【摘要】 目的:探讨非酒精性脂肪性肝病(NAFLD)在代谢综合征(MS)相关Ⅱ型糖尿病中的作用。方法:将64只大鼠随机分为8组,分别是3月正常对照组(3NC)、3月高糖高脂组(3H)、6月正常对照组(6NC)、6月高糖高脂组(6H)、9月正常对照组(9NC)、9月高糖高脂组(9H)、12月正常对照组(12NC)和12月高糖高脂组(12H)。测定血浆丙氨酸氨基转移酶(ALT)、游离脂肪酸(FFA)、内毒素(LPS)、肿瘤坏死因子α(TNFα)、C反应蛋白(CRP)、巨噬细胞趋化蛋白-1(MCP-1)、空腹血糖(FPG)、空腹胰岛素(FINS),并计算胰岛素抵抗指数(HOMA-IR)、β细胞功能指数(HOMA-β)。取肝组织和胰腺组织切片行苏木素-伊红(HE)染色和苏丹Ⅳ染色;内脏脂肪组织行苏木素-伊红(HE)染色。以TUNEL法检测胰岛内细胞凋亡水平。结果:与正常对照组相比,各阶段高糖高脂组大鼠血清ALT、FFA、LPS、TNFα、CRP、MCP-1、FPG、FINS和HOMA-IR水平都明显升高;而HOMA-β在第6个月出现代偿性增强后进行性衰退。高糖高脂组第3-12月胰岛凋亡细胞数量逐渐增加。结论:NAFLD(特别是脂肪肝与脂肪性肝炎)可以诱发MS相关的2型糖尿病。更多还原

【Abstract】 AIM: To investigate the effect of non-alcoholic fatty liver disease(NAFLD) on metabolic syndrome(MS)-related type 2 diabetes.METHODS: Sixty-four rats were randomly divided into 8 groups: normal control groups of 3 months(3NC),6 months(6NC),9 months(9NC) and 12 months(12NC),and high-sucrose and high-fat groups of 3 months(3H),6 months(6H),9 months(9H) and 12 months(12H).The serum levels of alanine transaminase(ALT),free fatty acid(FFA),endotoxin(LPS),tumor necrosis factor alpha(TNFα),C-reactive protein(CRP),monocyte chemotactic protein-1(MCP-1),fasting plasma glucose(FPG) and fasting plasma insulin(FINS) were measured.The insulin resistance index(HOMA-IR) and beta cell function index(HOMA-β) were also calculated.The specimens of liver and pancreas were prepared for microscopic observation with HE and Sudan Ⅳ staining.The visceral adipose specimens were also prepared with HE staining.The apoptosis of islet cells was detected by TUNEL.RESULTS: Compared with normal control groups,the levels of ALT,FFA,LPS,TNFα,CRP,MCP-1,FPG,FINS and HOMA-IR in high-sucrose and high-fat groups of every phase were higher,but the level of HOMA-β in 6H group showed a compensatory increase first and then progressively decreased.Compared with normal control groups,TUNEL results showed that the number of apoptotic islet cells in high-sucrose and high-fat groups gradually increased from the 3rd to the 12th month.CONCLUSION: The NAFLD plays a trigger role in the start of MS-related type 2 diabetes.更多还原