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Toward an integrated phenotype in pre-NIDDM

R N Bergman1, R Watanabe, K Rebrin

  • 1Department of Physiology and Biophysics, University of Southern California School of Medicine, Los Angeles 90033, USA.

Diabetic Medicine : a Journal of the British Diabetic Association
|September 1, 1996
PubMed
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Understanding pre-diabetes requires quantifying glucose regulation processes. This research quantifies insulin sensitivity, secretion, and glucose effectiveness to better represent the pre-NIDDM phenotype for genetic studies.

Area of Science:

  • Endocrinology and Metabolism
  • Genetics and Genomics
  • Physiology

Background:

  • The genetic basis of Non-Insulin-Dependent Diabetes Mellitus (NIDDM) necessitates a precise phenotype representation.
  • Current understanding of NIDDM molecular causes is limited, requiring alternative approaches to identify contributing factors.

Purpose of the Study:

  • To quantitatively assess key physiological processes determining blood glucose regulation.
  • To establish a framework for relating genomic mutations to NIDDM development through quantitative phenotypes.

Main Methods:

  • Review of methods for measuring glucose tolerance determinants: minimal model analysis (quantifying insulin sensitivity [S_I] and glucose effectiveness [S_G]) and combined modeling (measuring insulin secretion).
  • Development of population-based methods for large-scale studies.

Related Experiment Videos

  • Exploration of the hyperbolic relationship between insulin secretion and insulin action.

    • Main Results:

    • The hyperbolic law of glucose tolerance highlights that insulin secretion assessment is dependent on insulin sensitivity.
    • Latent pancreatic islet-cell dysfunction may be significantly underestimated, even in individuals with impaired glucose tolerance.
    • Free fatty acids may control hepatic glucose output, with insulin's lipolysis effect being critical for fasting glucose levels.

    Conclusions:

    • Quantitative assessment of glucose regulation is crucial for understanding pre-NIDDM phenotypes and NIDDM etiology.
    • Insulin resistance in adipocytes may significantly influence fasting hyperglycemia and the overall phenotype in prediabetic and NIDDM individuals.
    • The hyperbolic relationship between insulin secretion and action provides critical insights into glucose intolerance and diabetes development.