| Objective Previous studies showed insulin resistance and insulin secretion deficiency is getting worse from normal glucose tolerance status to diabetes. However, whether the course of diseases affects insulin resistance and insulin secretion index in diabetes patients still remains unknown. The aim of this study was to evaluate the effect of diseases courses, BMI and age on insulin sensitivity and insulin secretion index in type2diabetes mellitus.Materials and Methods1. Subjects:147patients of type2diabetes from January to October2011were enrolled in department of endocrinology in Jinan central hospital.2. The clinical general conditions, laboratory examination, and oral glucose tolerance test results were recorded.3. Grouping of subjects (1) According to diabetes disease course, patients were divided into4groups:newly diagnosed, less than5years, between5and10years and longer than10years, their insulin resistance and insulin release index were assessed.(2)①According to BMI, patients were divided into3groups:normal weight group (18.5≤BMI<24), overweight group (24<BMI<28) and obese group (BMI>28).②Patients were divided into4groups according to age:younger than40years old, between40and50years old, between50and60years old and older than60years old.(3) Further studies would be done to analyze the effect of different diabetes disease courses on insulin sensitivity and insulin secretion in different BMI groups.4. Insulin sensitivity was evaluated by homeostasis model insulin resistance index (HOMA-IR) and Matsuda insulin sensitivity index (ISI), while pancreatic β cell function was evaluated by insulinogenic index (IGI) and disposition index (DI). Results1. The changes of indexes in process of the disease (1) With age, sex, BMI, blood pressure and lipids adjusting, HOMA-IR increased in longer than10years group compared with newly diagnosed or less than5years groups (36%, P<0.01), its ISI decreased only slightly(8%and7%, P<0.05).(2) With age, sex, BMI, blood pressure and lipids adjusting, a significant decreased in function of insulin secretion and compensatory secretion was observed in between5and10years group(IGI30-31%, DI30-24%, P<0.05, IGI120-66%, DI120-29%, P<0.01), compared with newly diagnosed, and further decreased in longer than10years group (IGI30-36%, DI30-30%, P<0.05, IGI120-88%, DI120-39%, P<0.001).2.(1) The changes of indexes in different BMI groups①Compared with normal weight group, HOMA-IR increased36%in obese group (P<0.05), while ISI decreased by-10%and-7%in overweight or obese group respectively (P<0.01, P<0.05) after age, sex, diabetes disease course, blood pressure and lipids were adjusted.②With age, sex, course of disease, blood pressure and lipids adjusting, insulin basal release increased in overweight group or obese group(P<0.05), and early-phase and total insulin secretion increased either in obese group (IGI3027%, P<0.01, IGI12028%, P<0.05), compared with normal weight group. Whereas no significant changes were observed in the function of insulin compensatory secretion.(2) With sex, BMI, diabetes disease course, blood pressure and lipids adjusting, there were no significant differences in different age groups.3. With age, sex, blood pressure and lipids adjusting, both insulin resistance and insulin secretion deficiency may play important roles in group of BMI>24, and only insulin secretion impaired in group of BMI<24.Conclusion1. Impairment in function of pancreatic β-cell secretion and compensatory secretion were observed in type2diabetes, especially in patients with diabetes disease course longer than5years, which earlier and more significant than the decrease of insulin sensitivity.2. The decrease of insulin sensitivity and slightly increased of insulin secretion were associated with weight increasing, whereas age did not seem to have a major effect on insulin sensitivity and insulin secretion.3. Both insulin resistance and insulin secretion deficiency may play important roles in overweight or obese patients with type2diabetes. However, only insulin secretion was impaired in normal weight patients with type2diabetes. |
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