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Gut and Adipocyte Peptides

Zachary T. Bloomgarden, MD, is a practicing endocrinologist in New York, New York, and is affiliated with the Division of Endocrinology, Mount Sinai School of Medicine, New York, New York

Abbreviations: AGRP, agouti-related peptide • ARIC, Atherosclerosis Risk in Communities • BBB, blood-brain barrier • CART, cocaine-amphetamine–regulated transcript • CNTF, ciliary neurotrophic factor • DPP, dipeptidyl peptidase • FFA, free fatty acid • GIP, glucose-dependent insulinotropic polypeptide • GLP, glucagon-like peptide • GLP-1R, GLP-1 receptor • MCH, melanin-concentrating hormone • NPY, neuropeptide Y • NTS, nucleus of the solitary tract • POMC, proopiomelanocortin • PPAR, peroxisome proliferator–activated receptor • REE, resting energy expenditure • SOCS, suppressor of cytokine signaling • STAT, signal transducers and activators of transcription • TLR, toll-like receptor • TNF, tumor necrosis factor

The first 300 words of the full text of this article appear below.

This is the third in a series of articles on presentations at the American Diabetes Association Annual Meeting, San Diego, California, 10–14 June 2005.

Glucagon-like peptide-1 (and related hormones)

Daniel Drucker (Toronto, Canada) reviewed evidence that the incretin effect, the phenomenon of enteral glucose loading increasing the insulin secretory response to an increase in blood glucose, is reduced in type 2 diabetes, and that the incretin glucagon-like peptide (GLP)-1 may ameliorate this defect. The major limitation to use of GLP-1 in clinical treatment is its rapid clearance by the enzyme dipeptidyl peptidase (DPP)-IV. GLP-1 stimulates insulin secretion, inhibits glucagon secretion, and delays gastric emptying. Loss-of-function studies with a mouse model not expressing the GLP-1 receptor (GLP-1R^–/–), and with the GLP-1R antagonist exendin-(9-39), show effects of GLP-1 on the hypothalamic-pituitary-adrenal (HPA) axis, the reproductive system, the portal glucose receptor, gastric motility, and a number of other potential targets. GLP-1R^–/– mice have normal insulin sensitivity, arguing against an effect of the system on insulin action, but have glucose intolerance, and administration of exendin-(9-39) similarly is associated with glucose intolerance in mice, in primates, and in humans. Drucker noted that there is controversy as to whether the product of DPP-IV degradation may act at a second GLP-1R, perhaps having additional effects on metabolism, but that GLP-1 does not lower glucose levels in GLP-1R^–/– mice, arguing against such a receptor. In the model, pancreatic insulin mRNA levels are reduced and somatostatin mRNA levels are increased. The perfused pancreas isolated from GLP-1R^–/– animals shows normal insulin response to glucose, although without response to GLP-1. GLP-1R^–/– ß-cells appear to have increased sensitivity to the incretin glucose-dependent insulinotropic polypeptide (GIP), perhaps representing an adaptive upregulation of GIP and/or of GIP response, and mice neither expressing the GLP-1 nor the GIP receptor show glucose intolerance with decreased insulin response to glucose, and . . . [Full Text of this Article]

Leptin and adiponectin

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This article has been cited by other articles:

				Z. T. Bloomgarden, R. Dodis, C. M. Viscoli, E. S. Holmboe, and S. E. Inzucchi Lower Baseline Glycemia Reduces Apparent Oral Agent Glucose-Lowering Efficacy: A meta-regression analysis. Diabetes Care, September 1, 2006; 29(9): 2137 - 2139. [Full Text] [PDF]