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作 者:李冰昱[1]
机构地区:[1]佛山市第二人民医院内分泌科,佛山528000
出 处:《重庆医科大学学报》2013年第9期1074-1077,共4页Journal of Chongqing Medical University
基 金:广东省卫生厅医学科研基金资助项目(编号:B2010304);佛山市医学类科技攻关资助项目(编号:201008038)
摘 要:目的:探讨慢性乙肝所致肝源性糖尿病(hepatogenous diabetes,HD)患者胰岛β细胞功能及胰岛素抵抗(insulin resistance,IR)特征以指导临床诊治。方法:对慢性乙肝致HD 37例,2型糖尿病(type 2 diabetes mellite,T2DM)58例行口服葡萄糖耐量实验+胰岛素释放实验,测定0、30、120、180 min血糖及胰岛素水平。计算胰岛β细胞基础分泌指数(homeostasis model assessment isletβcell function,HOMA-β)、早相胰岛素分泌指数(early phase insulin secretion index,EISI)、晚相胰岛素分泌指数(late phase insulin secretion index,LISI)以评估胰岛β细胞功能,胰岛抵抗指数(homeostasis model assessment-insulin resistance,HOMA-IR)、肝脏胰岛素抵抗指数(hepatic insulin resistance index,HIR)以评估IR。结果:HD组空腹血糖(fasting plasma glucose,FPG)低于T2DM组,但餐后2 h血糖及各时间点的胰岛素水平、HOMA-IR、HIR、HOMA-β、LISI均高于T2DM组(P<0.05),2组年龄、性别、糖尿病病程、糖化血红蛋白及EISI无统计学差异(P>0.05)。结论:慢性乙肝所致糖尿病患者主要表现为餐后血糖升高、早相胰岛素分泌受损、高胰岛素血症伴IR。Objective :To investigate islet cell function and insulin resistance (IR) in the patients with hepatogenous diabetes (HD). Methods:Oral glucose tolerance test and insulin releasing test were carried out on 37 patients with hepatogenous diabetes (HD) and 58 patients with type 2 diabetes (T2DM). Plasma glucose and insulin levels at 0,30,120, 180 min were measured. Homeostasis model assessment islet beta cell function (HOMA-β),early phase indexes of insulin secretion (EISI) and late phase indexes of insulin secretion (LISI) were used to evaluate islet beta cell function. Homeostasis model assessment-insulin resistance(HOMA-IR) and hepatic insulin resistance index(HIR) were used to assess IR. Results:Fasting plasma glucose level in HD group was lower than that in T2DM group,but 2-hour postprandial plasma glucose,insulin level at each time point,HOMA-IR,HIR,HOMA-β and LISI in HD group were significantly higher than those in T2DM group(P〈0.05). There was no significant difference in age, sex, disease course and glycosylated hemoglobin Alc and EISI between HD and T2DM groups(P〈0.05). Conclusions:Patients with HD may present high postprandial plasma glucose, early phase insulin secretion damage and hyperinsulinemia with IR.
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