糖调节受损合并非酒精性脂肪肝患者血清脂联素水平及临床意义
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摘要
目的:测定糖调节受损(IGR)与非酒精性脂肪性肝病(NAFLD)集结存在时血清脂联素水平并探讨脂联素在糖代谢紊乱及NAFLD发生发展中的作用。
方法:选取健康对照者30例(NC组),空腹血糖受损(IFG)合并NAFLD者31例(IFG+NAFLD组)、不合并脂肪肝者28例(IFG+无FL组),IFG+糖耐量异常(IGT)合并NAFLD者32例(IGT+NAFLD组)、不合并脂肪肝者30例(IGT+无FL组)。测定各组人群血糖、血脂、肝功、血清胰岛素及脂联素水平,计算稳态模型评估法胰岛素抵抗指数(HOMA-IR)。探讨随NAFLD和糖代谢紊乱发生血清脂联素水平的变化趋势及相关因素。
结果:各组血清脂联素水平为NC组5.84±0.96mg/l、IFG+无FL组5.56±1.26mg/l、IFG+NAFLD组4.96±0.77mg/l、IGT+无FL组4.80±1.21mg/l、IGT+NAFLD组4.07±0.86mg/l。IFG+NAFLD组血清脂联素显著高于IFG+无FL组(P＜0.05);IGT+NAFLD组血清脂联素显著高于IGT+无FL组(P＜0.05);IGT+NAFLD组血清脂联素显著高于IFG+NAFLD组(P＜0.05)。IGR+NAFLD组血清脂联素与FPG(r=-0.497,P＜0.05)、Fins(r=-0.554,P＜0.05)、HOMA-IR(r=-0.584,P＜0.01)成显著负相关,与HDL-C(r=0.296,P＜0.01)成显著正相关。校正年龄、性别、体重、BMI后,上述相关关系仍然存在。多元线性逐步回归分析显示,HOMA-IR(回归系数=-0.826,t=-5.499,P＜0.05)、腰围(回归系数=-0.027,t=-2.423,P=0.001)为脂联素的显著相关因素。
结论:IGR期已存在血清脂联素水平降低、胰岛素抵抗状态,合并NAFLD或糖代谢紊乱加重都会使情况更加恶化。脂联素水平下降、糖脂代谢紊乱、胰岛素抵抗相互作用、相互影响,共同参与NAFLD、糖尿病及其并发症的发生发展。早期纠正糖脂毒性、改善胰岛素敏感性、提高血清脂联素的靶向治疗可能有助于改善机体代谢状态、预防或逆转NAFLD、糖尿病的发生发展。
Objective: To test levels of adiponectin in patients with impaired glucose regulation(IGR) and nonalcoholic fatty liver disease(NAFLD) and investigate the role of adiponectin in the develepment of glucose intolerance and nonalcoholic fatty liver disease.
Methods: Clicical and lavoratory data were collected from thirty healthy controls, thirty-one cases of impaired fasting glucose(IFG) with NAFLD, twenty-eight cases of IFG without NAFLD, thirty-two cases of impaired glucose tolerance(IGT) and IFG with NAFLD, thirty cases of IFG and IGT without NAFLD. Fasting plasma glucose, insulin, adiponectin and lipid profile were measured. The index of insulin resistance was caleulated according to the homeostasis model assessment method (HOMA-IR).
Results: In patients with IGR, serum adiponectin levels were statistically significantly lower, while HOMA-IR and triglycerid were higher in patients with NAFLD than without, and the situation became worse when glucose intolerance deteriorated. A statistically negative correlation was found between adiponectin and fasting plasma glucose(FPG), insulin and HOMA -IR in NAFLD patients with IGR. Adiponectin levels were of positive correlation with HDL-cholesterol in NAFLD patients with IGR. And the relationship still exited after controling for age, sex, weight and body mass index(BMI). HOMA -IR and waist circumstance played the major role in affecting adiponectin in NAFLD patients with IGR.
Conclusion: In patients with IGR, serum adiponectin levels were statistically significantly lower, HOMA-IR and triglycerid was higher than healthy controls, and the occurrance of NAFLD or deteriorated glucose intolerance only made the situation worse . Low adiponectin , intolerance of glucose-lipid and insulin resistance interact with one another and may eventually induce NAFLD and diabetes.
