Does abnormal insulin action or insulin secretion explain the increase in prevalence of impaired glucose metabolism with age in populations of different ethnicities?
✍ Scribed by F. Ning; Q. Qiao; J. Tuomilehto; N. Hammar; S. Y. Ho; S. Söderberg; P. Z. Zimmet; J. E. Shaw; T. Nakagami; V. Mohan; A. Ramachandran; T. H. Lam; S. W. Andersson; E. D. Janus; E. J. Boyko; W. Y. Fujimoto; Z. C. Pang
- Publisher
- John Wiley and Sons
- Year
- 2010
- Tongue
- English
- Weight
- 212 KB
- Volume
- 26
- Category
- Article
- ISSN
- 1520-7552
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✦ Synopsis
Abstract
Background
Age is associated with both impaired glucose and insulin metabolism. To what extent the age‐related changes in insulin resistance (IR) and β‐cell function contribute to the increase in prevalence of impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) is less known, and this is investigated in this study.
Methods
This study included 6610 men and 7664 women of different ethnic groups aged 30‐69 years. IR and β‐cell function were examined by the homeostasis model assessment of insulin resistance (HOMA‐IR) and homeostasis model assessment of β‐cell function (HOMA‐B). Odds ratios (ORs) and 95% confidence intervals (95% CIs) were estimated using logistic regression analysis adjusting for body mass index and study.
Results
In Chinese men, the ORs (95% CIs) for IFG were 2.69 (1.70, 4.26), 2.51 (1.49, 4.21) and 2.89 (1.68, 4.97), respectively, in age groups of 40–49, 50–59 and 60–69 years compared with 30–39 years (p < 0.001 for trend); the corresponding figures for IGT were 1.73 (1.25, 2.38), 2.54 (1.78, 3.63) and 3.57 (2.46, 5.19) (p < 0.001 for trend). Similar trends for IGT were observed also in Chinese women and other ethnic groups, but not for IFG in Mauritius Indian and Creole men. Adjustment for HOMA‐IR and HOMA‐B reduced the ORs in all age groups of all ethnicities for both IFG and IGT, but the risk gradient between age groups remained particularly for the IGT.
Conclusions
The age‐related increase in glucose intolerance may not be fully explained by the defect in HOMA‐IR and HOMA‐B. As HOMA‐IR and HOMA‐B are only surrogate measures of insulin sensitivity and insulin secretion, the results need to be further investigated. Copyright © 2010 John Wiley & Sons, Ltd.