葡萄糖和胰岛素对3T3-L1脂肪细胞内脏脂肪素mRNA表达的影响

目的研究不同浓度葡萄糖和胰岛素对3T3-L1脂肪细胞中内脏脂肪素（Visfatin）mRNA表达的影响。方法通过real—time RT-PCR方法检测不同浓度葡萄糖和胰岛素培养下3T3-L1脂肪细胞Visfatin mRNA的表达。结果葡萄糖增加了3T3-L1脂肪细胞Visfatin mRNA的表达;胰岛素降低其表达。结论葡萄糖和胰岛素对3T3-L1脂肪细胞中Visfatin mRNA的表达有凋控作用。     

Infusion of insulin impairs human adipocyte glucose metabolism in vitro without decreasing adipocyte insulin receptor binding

Summary To determine whether hyperinsulinaemia can cause insulin resistance in man and, if so, whether this occurs at a receptor or post-receptor site, nine normal volunteers were infused with insulin for 6 h at a rate (2 mU·kg^-1·min^-1) which resulted in steady-state plasma insulin concentrations of 140±13mU/l and four subjects were infused with saline (0.45%). Isolated adipocytes and monocytes were used as models for studying insulin binding, while adipocytes were also used to study insulin action in vitro. Adipocyte insulin binding did not decrease following infusion of insulin (4.6±0.5 versus 4.4±0.4% per 2×10⁵ cells, before and after, respectively), whereas monocyte insulin binding did (7.2±0.6 versus 6.2±0.6% per 10⁷ cells, p<0.05). Initial rates of adipocyte 3-0-methyl glucose transport were decreased in the absence of insulin (basal) and at submaximally effective (33.3pmol/l) but not at maximally effective insulin concentrations. At all insulin concentrations and in the absence of insulin, rates of glucose conversion to lipids were decreased more than 50% (p<0.05), whereas rates of glucose oxidation were unaffected. This decrease in the rates of conversion of glucose to lipids could not be accounted for by the decrease in rates of glucose transport. These results suggest that hyperinsulinaemia can cause insulin resistance in man and that, at least initially, this occurs at a post-receptor site. Furthermore, the discordant effect of hyperinsulinaemia on monocyte and adipocyte insulin binding indicates that monocyte insulin binding may not always reflect insulin binding in insulin-sensitive tissues.     

Plasma visfatin levels in patients with newly diagnosed and untreated type 2 diabetes mellitus and impaired glucose tolerance

Visfatin, a new adipokine, facilitates adipogenesis and has insulin-mimetic properties. We aimed to investigate the plasma visfatin levels in patients with newly diagnosed and untreated type 2 diabetes mellitus (T2DM) and impaired glucose tolerance (IGT), who had no obesity or hypertension. Twenty-two patients with T2DM, 18 subjects with IGT and 40 healthy controls were enrolled. Visfatin levels were measured along with the BMI, blood pressure, lipids, glucose, insulin, adiponectin and hsCRP levels, and HOMA-IR indexes. Age, sex and BMI were similar in all groups. Visfatin levels were higher in the diabetic group than the controls (p=0.01). There was no significant difference in the visfatin levels between the T2DM and IGT groups as well as IGT group and healthy controls. Plasma visfatin concentrations did not differ between men and women. Visfatin levels did not correlate with BMI, blood pressure, plasma adiponectin, insulin, hsCRP, glucose and lipid levels or HOMA-IR indexes in the three groups. These results indicate that hyperglycemia causes an increase in plasma visfatin levels and, as in people with T2DM but not with IGT, this increase gets more prominent as the glucose intolerance worsens.     

Serum visfatin levels, adiposity and glucose metabolism in obese adolescents

Objective: Visfatin, an adipokine, has insulin-mimetic effects. The main determinants of both the production and the physiologic role of visfatin are still unclear. The aim of this study is to determine the relation of serum visfatin to adiposity and glucose metabolism.Methods: 40 pubertal adolescents (20 females, 20 males; age range: 9-17 years) with exogenous obesity and 20 age- and sex-matched healthy adolescents (10 females, 10 males) were enrolled in the study. Oral glucose tolerance test (OGTT) was performed in the obese group. Serum glucose, insulin and visfatin levels were analyzed in the fasting state in the controls and at 0, 60 and 120 minutes during the OGTT in the obese group.Results: The obese group had higher serum visfatin levels than the control group [11.6 (3.3-26) ng/mL vs. 7.5 (3.3-10.5) ng/mL, p<0.001]. Visfatin levels were correlated positively with body mass index, waist/hip ratio, insulin, and homeostasis model assessment for insulin resistance and negatively with glucose/insulin ratio in the combined group (obese subjects plus controls). Visfatin levels were essentially similar in obese subjects with and without insulin resistance (p>0.05). Serum visfatin levels did not change at 60 and 120 minutes of the OGTT compared to the baseline levels (p>0.05).Conclusions: Serum visfatin levels are elevated in obese adolescents and do not change with acute changes in glucose metabolism. Visfatin levels are related with adiposity and glucose metabolism parameters. However, the role and contribution of adiposity and glucose metabolism to the circulating visfatin levels in obese patients remain to be explored. Conflict of interest:None declared.     

