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Fatty acids and insulin secretion.

V Grill1, E Qvigstad

  • 1Department of Internal Medicine, Norwegian University of Science and Technology, Trondheim, Norway. valdemar.grill@medisin.ntnu.no

The British Journal of Nutrition
|July 13, 2000
PubMed
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Longer exposure to elevated non-esterified fatty acids (NEFA) inhibits glucose-stimulated insulin secretion by affecting fatty acid oxidation in pancreatic beta cells. This effect was observed in rats, human islets, and db/db mice, suggesting a role in type 2 diabetes.

Area of Science:

  • Endocrinology
  • Metabolic Research
  • Cell Biology

Background:

  • Acute elevation of non-esterified fatty acids (NEFA) moderately stimulates insulin secretion.
  • The impact of chronic NEFA elevation on insulin secretion has been less understood.

Purpose of the Study:

  • To investigate the time-dependent effects of elevated NEFA on insulin secretion.
  • To explore the mechanisms underlying NEFA's impact on pancreatic beta cells.
  • To assess the role of NEFA in a mouse model of type 2 diabetes.

Main Methods:

  • In vivo and in vitro studies using rats and human pancreatic islets.
  • Exposure to Intralipid and specific fatty acids (palmitate, oleate, octanoate).
  • Assessment of glucose-induced insulin secretion, fatty acid oxidation, and pyruvate dehydrogenase activity.

Related Experiment Videos

  • Studies in db/db mice, a model for type 2 diabetes.

    • Main Results:

    • Longer-term NEFA exposure (6-24h) inhibited glucose-induced insulin secretion in rats and human islets.
    • Inhibitory effects were linked to fatty acid oxidation in beta cells, reducing glucose oxidation and pyruvate dehydrogenase activity.
    • Elevated NEFA contributed to decreased insulin secretion in db/db mice.
    • NEFA also inhibited insulin biosynthesis and altered the proinsulin:insulin secretion ratio.

    Conclusions:

    • Chronic elevation of NEFA impairs glucose-induced insulin secretion through mechanisms involving beta-cell fatty acid oxidation.
    • Elevated NEFA may play a significant role in the pathophysiology of type 2 diabetes.
    • Further clinical studies are required to confirm the impact of elevated NEFA in humans.