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Mol Cell Endocrinol. 2015 Dec 15;418 Pt 1:27-32. doi: 10.1016/j.mce.2015.02.017. Epub 2015 Feb 24.

Brain GLP-1 and insulin sensitivity.

Author information

1
Department of Surgery, University of Michigan, Ann Arbor, MI, United States.
2
Department of Pediatrics, Division of Nutrition, Baylor College of Medicine, Houston, TX, United States. Electronic address: sisley@bcm.edu.

Abstract

Type 2 diabetes is often treated with a class of drugs referred to as glucagon-like peptide-1 (GLP-1) analogs. GLP-1 is a peptide secreted by the gut that acts through only one known receptor, the GLP-1 receptor. The primary function of GLP-1 is thought to be lowering of postprandial glucose levels. Indeed, medications utilizing this system, including the long-acting GLP-1 analogs liraglutide and exenatide, are beneficial in reducing both blood sugars and body weight. GLP-1 analogs were long presumed to affect glucose control through their ability to increase insulin levels through peripheral action on beta cells. However, multiple lines of data point to the ability of GLP-1 to act within the brain to alter glucose regulation. In this review we will discuss the evidence for a central GLP-1 system and the effects of GLP-1 in the brain on regulating multiple facets of glucose homeostasis including glucose tolerance, insulin production, insulin sensitivity, hepatic glucose production, muscle glucose uptake, and connections of the central GLP-1 system to the gut. Although the evidence indicates that GLP-1 receptors in the brain are not necessary for physiologic control of glucose regulation, we discuss the research showing a strong effect of acute manipulation of the central GLP-1 system on glucose control and how it is relevant to type 2 diabetic patients.

KEYWORDS:

Brain; GLP-1; GLP-1R; Glucagon-like peptide-1; Glucose; Insulin sensitivity

PMID:
25724479
PMCID:
PMC4547906
DOI:
10.1016/j.mce.2015.02.017
[Indexed for MEDLINE]
Free PMC Article

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