• Hitomi Nakayama, Tomoko Kato, Satoshi Nakayama, Hiroh Kaku, Kazuhisa Muraishi, Ichiro Tokubuchi, Kento Hara, Tamotsu Kato, Nobuhiko Wada, Munehisa Tsuruta, Tsuyoshi Ohki, Kayo Tanaka, Kenshi Mitsuzaki, Yuji Tajiri, and Kentaro Yamada.
• Division of Endocrinology and Metabolism, Department of Medicine, Kurume University School of Medicine, Japan.
• Intern. Med. 2015 Jan 1; 54 (16): 197119761971-6.

ObjectiveType 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.MethodsThe subjects consisted of 382 patients with type 2 diabetes, aged 57±13 years. We estimated the β-cell function using 6-min post-glucagon increments in C-peptide (ΔCPR).ResultsA significant inverse correlation was observed between the time since the diagnosis of diabetes and ΔCPR. A simple liner regression analysis showed that ΔCPR 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 ΔCPR. Time since the diagnosis of diabetes, diabetes in 1st degree relatives, the presence of diabetic retinopathy, and HbA1c were inversely correlated with ΔCPR. In 50 patients who underwent the glucagon stimulation test twice, the ΔCPR 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 ΔCPR.ConclusionThe duration of diabetes, a low BMI, genetic factors, and the presence of microangiopathy may be associated with β-cell dysfunction in diabetic patients. The observations in this study suggest that obese subjects showed a rapid decline in the β-cell function despite an initial high CPR response. Environmental factors causing insulin resistance and glucotoxicity may therefore be involved in progressive β-cell failure.

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