modulator of the pro-inflammatory state observed in obesity and type 2 diabetes.
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PMID:Glycine increases mRNA adiponectin and diminishes pro-inflammatory adipokines expression in 3T3-L1 cells. 1849 99

Insulin resistance is extremely common and frequently is associated with comorbid conditions such as cardiovascular disease, hypertension, obesity, infertility, and neurodegeneration. In addition, insulin resistance is the driving force for type 2 diabetes mellitus. Interestingly, co-existence of insulin resistance and chronic hepatitis C occurs more often than predicted by chance, with recent estimates indicating that 30% to 70% of patients with chronic hepatitis C display some evidence of insulin resistance. Recent research revealed several molecules, including tumor necrosis factor alpha, suppressor of cytokine signaling 1 and 3 proteins, insulin-receptor substrates 1 and 2, and other adipocytokines, potentially are involved in the development of insulin resistance in patients with chronic hepatitis C. Unfortunately, baseline insulin resistance has a negative impact on treatment outcomes in patients with chronic hepatitis C. However, successfully managing insulin resistance or diabetes mellitus in these patients may improve patients' likelihoods of successful outcomes with antiviral therapy. Likewise, eradication of hepatitis C virus in patients with insulin resistance or diabetes mellitus appears to improve glucose metabolism. Although adjunctive therapies such as insulin sensitizers and weight loss often are recommended, their ability to improve antiviral treatment response in patients with chronic hepatitis C is unproven. Studies are under way to determine whether improving insulin sensitivity results in better outcomes in patients receiving pegylated interferon alfa plus ribavirin therapy for chronic hepatitis C.
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PMID:Insulin resistance among patients with chronic hepatitis C: etiology and impact on treatment. 1858 70

The present review focuses on the possible role of interleukin-(IL)-6 in vascular insulin resistance. The endothelium plays an important role in regulating the tone of the vasculature by releasing nitric oxide (NO) to the smooth muscles of the vessels, thereby regulating the distribution of blood flow to the various tissues in relation to their energy demand. A dysfunctioning endothelium has been associated with both initiation and progression of atherosclerotic cardiovascular (CV) disease and has been shown to predate the onset of hyperglycemia in the natural history of type 2 diabetes. It is likely that chronic low-level inflammation plays an important role in developing endothelial dysfunction mainly through proinflammatory actions of tumor necrosis factor alpha (TNF-alpha). TNF-alpha induces production of IL-6 and it has been suggested that a causal relationship exists between endothelial dysfunction and these cytokines. With regard to vascular insulin resistance, the available data point to a direct pathogenic role of TNF-alpha in mediating endothelial dysfunction, whereas with regard to IL-6 evidence is sparse and does not allow any firm conclusions.
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PMID:The role of inflammation in vascular insulin resistance with focus on IL-6. 1879 75

Ingestion of 75 g glucose during an oral glucose tolerance test (OGTT) increases systemic inflammation and oxidative stress in healthy subjects and patients with type 2 diabetes mellitus, but the effect in overweight/obese nondiabetic individuals is uncertain. The aim of the present study was to determine the effect of an OGTT on plasma concentrations of inflammatory cytokines and peroxides in 33 subjects with body mass index >27 kg/m(2). After an overnight fast, blood samples were taken from participants immediately before and at 30, 60, 90, and 120 minutes after ingestion of 75 g glucose. Plasma glucose, insulin, free fatty acid, interleukin (IL)-6, tumor necrosis factor alpha, and peroxides were measured during the tests. Plasma IL-6 concentrations decreased (13%) significantly (P < .001) at 30 and 60 minutes, whereas plasma peroxide concentrations decreased slightly (3%, P = .003) at 30 minutes during the tests. The 30-minute decrease in plasma IL-6 was correlated significantly and inversely with the concomitant increase in plasma insulin (r = -0.410, P = .02) and with the ratio of insulin to glucose at 30 minutes during the OGTT (r = -0.366, P = .04). These data suggest that plasma concentrations of IL-6 are acutely decreased possibly because of the predominance of the anti-inflammatory effect of hyperinsulinemia over the proinflammatory effect of hyperglycemia after ingestion of a large quantity of glucose in obese individuals.
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PMID:The effect of glucose ingestion on inflammation and oxidative stress in obese individuals. 1880 36

The aim of this study was to evaluate the effect of pioglitazone on nitric oxide in patients with type 2 diabetes and coronary artery disease. Twenty-seven patients with coronary artery disease and diabetes mellitus who had received coronary stenting were eligible for the study. They were assigned to the no insulin resistance (NIR) group, the insulin resistance (IR) group, and the pioglitazone group (30 mg once a day). Endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), tumor necrosis factor alpha (TNF-alpha), interleukin-6, leptin, and adiponectin were measured. In the pioglitazone group, eNOS, iNOS, and leptin were significantly lower and adiponectin was significantly higher than those in the IR group. Stepwise multiple regression analyses showed that eNOS correlated with TNF-alpha and iNOS correlated with leptin and TNF-alpha. Leptin was the strongest predictor of iNOS. Treatment with pioglitazone significantly reduced eNOS and iNOS by improving adipocytokine levels.
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PMID:The effect of pioglitazone on nitric oxide synthase in patients with type 2 diabetes mellitus. 1904 May 87


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