Glucagon-Like Peptide 1 Secretion by the L-Cell

The View From Within

  1. Gareth E. Lim1 and
  2. Patricia L. Brubaker12
  1. 1Department of Physiology, University of Toronto, Toronto, Ontario, Canada
  2. 2Department of Medicine, University of Toronto, Toronto, Ontario, Canada
  1. Address correspondence and reprint requests to Dr. P.L. Brubaker, Room 3366, Medical Sciences Building, University of Toronto, 1 King’s College Circle, Toronto, ON M5S 1A8 Canada. E-mail: p.brubaker{at}


Glucagon-like peptide 1 (GLP-1) is a gut-derived peptide secreted from intestinal L-cells after a meal. GLP-1 has numerous physiological actions, including potentiation of glucose-stimulated insulin secretion, enhancement of β-cell growth and survival, and inhibition of glucagon release, gastric emptying, and food intake. These antidiabetic effects of GLP-1 have led to intense interest in the use of this peptide for the treatment of patients with type 2 diabetes. Oral nutrients such as glucose and fat are potent physiological regulators of GLP-1 secretion, but non-nutrient stimulators of GLP-1 release have also been identified, including the neuromodulators acetylcholine and gastrin-releasing peptide. Peripheral hormones that participate in energy homeostasis, such as leptin, have also been implicated in the regulation of GLP-1 release. Recent studies have begun to elucidate the intracellular signaling pathways that mediate the effects of GLP-1 secretagogues on the intestinal L-cell. The purpose of this review is to summarize the known signaling mechanisms of GLP-1 secretagogues based on the available literature. A better understanding of the pathways underlying GLP-1 secretion may lead to novel approaches by which the levels of this important insulinotropic hormone can be enhanced in patients with type 2 diabetes.


  • P.L.B. has received honoraria from and is a consultant for Amgen.

    This article is based on a presentation at a symposium. The symposium and the publication of this article were made possible by an unrestricted educational grant from Servier.

    The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

    • Accepted May 2, 2006.
    • Received March 23, 2006.
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