【摘要】 目的 探讨血浆内脏脂肪素(visfatin)与2型糖尿病的关系。方法 2007年7月—9月选取2型糖尿病患者和正常对照组各40例。根据体重指数再分为超重肥胖组和非超重肥胖组。检测visfatin水平、空腹血糖、空腹胰岛素、血脂、血压等,计算腰臀比、体重指数、稳态模型胰岛素抵抗指数homeostasis model assessment of insulin resistance,HOMAIR)及胰岛素分泌功能(HOMAβ)。结果 2型糖尿病组血浆visfatin水平显著低于正常对照组(Plt;0.05)。多元逐步相关分析表明,在肥胖的2型糖尿病个体中visfatin与高密度脂蛋白胆固醇、空腹血糖、体重指数呈负相关。二分类Logstic回归分析显示血浆visfatin及胰岛素抵抗指数与2型糖尿病的发生显著相关,回归方程式为Y=7.681+2.417 ln HOMAIR-2.549 visfatin。结论 visfatin的变化可能对2型糖尿病的发生、发展具有一定作用。
ObjectiveTo study the characteristics of carotid atherosclerotic plaque and investigate the relationship between visfatin and plaque stabilization. Methodsfifty-six patients with carotid stenosis were divided into symptomatic group (n=31) and asymptomatic group (n=25) based on the clinical manifestation and onset time.All plaque specimens were stained with HE and Masson trichrome staining and studied pathologically.The plaques were grouped into stable and unstable plaques based on thickness of the fibrous cap and the area of lipid-rich core in the plaques.The expression of visfatin was detected by immunohistochemistry staining. Results①The proportion of unstable plaques were significantly higher in symptomatic group than in asymptomatic group (67.74% vs 36.00%, P < 0.05).②Compared with stable plaques, unstable plaques had thinner fibrous cap, larger lipid necrotic core, and higher proportion of hemorrhage: (49.87±8.75)μm vs (74.54±6.80)μm (P < 0.001), (65.63±12.97)% vs (31.81±5.13)% (P < 0.001), and 63.33% vs 30.77% (P < 0.05).③The integral optical density value of expressed visfatin in unstable plaques was significantly more than in stable plaques (84 165.47±9 183.12 vs 55 694.08±4 818.57, P < 0.001). ConclusionsThe plaque destabilization is closely related to the clinical symptoms of atherosclerosis.The thickness of fibrous cap, area of lipid-rich core, and hemorrhage play an important role in the plaque stabilization.The visfatin is related to atherogenesis and plaque destabilization.
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.
Objective To investigate the correlation between serum level of visfatin and obesity in patients with obstructive sleep apnea hypopnea syndrome ( OSAHS) . Methods Forty-seven patients with OSAHS and 20 healthy controls were recruited in this study. Polysomnography was performed in all subjects to detect apnea-hypopnea index ( AHI) . The serumlevels of cisfatin, C-reactive protein ( CRP) , TNF-α, and IL-6 were measured by enzyme linked immunosorbent assay. The body mass inex ( BMI) was calculated.The level of cisfatin was compared between the OSAHS patients with different severity and the controls, and its relationship with the levels of AHI, BMI, CRP, TNF-α, and IL-6 was analyzed. Results The serumlevel of visfatin in the OSAHS patients was higher significantly than that in the controls ( P lt;0. 01) and increased by the severity of OSAHS. There were positive correlations between the serum level of visfatin and AHI,BMI, CRP, TNF-α, IL-6 in the OSAHS patients ( P lt;0. 05) . Conclusion The expression of visfatin may play an important role in the pathogenesis of OSAHS.