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Ann. N.Y. Acad. Sci. ISSN 0077-8923 ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
 

Summary: Ann. N.Y. Acad. Sci. ISSN 0077-8923
ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
Issue: The Year in Diabetes and Obesity
Gastrointestinal hormones and the regulation
of -cell mass
Jeremy A. Lavine and Alan D. Attie
Department of Biochemistry, University of Wisconsin-Madison, Madison, Wisconsin
Address for correspondence: Alan Attie, 433 Babcock Drive, Madison, WI 53706. adattie@wisc.edu
Type 2 diabetes occurs due to a relative deficit in -cell mass or function. Glucagon-like peptide 1 (GLP-1), glucose-
dependent insulinotropic polypeptide (GIP), cholecystokinin (CCK), and gastrin are gastrointestinal hormones that
are secreted in response to nutrient intake, regulating digestion, insulin secretion, satiety, and -cell mass. In this
review, we focus upon -cell mass regulation. -cell mass expands through -cell proliferation and islet neogenesis;
-cell mass is lost via apoptosis. GLP-1 and GIP are well-studied gastrointestinal hormones and influence -cell
proliferation, apoptosis, and islet neogenesis. CCK regulates -cell apoptosis and mitogenesis, and gastrin stimulates
islet neogenesis. GLP-1 and GIP bind to G protein-coupled receptors and regulate -cell mass via multiple signaling
pathways. The protein kinase A pathway is central to this process because it directly regulates proliferative and anti-
apoptotic genes and transactivates several signaling cascades, including Akt and mitogen-activated protein kinases.
However, the signaling pathways downstream of G protein-coupled CCK receptors that influence -cell mass remain
unidentified. Gastrointestinal hormones integrate nutrient signals from the gut to the -cell, regulating insulin
secretion and -cell mass adaptation.

  

Source: Attie, Alan D. - Department of Biochemistry, University of Wisconsin at Madison

 

Collections: Biology and Medicine