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From obesity to type 2 diabetes.
1Division of Diabetes, Nutrition and Metabolic Disorders, Department of Medicine, CHU Liège.
Acta Clinica Belgica. Supplementum
|January 1, 1992
Summary
Obesity worsens insulin resistance, a primary defect leading to impaired glucose tolerance. Beta-cell dysfunction is crucial for progressing from impaired glucose tolerance to non-insulin-dependent diabetes mellitus (NIDDM).
Area of Science:
- Endocrinology
- Metabolic Disorders
- Diabetes Research
Background:
- Obesity is a significant risk factor for non-insulin-dependent diabetes mellitus (NIDDM).
- Development of NIDDM requires both insulin resistance and beta-cell dysfunction.
- Insulin resistance, exacerbated by obesity, is the primary defect causing impaired glucose tolerance.
Purpose of the Study:
- To elucidate the roles of insulin resistance and beta-cell dysfunction in the pathogenesis of NIDDM.
- To understand the progression from impaired glucose tolerance to overt NIDDM.
Main Methods:
- This study is a review of existing literature on NIDDM pathogenesis.
- Analysis of genetic and environmental factors contributing to insulin resistance.
- Examination of beta-cell function in various stages of glucose intolerance.
Main Results:
- Insulin resistance, potentially genetically influenced and worsened by obesity, is identified as the initial defect.
- Beta-cell dysfunction is critical for the transition from impaired glucose tolerance to severe NIDDM.
- Obesity significantly exacerbates insulin resistance, accelerating disease development.
Conclusions:
- Both insulin resistance and beta-cell dysfunction are essential components in NIDDM development.
- Insulin resistance is the primary defect, while beta-cell dysfunction drives disease progression.
- Managing obesity is crucial for preventing or delaying NIDDM onset and progression.