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不同糖耐量个体胰岛β细胞功能观察及评价
引用本文:Liu J,Li YB,Shao H,Li YX,Yuan YH,Xiao YB,Weng JP. 不同糖耐量个体胰岛β细胞功能观察及评价[J]. 中华医学杂志, 2007, 87(18): 1252-1255
作者姓名:Liu J  Li YB  Shao H  Li YX  Yuan YH  Xiao YB  Weng JP
作者单位:1. 510080,广州,中山大学第一附属医院内分泌科
2. 佛山市第二人民医院体检中心
基金项目:广东省自然科学基金重点资助项目(5100981),广东省科技计划基金资助项目(2006A26001001)
摘    要:目的评价正常糖耐量(NGT)、糖调节受损(IGR)、新诊断2型糖尿病(T2DM)个体胰岛β细胞功能及其相关指标的适用性。方法178例入选者行口服和静脉葡萄糖耐量试验。检测胰岛素生成指数(ΔI30/ΔG30)、胰岛素急性分泌时相(AIR)、β细胞功能指数(HOMA β)、空腹胰岛素原(FPI)及胰岛素原/胰岛素(PI/I)比值反映胰岛素分泌功能。结果IGR组的ΔI30/ΔG30、AIR较NGT组分别下降了38%、39%,HOMA β轻度下降(19%);T2DM组的胰岛β细胞功能降低更明显,其中AIR下降84%,ΔI30/ΔG30下降70%、HOMA β下降62%。T2DM组FPI和PI/I比值也比NGT组明显升高(24.4pmol/L±18.0pmol/L or 10.9pmol/L±6.7pmol/L;14.7%±10.5%or10.0%±6.5%,P〈0.05)。ΔI30/ΔG30和AIR相关性好(r=0.75,P〈0.001)。结论IGR患者主要表现胰岛素分泌时相缺陷和HOMA β降低,至糖尿病阶段则伴有胰岛素分泌质量下降。ΔI30/ΔG30和AIR均可准确反映IGR患者胰岛β细胞功能,而在新诊断2型糖尿病患者中AIR更适用,若应用ΔI30/ΔG30须校正胰岛素抵抗。

关 键 词:糖尿病  非胰岛素依赖型 胰岛素分泌 糖调节受损
修稿时间:2006-08-28

Evaluation of islet beta cell function in subjects with normal glucose tolerance, impaired glucose regulation, and type 2 diabetes mellitus
Liu Juan,Li Yan-bing,Shao Hong,Li Yue-xia,Yuan Yong-hong,Xiao Yi-Bin,Weng Jian-ping. Evaluation of islet beta cell function in subjects with normal glucose tolerance, impaired glucose regulation, and type 2 diabetes mellitus[J]. Zhonghua yi xue za zhi, 2007, 87(18): 1252-1255
Authors:Liu Juan  Li Yan-bing  Shao Hong  Li Yue-xia  Yuan Yong-hong  Xiao Yi-Bin  Weng Jian-ping
Affiliation:1.Department of Endocrinology, First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China
Abstract:OBJECTIVE: To investigate the function of islet beta cells in subjects with normal glucose tolerance (NGT), impaired glucose regulation (IGR), and type 2 diabetes mellitus (T2DM). Different indexes of insulin secretion, including DeltaI30/DeltaG30, AIR or HOMAbeta, were compared. METHODS: 178 subjects without overt diabetes were classified into three groups according to the results of 75 g oral glucose tolerance test (OGTT): NGT group (n = 68), IGR group (n = 75), and T2DM group (n = 35). Intravenous glucose tolerance test (IVGTT) was carried out 1 approximately 3 days later in all participants, with measurement of plasma insulin. The ratio of insulin-to-glucose levels increment during the first 30 min of OGTT (DeltaI30/DeltaG30) and the acute insulin response (AIR) in IVGTT were used as indexes of early insulin secretion. Homeostasis model assessment of insulin secretion (HOMAbeta) was another indicator of insulin secretion. The fasting plasma proinsulin level (FPI) was measured and the ratio fasting proinsulin to fasting insulin (PI/I) was calculated. HOMA insulin resistance index (HOMA IR) was used to assess the insulin resistance. RESULTS: The DeltaI30/DeltaG30 and AIR of the IGR group, adjusted by age, sex, and BMI, were both significantly lower than those of the NGT group. But the HOMAbeta of the IGR group was only slightly lower than that of the NGT group. Compared with the NGT subjects, the T2DM patients had a very severe islet beta cell dysfunction (84% decrease in AIR, 70% decrease in DeltaI30/DeltaG30 and 62% decrease in HOMA beta). When the DeltaI30/DeltaG30 was adjusted by HOMR IR, the extent of impairment in early insulin response was similar to that of AIR (87% versus 84% lower than that of the NGT group). The FPI and ratio of proinsulin to insulin were higher in the T2DM subjects compared with the NGT subjects (24.4 pmol/L +/- 18.0 pmol/L vs 10.9 pmol/L +/- 6.7 pmol/L; and 14.7% +/- 10.5% vs. 10.0% +/- 6.5%, both P < 0.05). There was a significantly positive correlation between DeltaI30/DeltaG30 and AIR (r = 0.75, P < 0.001). CONCLUSION: In the stage of IGR, an evident deficit in phasic insulin secretion after glucose load and a decreasing HOMAbeta are exhibited. In addition to this, qualitative decrease of insulin secretion appears in the DM stage. AIR is a reliable index of isletbeta cell function. DeltaI30/DeltaG30 is an alternative one in the subjects with NGT and IGR. But it should be adjusted by IR in diabetic patients.
Keywords:Diabetes mellitus, non insulin dependent   Insulin secretion   Impaired glucose regulation
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