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Decrease in glucose-stimulated insulin secretion with aging is independent of insulin action.

Radhika Muzumdar1, Xiaohui Ma, Gil Atzmon

  • 1Division of Pediatric Endocrinology, Children's Hospital at Montefiore, Institute for Aging Research and Diabetes Research and Training Center, and the Department of Medicine, Albert Einstein College of Medicine, Bronx, New York, USA.

Diabetes
|January 30, 2004
PubMed
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Aging impairs beta-cell function, decreasing insulin secretion independent of insulin resistance. Prolonged glucose stimulation reveals this defect, suggesting a new diagnostic tool for diabetes risk in older adults.

Area of Science:

  • Endocrinology
  • Gerontology
  • Metabolic Research

Background:

  • Diabetes incidence rises with age.
  • Age-related decline in beta-cell function independent of insulin resistance is not fully understood.
  • Understanding age-related changes in insulin secretion is crucial for diabetes prevention.

Purpose of the Study:

  • To investigate age-related changes in insulin secretion.
  • To determine if impaired insulin secretion with aging is linked to insulin resistance.
  • To explore the effect of prolonged hyperglycemia on beta-cell function.

Main Methods:

  • Hyperglycemic clamp studies in young (3-month), middle-aged (9-month), and old (20-month) Sprague Dawley rats.
  • Modulation of insulin action via caloric restriction and visceral fat removal in old rats.

Related Experiment Videos

  • Assessment of insulin secretion and resistance under varying glucose and free fatty acid levels.

    • Main Results:

    • Aging rats showed decreased ability to maintain insulin secretion during prolonged hyperglycemia.
    • The age-related defect in insulin secretion was independent of insulin resistance.
    • Insulin secretion responded robustly to free fatty acid elevation in both young and old rats, but not to prolonged high glucose in aging rats.

    Conclusions:

    • Prolonged hyperglycemia reveals a functional defect in insulin secretion associated with aging.
    • This defect is specific to glucose stimulation and not related to insulin resistance.
    • Prolonged hyperglycemic stimulation may serve as a diagnostic tool for identifying impaired insulin secretion in at-risk individuals.