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From obesity to type 2 diabetes.

A J Scheen1

  • 1Division of Diabetes, Nutrition and Metabolic Disorders, Department of Medicine, CHU Liège.

Acta Clinica Belgica. Supplementum
|January 1, 1992
PubMed
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).

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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.

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