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Cited by 8Diabetes Treatment and ManagementRegulation of Appetite and ObesityPancreatic function and diabetes

Glucagon-like peptide 1: continued advances, new targets and expanding promise as a model therapeutic

Aulinger, Benedikt, D'Alessio, David·2007·Current Opinion in Endocrinology, Diabetes & Obesity
DOI 10.1097/med.0b013e328013e79e
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Abstract

PURPOSE OF REVIEW: This article discusses glucagon-like peptide 1 physiology and its various sites of action beyond the incretin effect and highlights recent findings (2005 and 2006). RECENT FINDINGS: Glucagon-like peptide 1 is a physiological incretin in humans and promotes insulin secretion after nutrient ingestion. It is secreted from intestinal L cells after meals and may be partially responsible for the improved glycemic control and weight loss after bariatric surgery. In vivo, glucagon-like peptide 1 is quickly degraded by dipetidyl peptidase IV to glucagon-like peptide 1(9-36), which has unclear physiologic activity. Glucagon-like peptide 1 and its specific receptor are also expressed in the brain, and central nervous system. Glucagon-like peptide 1 can reduce food intake, mediate toxic illness responses and control muscle and liver glucose disposal. In the heart, glucagon-like peptide 1 receptor activation improves cardiac hemodynamics in patients following angioplasty and has a beneficial effect on myocardial function in heart failure and postischemic animal models. Finally, glucagon-like peptide 1 augments islet mass and recent studies have identified cellular mechanisms by which glucagon-like peptide 1 receptor signaling affects this process. SUMMARY: Glucagon-like peptide 1 is emerging as a regulatory factor with a broad range of actions related to substrate and energy metabolism. With the recent development of medications based on glucagon-like peptide 1 receptor signaling for diabetes treatment, these new findings suggest the promise of further application of this system for the treatment of other conditions such as obesity and cardiovascular disease.

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Crossref · 10.1097/med.0b013e328013e79e

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51 of 51 references verified0 citation errors · 0 not checkable

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  • Increased GLP-1 and PYY levels together with an absence of a compensatory rise in ghrelin in most RYGB patients would be expected to favor improved insulin sensitivity.

    “Increased GLP-1 and PYY levels together with an absence of a compensatory rise in ghrelin in most RYGB patients would be expected to favor improved insulin sensitivity as these hormone affect glucose homeostasis in addition to appetitive behavior (8, 30–32).”

    From Prospective study of gut hormone and metabolic changes after adjustable gastric banding and Roux-en-Y gastric bypass (2009) · cites this paper as [32]

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Authors
Aulinger, B., & D'Alessio, D.
Affiliations
University of Cincinnati (US)
ORCID
Aulinger, Benedikt
Venue
Current Opinion in Endocrinology, Diabetes & Obesity
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2007-02
Volume
14
Issue
1
Pages
68-73
ISSN
1752-296X (ISSN-L)
DOI
10.1097/med.0b013e328013e79e
OpenAlex
W2321660256
Cited by
8
References
53
Citations by year
2013: 1
FWCI
0.29
Type
journal article
Language
en
Open access
closed
Locations
  • Current Opinion in Endocrinology Diabetes and Obesity (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
Keywords
glucagon-like peptide-1, incretin effect, GLP-1 receptor, GLP-1 receptor agonists, insulin secretion, intestinal L cells, bariatric surgery, food intake regulation, cardiac hemodynamics, heart failure, myocardial ischemia, islet mass, energy metabolism, obesity, diabetes treatment, cardiovascular disease
MeSH terms
Glucagon-Like Peptide-1 Receptor, Insulin Secretion, Animals, Central Nervous System, Diabetes Mellitus, Energy Metabolism, Humans, Insulin, Intestinal Mucosa, Nutritional Physiological Phenomena, Signal Transduction, Receptors, Glucagon, Glucagon-Like Peptide 1

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