目的:探讨visfatin与老年2型糖尿病及其大血管并发症和相关代谢指标的关系。方法:将66例老年糖尿病患者分为合并大血管病变组（MCV）35例和非大血管病变组（nMCV）31例，并选64例健康人做对照。采取酶联免疫测定法（ELISA）测定空腹血清visfatin浓度；并测定各组的空腹血糖、胰岛素、血压和血脂水平；用胰岛素抵抗指数（HOMAIR）HOMAIR评价胰岛素抵抗，分析各指标间的相关性及与大血管并发症的相关性。结果:①老年2型糖尿病组血清visfatin浓度高于正常对照组，差异有统计学意义（Plt;0.01）。但正常对照组与2型糖尿病组中nMCV组比较，visfatin浓度差异无统计学意义（Pgt;0.05）。②老年2型糖尿病组中大血管病变组（MCV）血清visfatin浓度明显高于非大血管病变组（nMCV），差异有统计学意义（Plt;0.01）。③相关分析显示，老年2型糖尿病组血清visfatin浓度与腰围（WC）、甘油三酯（TG）均呈显著正相关，与性别、年龄、HOMAIR呈正相关。进一步以visfatin为应变量，以年龄、性别、BMI、WC、收缩压（SBP）、舒张压（DBP）、总胆固醇（TC）、甘油三酯（TG）、低密度脂蛋白胆固醇（LDL-C）、高密度脂蛋白胆固醇（HDL-C）、空腹血糖（FPG）、空腹胰岛素（FINS）、HOMAIR为自变量进行多元逐步回归分析，TG、WC和年龄是血清visfatin独立相关因素。④在老年T2DM组，以有无大血管并发症为应变量（Y=1，n=0），各指标为自变量，进行logistic回归分析，visfatin进入回归方程。结论:血清visfatin与2型糖尿病的发病不相关，但在老年2型糖尿病中与其大血管并发症有关。
The aim of the current study is to investigate the effect of visfatin on cardiomyocyte hypertrophy. Cultured H9c2 cardiomyocytes were exposed to visfatin at different concentrations for different periods of time, and the markers of cardiomyocyte hypertrophy were detected. Moreover, pravastatin, the inhibitor of endoplasmic reticulum stress (ERS) or thapsigargin, an ERS agonist was used respectively to pre-treat the cells before visfatin stimulation. F-actin staining was performed to measure the cell surface change. The mRNA expressions of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP)and ERS markers including glucose-regulated protein 78(GRP78), C/EPB homologous protein (CHOP) and activating transcription factor 6 (ATF6) were assessed by real time RT-PCR. The change of protein level of GRP78 and CHOP was detected by Western blot. The experimental data demonstrated that exposure to 100 or 150 ng/mL concentrations of visfatin for 24 h, or 100 ng/mL of visfatin for 24 or 48 h, significantly increased the expression of markers for cardiomyocyte hypertrophy. Visfatin stimulation provoked ERS in H9c2 cells. Furthermore, pre-treatment with pravastatin partially inhibited the visfatin-induced mRNA expression of ANP and BNP in H9c2 cells, whereas thapsigargin promoted the visfatin-induced expression of cardiomyocyte hypertrophy markers. The results suggest that visfatin might induce cardiomyocyte hypertrophy via ERS -dependent pathways.
The aim of the study is to identify the effects and underlying mechanisms of visfatin on inflammation and necroptosis in vascular endothelial cells. Human umbilical vein endothelial cells (HUVECs) were stimulated with visfatin or pretreated with Polyinosinic acid (LOX-1 inhibitor). By using the Western blot, RT-PCR, immunocytochemistry, enzyme-linked immunosorbent assay (ELISA), MTT and flow cytometry technique, the occurrence of inflammation and necroptosis in HUVECs were evaluated. Our results showed that 100 ng/mL visfatin significantly increased the mRNA and protein expression of monocyte chemotactic protein 1 (MCP-1) and LOX-1 after 24 hours’ treatment in HUVECs. However, pretreatment with Polyinosinic acid could significantly reduce the expression of MCP-1 compared with visfatin group. Additionally, 100 ng/mL visfatin could induce the production of necrotic features and increase the mRNA expression of BMF (one of the markers of necroptosis), while pretreating with Polyinosinic acid markedly downregulated the mRNA expression of BMF gene and promoted the cell proliferation. These results indicate that visfatin might induce inflammation and necroptosis via LOX-1 in HUVECs, suggesting that visfatin plays a central role in the development of atherosclerosis.