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Potential incretins.

L T Shuster1, V L Go, R A Rizza

  • 1Department of Internal Medicine, Mayo Clinic, Rochester, MN 55905.

Mayo Clinic Proceedings
|August 1, 1988
PubMed
Summary
This summary is machine-generated.

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The incretin effect, a rise in insulin after oral glucose, may involve more than just gastric inhibitory polypeptide. Other gastrointestinal hormones like gastrin and peptide YY also show differential responses, suggesting they contribute to this glucose regulation phenomenon.

Area of Science:

  • Gastroenterology
  • Endocrinology
  • Metabolic Research

Background:

  • The incretin effect describes a higher insulin response to oral glucose compared to intravenous glucose.
  • Gastric inhibitory polypeptide (GIP) is the primary known mediator, but may not fully explain the effect.

Purpose of the Study:

  • To investigate other gastrointestinal polypeptides as potential mediators of the incretin effect.
  • To compare the plasma responses of various gastrointestinal hormones to oral versus intravenous glucose administration.

Main Methods:

  • Participants received either oral or intravenous glucose infusions, matched for arterial plasma glucose levels.
  • Plasma concentrations of several gastrointestinal hormones (gastrin, GIP, peptide histidine methionine, peptide YY, neurotensin, vasoactive intestinal polypeptide) were measured.

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Main Results:

  • Gastrin, peptide histidine methionine, peptide YY, and neurotensin showed increased plasma levels after oral glucose but not intravenous glucose.
  • Vasoactive intestinal polypeptide did not show increased concentrations with either administration route.
  • These differential responses suggest a broader role for gastrointestinal hormones in the incretin effect.

Conclusions:

  • Several gastrointestinal polypeptides, beyond GIP, exhibit differential responses to oral glucose, supporting their role as incretin effect mediators.
  • Further research is warranted to elucidate the specific contributions of these hormones to glucose homeostasis.