Earlier Appearance of Impaired Insulin Secretion Than of Visceral Adiposity in the Pathogenesis of NIDDM: 5-Year Follow-up of Initially Nondiabetic Japanese-American Men
- Kwang-Wen Chen, MD,
- Edward J Boyko, MD,
- Richard W Bergstrom, MD,
- Donna L Leonetti, PHD,
- Laura Newell-Morris, PHD,
- Patricia W Wahl, PHD and
- Wilfred Y Fujimoto, MD
- Departments of Medicine, University of Washington Seattle, Washington
- Departments of Anthropology, and Biostatistics University of Washington Seattle, Washington
- Address correspondence and reprint requests to Wilfred Y. Fujimoto, MD, Department of Medicine RG-26, University of Washington School of Medicine, Seattle, WA 98195.
Abstract
OBJECTIVE To identify risk factors for development of non-insulin-dependent diabetes mellitus (NIDDM) during a 5-year longitudinal follow-up of second-generation Japanese-American (Nisei) men.
RESEARCH DESIGN AND METHODS For 5 years, 137 initially nondiabetic Nisei men were followed with 75-g oral glucose tolerance tests at the initial visit and at 2.5- and 5-year follow-up visits. Body fat distribution was assessed by computed tomography (CT) and body mass index (BMI) calculated at each visit. Fasting insulin and C-peptide, the increment of insulin and C-peptide at 30 min after the oral glucose load, intra-abdominal and total subcutaneous fat by CT, and BMI were compared between those who remained nondiabetic (non-DM) and those who had developed NIDDM at 2.5 years (DM-A) and 5 years (DM-B).
RESULTS At baseline, the DM-A group had significantly increased intra-abdominal fat, elevated fasting plasma C-peptide, and lower C-peptide response at 30 min after oral glucose. At the 2.5-year follow-up, this group had markedly increased fasting plasma insulin and decreased 30-min insulin and C-peptide response to oral glucose. The DM-B group also had significantly lower insulin response at 30 min after oral glucose at baseline but no significant difference in intra-abdominal fat or fasting plasma insulin and C-peptide levels. When this group developed NIDDM by 5-year follow-up, however, an increase of intra-abdominal fat was found superimposed on the pre-existing lower insulin response. Fasting plasma insulin and C-peptide remained low.
CONCLUSION In DM-A, lower 30-min insulin response to oral glucose (an indicator of β-cell lesion) and increased intra-abdominal fat and fasting C-peptide (indicators of insulin resistance) were the risk factors related to the development of NIDDM. DM-B subjects had a lower 30-min insulin response to oral glucose at baseline and increased intra-abdominal fat at 5-years, when they were found to have NIDDM. Thus, both insulin resistance and impaired β-cell function contribute to the development of NIDDM in Japanese-Americans, and impaired β-cell function may be present earlier than visceral adiposity in some who subsequently develop NIDDM.
- Received October 20, 1994.
- Revision received February 2, 1995.
- Accepted February 2, 1995.
- Copyright © 1995 by the American Diabetes Association
