Korean J Obes 2006; 15(3): 146-158
Published online July 1, 2006
Copyright © Korean Society for the Study of Obesity.
Suk Chon*.**, Sang Youl Rhee*, Seungjoon Oh*.**, Sung-Woon Kim*.**, Jin-Woo Kim*.**, Young Seol Kim*.**, Jeong-taek Woo*.**
Department of Endocrinology and Metabolism*, Research Institute of Endocrinology**;
School of Medicine, Kyung Hee University
Background: The development of type 2 diabetes mellitus is characterized by both an impaired β-cell function and increased insulin resistance. Obesity may cause insulin resistance, impaired glucose tolerance and T2DM. However, the precise mechanism of β-cell dysfunction in obesity is unclear.
The aim of this study is to evaluate the relationship between obesity and the pancreatic β-cell function in Korean young adults with normal glucose tolerance.
Subject and Methods: 75 g OGTT was performed in 152 young adults. The subjects were grouped as follows: Normal (BMI < 23 kg/m2), Overweight (23 ≤ BMI < 25), Obese (BMI ≥ 25). In the normal subjects, insulin sensitivity (WBISI) and HOMAIR, pancreatic β-cell function (Acute Insulin Response: AIR, Acute C-Peptide Response: ACR, Disposition Index (DI): AIR × WBISI, AIR/HOMAIR) were measured.
Results: The HOMAIR was similar in the three groups. The WBISI decreased in the obese group compared with the normal BMI group at the NFG/NGT status. Compensatory β-cell functions (DI, AIR/HOMAIR) were significantly higher in the overweight group than in the normal BMI group. Despite the NFG/NGT status, the compensatory pancreatic β-cell functions were significantly lower in the obese group than in the overweight group.
Conclusion: Obesity is associated with a decrease in the compensatory β-cell function to glucose stimulation in young adults with a NFG/NGT status.
Keywords: Obesity, β-cell function, Type 2 Diabetes Mellitus