Pancreas beta-Cell Function Impaired in Obese Normal Young Adults

Chon, Suk; Rhee, Sang Youl; Oh, Seungjoon; Kim, Sung Woon; Kim, Jin Woo; Kim, Young Seol; Woo, Jeong Taek

Abstract

BACKGROUND: The development of type 2 diabetes mellitus is characterized by both an impaired beta-cell function and increased insulin resistance. Obesity may cause insulin resistance, impaired glucose tolerance and T2DM. However, the precise mechanism of beta-cell dysfunction in obesity is unclear. The aim of this study is to evaluate the relationship between obesity and the pancreatic beta-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 < or = BMI < 25), Obese (BMI > or = 25). In the normal subjects, insulin sensitivity (WBISI) and HOMAIR, pancreatic beta-cell function (Acute Insulin Response: AIR, Acute C-Peptide Response: ACR, Disposition Index (DI): AIR x 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 beta-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 beta-cell functions were significantly lower in the obese group than in the overweight group.
CONCLUSION
Obesity is associated with a decrease in the compensatory beta-cell function to glucose stimulation in young adults with a NFG/NGT status.