Visfatin inhibits apoptosis of pancreatic β-cell line, MIN6, via the mitogen-activated protein kinase/phosphoinositide 3-kinase pathway

Visfatin is an adipocytokine that plays an important role in attenuating insulin resistance by binding to insulin receptor. It has been suggested that visfatin plays a role in the regulation of cell apoptosis and inflammation by an as yet unidentified mechanism. This study investigated the protective effects of visfatin on palmitate-induced islet β-cell apoptosis in the clonal mouse pancreatic β-cell line MIN6. The cells were treated with palmitate and/or recombinant visfatin. An 1-(4,5-dimethylthiazol-2-yl)-3,5-diphenylformazan assay was used to detect cell proliferation, V-FITC/propidium iodide staining was used to measure cell apoptosis and necrosis, and western blot analysis was used to detect the expression of proapoptotic proteins. The incubation of the cells with visfatin led to a concentration-dependent increase of cell proliferation (1.55-fold at 10(-7) M and 24 h compared with control, P<0.05). Visfatin significantly reduced the cell apoptosis induced by palmitate and caused a significant change in the expression of several proapoptotic proteins, including upregulation of Bcl-2 and a marked downregulation of cytochrome c and caspase 3. Visfatin also activated the ERK1/2 and the phosphoinositide 3-kinase (PI3K)/AKT signaling pathways in a time- and concentration-dependent manner, and the effect of visfatin on apoptosis was blocked by the specific ERK1/2 and PI3K/AKT inhibitors, PD098059 and LY294002. We conclude that visfatin can increase β-cell proliferation and prevent apoptosis, activate intracellular signaling, and regulate the expression of proapoptotic proteins. The antiapoptotic action of visfatin is mediated by activation of mitogen-activated protein kinase-dependent and PI3K-dependent signaling pathways.     

Visfatin及其基因多态性与糖脂代谢的关系

Visfatin是新近发现的一种脂肪细胞因子,主要由内脏脂肪组织分泌产生.目前许多研究表明,visfatin与胰岛素抵抗、脂代谢、2型糖尿病及其并发症密切相关,具有降血糖和类胰岛素作用,在2型糖尿病伴动脉粥样硬化、冠心病及糖尿病肾病患者中血浆水平明显升高.因此,visfatin可能与上述疾病的发生有一定关系.此外,visfatin基因多态性与糖脂代谢相关,而且受遗传背景和环境凶素的影响.本文就visfatin及其基因多态性与糖脂代谢关系的研究进展作一综述.     

Visfatin及其基因多态性与糖脂代谢的关系

Visfatin是新近发现的一种脂肪细胞因子,主要由内脏脂肪组织分泌产生.目前许多研究表明,visfatin与胰岛素抵抗、脂代谢、2型糖尿病及其并发症密切相关,具有降血糖和类胰岛素作用,在2型糖尿病伴动脉粥样硬化、冠心病及糖尿病肾病患者中血浆水平明显升高.因此,visfatin可能与上述疾病的发生有一定关系.此外,visfatin基因多态性与糖脂代谢相关,而且受遗传背景和环境凶素的影响.本文就visfatin及其基因多态性与糖脂代谢关系的研究进展作一综述.     

Visfatin及其基因多态性与糖脂代谢的关系

Visfatin是新近发现的一种脂肪细胞因子,主要由内脏脂肪组织分泌产生.目前许多研究表明,visfatin与胰岛素抵抗、脂代谢、2型糖尿病及其并发症密切相关,具有降血糖和类胰岛素作用,在2型糖尿病伴动脉粥样硬化、冠心病及糖尿病肾病患者中血浆水平明显升高.因此,visfatin可能与上述疾病的发生有一定关系.此外,visfatin基因多态性与糖脂代谢相关,而且受遗传背景和环境凶素的影响.本文就visfatin及其基因多态性与糖脂代谢关系的研究进展作一综述.     

Visfatin及其基因多态性与糖脂代谢的关系

Visfatin是新近发现的一种脂肪细胞因子,主要由内脏脂肪组织分泌产生.目前许多研究表明,visfatin与胰岛素抵抗、脂代谢、2型糖尿病及其并发症密切相关,具有降血糖和类胰岛素作用,在2型糖尿病伴动脉粥样硬化、冠心病及糖尿病肾病患者中血浆水平明显升高.因此,visfatin可能与上述疾病的发生有一定关系.此外,visfatin基因多态性与糖脂代谢相关,而且受遗传背景和环境凶素的影响.本文就visfatin及其基因多态性与糖脂代谢关系的研究进展作一综述.