方法:选取健康对照者30例(NC组),空腹血糖受损(IFG)合并NAFLD者31例(IFG+NAFLD组)、不合并脂肪肝者28例(IFG+无FL组),IFG+糖耐量异常(IGT)合并NAFLD者32例(IGT+NAFLD组)、不合并脂肪肝者30例(IGT+无FL组)。测定各组人群血糖、血脂、肝功、血清胰岛素及脂联素水平,计算稳态模型评估法胰岛素抵抗指数(HOMA-IR)。探讨随NAFLD和糖代谢紊乱发生血清脂联素水平的变化趋势及相关因素。
结果:各组血清脂联素水平为NC组5.84±0.96mg/l、IFG+无FL组5.56±1.26mg/l、IFG+NAFLD组4.96±0.77mg/l、IGT+无FL组4.80±1.21mg/l、IGT+NAFLD组4.07±0.86mg/l。IFG+NAFLD组血清脂联素显著高于IFG+无FL组(P＜0.05);IGT+NAFLD组血清脂联素显著高于IGT+无FL组(P＜0.05);IGT+NAFLD组血清脂联素显著高于IFG+NAFLD组(P＜0.05)。IGR+NAFLD组血清脂联素与FPG(r=-0.497,P＜0.05)、Fins(r=-0.554,P＜0.05)、HOMA-IR(r=-0.584,P＜0.01)成显著负相关,与HDL-C(r=0.296,P＜0.01)成显著正相关。校正年龄、性别、体重、BMI后,上述相关关系仍然存在。多元线性逐步回归分析显示,HOMA-IR(回归系数=-0.826,t=-5.499,P＜0.05)、腰围(回归系数=-0.027,t=-2.423,P=0.001)为脂联素的显著相关因素。
结论:IGR期已存在血清脂联素水平降低、胰岛素抵抗状态,合并NAFLD或糖代谢紊乱加重都会使情况更加恶化。脂联素水平下降、糖脂代谢紊乱、胰岛素抵抗相互作用、相互影响,共同参与NAFLD、糖尿病及其并发症的发生发展。早期纠正糖脂毒性、改善胰岛素敏感性、提高血清脂联素的靶向治疗可能有助于改善机体代谢状态、预防或逆转NAFLD、糖尿病的发生发展。
Objective: To test levels of adiponectin in patients with impaired glucose regulation(IGR) and nonalcoholic fatty liver disease(NAFLD) and investigate the role of adiponectin in the develepment of glucose intolerance and nonalcoholic fatty liver disease.
Methods: Clicical and lavoratory data were collected from thirty healthy controls, thirty-one cases of impaired fasting glucose(IFG) with NAFLD, twenty-eight cases of IFG without NAFLD, thirty-two cases of impaired glucose tolerance(IGT) and IFG with NAFLD, thirty cases of IFG and IGT without NAFLD. Fasting plasma glucose, insulin, adiponectin and lipid profile were measured. The index of insulin resistance was caleulated according to the homeostasis model assessment method (HOMA-IR).
Results: In patients with IGR, serum adiponectin levels were statistically significantly lower, while HOMA-IR and triglycerid were higher in patients with NAFLD than without, and the situation became worse when glucose intolerance deteriorated. A statistically negative correlation was found between adiponectin and fasting plasma glucose(FPG), insulin and HOMA -IR in NAFLD patients with IGR. Adiponectin levels were of positive correlation with HDL-cholesterol in NAFLD patients with IGR. And the relationship still exited after controling for age, sex, weight and body mass index(BMI). HOMA -IR and waist circumstance played the major role in affecting adiponectin in NAFLD patients with IGR.
Conclusion: In patients with IGR, serum adiponectin levels were statistically significantly lower, HOMA-IR and triglycerid was higher than healthy controls, and the occurrance of NAFLD or deteriorated glucose intolerance only made the situation worse . Low adiponectin , intolerance of glucose-lipid and insulin resistance interact with one another and may eventually induce NAFLD and diabetes.
引文
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[2]Gabir MM,Hanson RL,Dabelea D,et al.The 1997 American Diabetes Association and 1999 World Health Organization criteria for hyperglycemia in the diagnosis and prediction of diabetes.Diabetes Care.2000,23:1108-1112
[3]Hui JM,Hodge A,Farrell GC,et al.Beyond insulin resistance in NASH:TNF-a or adiponectin? Hepatology,2004,40:46-54
[4]Bugianesi E,McCullough AJ,Marchesini G.Insulin resistance:a metabolic pathway to chronic liver disease.Hepatology,2005,42:987-1000
[5]赵向彤,潘优津,吴朝明等.糖调节受损患者血清脂联素水平及相关因素研究.中国慢性病预防与控制,2007,15:36-37
[6]The Expert Committee on the Diagnosis and Classification of Diabetes Mellitus:Follow-up report on the diagnosis of diabetes mellitus.Diabetes Care,2003,26:3160-3167
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