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Related Experiment Videos

Effects in liver.

Andrew Young1

  • 1Amylin Pharmaceuticals, Inc., San Diego, California, USA.

Advances in Pharmacology (San Diego, Calif.)
|February 24, 2006
PubMed
Summary
This summary is machine-generated.

Amylin and calcitonin gene-related peptide (CGRP) stimulate glucose production in rats, but not in isolated liver cells. Further studies suggest additional mechanisms beyond lactate release are involved in amylin

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Area of Science:

  • Endocrinology
  • Metabolism
  • Physiology

Background:

  • Amylin and calcitonin gene-related peptide (CGRP) are known to influence glucose metabolism.
  • Previous studies suggested these peptides might stimulate endogenous glucose production (EGP).

Purpose of the Study:

  • To investigate the mechanisms by which amylin and CGRP affect glucose production.
  • To determine if the effects observed in vivo are mediated by changes in intermediary carbohydrate metabolism.
  • To explore the role of lactate release from muscle in mediating amylin's effect on EGP.

Main Methods:

  • In vivo studies in rats to measure EGP.
  • In vitro studies using isolated rat hepatocytes and perfused liver to assess intermediary carbohydrate metabolism.
  • Hyperlactemic clamp preparations in rats to directly measure lactate release and its impact on gluconeogenesis.

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Main Results:

  • Both amylin and CGRP stimulated EGP in vivo in rats.
  • Neither peptide affected intermediary carbohydrate metabolism in isolated hepatocytes or perfused liver.
  • Hyperlactemic clamp studies indicated that lactate release alone did not fully explain amylin's stimulation of EGP, suggesting additional mechanisms.
  • No evidence suggests amylin increases EGP in humans.

Conclusions:

  • Amylin and CGRP stimulate EGP in rats through mechanisms not solely dependent on direct hepatic effects or lactate-induced gluconeogenesis.
  • The augmentation of EGP by amylin in rats involves complex pathways.
  • Current findings do not support a similar role for amylin in human EGP.