Early insulin secretion failure leads to diabetes in Chinese subjects with impaired glucose regulation
- 30 December 2008
- journal article
- research article
- Published by Wiley in Diabetes/Metabolism Research and Reviews
- Vol. 25 (2), 144-149
- https://doi.org/10.1002/dmrr.922
Abstract
Background Both beta-cell dysfunction and decreased insulin sensitivity are involved in the pathogenesis of impaired glucose tolerance (IGT) and impaired fasting glucose (IFG), while their relative contribution in the progression to type 2 diabetes still remains controversial. The aim of the present study is to clarify this process in Chinese subjects by using cross-sectional method. Methods 2975 Chinese subjects were classified into: normal glucose tolerance (NGT), impaired glucose regulations (IGR), and diabetes mellitus (DM) based on oral glucose tolerance test (OGTT). The IGR group was sub-classified as isolated IFG, isolated IGT and combined glucose intolerance (CGI). The DM group was sub-classified as normal fasting plasma glucose and 2-hour hyperglycemia (N0D2), fasting hyperglycemia and normal 2-hour plasma glucose (D0N2), and both fasting and 2-hour hyperglycemia (D0D2). Results As far as insulinogenic index (IGI) was concerned, there was no difference between IFG and IGT in either gender, however, HOMA2-B% (homeostasis model assessment for beta-cell function) of IGT was higher than that of IFG and CGI in both male and female (P < 0.05). In the diabetic sub-groups, IGI of N0D2 was higher than that of D0N2, and both deteriorated compared with those of IGT and IFG, respectively. HOMA2-B% of N0D2 was still higher than that of D0N2 and D0D2. No significant difference was detected in OGIS and HOMA2-S% (homeostasis model assessment for insulin sensitivity) between IFG and IGT, and this was the case between N0D2 and D0N2. OGIS and HOMA-IR of IGR sub-groups were not different from those of their diabetic counterparts. Conclusion Failure of beta-cell function might be the main reason for both IGT and IFG developing into diabetes instead of aggravated insulin resistance. Copyright © 2008 John Wiley & Sons, Ltd.Keywords
This publication has 23 references indexed in Scilit:
- Metabolic characteristics of subjects with normal glucose tolerance and 1‐h hyperglycaemiaClinical Endocrinology, 2008
- Different Mechanisms for Impaired Fasting Glucose and Impaired Postprandial Glucose Tolerance in HumansDiabetes Care, 2006
- Assessing 1-h plasma glucose and shape of the glucose curve during oral glucose tolerance testActa Endocrinologica, 2006
- Contributions of β-Cell Dysfunction and Insulin Resistance to the Pathogenesis of Impaired Glucose Tolerance and Impaired Fasting GlucoseDiabetes Care, 2006
- Use and Abuse of HOMA ModelingDiabetes Care, 2004
- Follow-up Report on the Diagnosis of Diabetes MellitusDiabetes Care, 2003
- Methods for clinical assessment of insulin sensitivity and β-cell functionBest Practice & Research Clinical Endocrinology & Metabolism, 2003
- The Significance of Impaired Fasting Glucose Versus Impaired Glucose ToleranceDiabetes Care, 2003
- Post‐challenge hyperglycaemia relates more strongly than fasting hyperglycaemia with carotid intima‐media thickness: the RIAD StudyDiabetic Medicine, 2000
- Increased Insulin Concentrations in Nondiabetic Offspring of Diabetic ParentsNew England Journal of Medicine, 1988