Cross-sectional and Longitudinal Analyses of Factors Contributing to the Progressive Loss of the β-cell Function in Type 2 Diabetes
Cross-sectional and Longitudinal Analyses of Factors Contributing to the Progressive Loss of the β-cell Function in Type 2 Diabetes
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DOI:
10.2169/internalmedicine.54.4351
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发表时间:
2015-01-01
影响因子:
1.2
通讯作者:
Yamada, Kentaro
中科院分区:
文献类型:
--
作者:
Nakayama, Hitomi;Kato, Tomoko;Yamada, Kentaro
Objective Type 2 diabetes is a progressive disease characterized by insulin resistance and insulin secretory dysfunction. In this study, we assessed the factors contributing to an insulin secretory defect in type 2 diabetes patients.Methods The subjects consisted of 382 patients with type 2 diabetes, aged 57+/-13 years. We estimated the beta-cell function using 6-min post-glucagon increments in C-peptide (Delta CPR).Results A significant inverse correlation was observed between the time since the diagnosis of diabetes and Delta CPR. A simple liner regression analysis showed that Delta CPR decreases at a rate of 0.056 ng/mL/year. According to a multiple regression model, body mass index (BMI) and log (triglyceride) were positively correlated with Delta CPR. Time since the diagnosis of diabetes, diabetes in 1st degree relatives, the presence of diabetic retinopathy, and HbA1c were inversely correlated with Delta CPR. In 50 patients who underwent the glucagon stimulation test twice, the Delta CPR decreased from 2.27+/-1.47 to 1.72+/-1.08 ng/mL over a period of 6.5+/-0.9 years. A multiple regression analysis revealed the BMI and fasting plasma glucose level to be significant contributing factors to the decline in Delta CPR.Conclusion The duration of diabetes, a low BMI, genetic factors, and the presence of microangiopathy may be associated with beta-cell dysfunction in diabetic patients. The observations in this study suggest that obese subjects showed a rapid decline in the beta-cell function despite an initial high CPR response. Environmental factors causing insulin resistance and glucotoxicity may therefore be involved in progressive beta-cell failure.