Enteroendocrine secretion of gut hormones in diabetes, obesity and after bariatric surgery

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Enteroendocrine secretion of gut hormones in diabetes, obesity and after bariatric surgery. / Holst, Jens Juul.

In: Current Opinion in Pharmacology, Vol. 13, No. 6, 12.2013, p. 983-8.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Holst, JJ 2013, 'Enteroendocrine secretion of gut hormones in diabetes, obesity and after bariatric surgery', Current Opinion in Pharmacology, vol. 13, no. 6, pp. 983-8. https://doi.org/10.1016/j.coph.2013.09.014

APA

Holst, J. J. (2013). Enteroendocrine secretion of gut hormones in diabetes, obesity and after bariatric surgery. Current Opinion in Pharmacology, 13(6), 983-8. https://doi.org/10.1016/j.coph.2013.09.014

Vancouver

Holst JJ. Enteroendocrine secretion of gut hormones in diabetes, obesity and after bariatric surgery. Current Opinion in Pharmacology. 2013 Dec;13(6):983-8. https://doi.org/10.1016/j.coph.2013.09.014

Author

Holst, Jens Juul. / Enteroendocrine secretion of gut hormones in diabetes, obesity and after bariatric surgery. In: Current Opinion in Pharmacology. 2013 ; Vol. 13, No. 6. pp. 983-8.

Bibtex

@article{7be13276988c48ebb7f98a271de86729,
title = "Enteroendocrine secretion of gut hormones in diabetes, obesity and after bariatric surgery",
abstract = "Gastric bypass surgery is associated with a major weight loss and often causes remission in patients with type 2 diabetes. Surgery is also associated with dramatic increases in the secretion of the gut hormones, glucagon-like peptide-1 (GLP-1) and peptide YY (PYY), both of which regulate appetite and food intake, while GLP-1 in addition functions as an incretin hormone, stimulating insulin secretion. It has been possible to probe the role of GLP-1 for the diabetes resolution after gastric bypass using a GLP-1 receptor antagonist, and it is clear that the enhanced beta cell sensitivity to glucose which underlies the enhanced insulin secretion in the patients after the operation depends critically on the increased GLP-1 secretion. Both hormones seem to contribute importantly to the reduction in food intake after bypass and, therefore, to the weight loss. Currently, there are no data to indicate that decreased secretion of the hormones is involved in the pathogenesis of obesity and/or diabetes, but impaired secretion generally observed in obesity (and hence also in diabetes) may contribute to the development. Because of these effects receptor agonists for both hormones are currently being developed for the treatment of obesity and diabetes.",
keywords = "Bariatric Surgery, Diabetes Mellitus, Type 2, Eating, Enteroendocrine Cells, Gastrointestinal Hormones, Gastrointestinal Tract, Humans, Obesity",
author = "Holst, {Jens Juul}",
note = "Copyright {\textcopyright} 2013 Elsevier Ltd. All rights reserved.",
year = "2013",
month = dec,
doi = "10.1016/j.coph.2013.09.014",
language = "English",
volume = "13",
pages = "983--8",
journal = "Current Opinion in Pharmacology",
issn = "1471-4892",
publisher = "Elsevier Ltd. * Current Opinion Journals",
number = "6",

}

RIS

TY - JOUR

T1 - Enteroendocrine secretion of gut hormones in diabetes, obesity and after bariatric surgery

AU - Holst, Jens Juul

N1 - Copyright © 2013 Elsevier Ltd. All rights reserved.

PY - 2013/12

Y1 - 2013/12

N2 - Gastric bypass surgery is associated with a major weight loss and often causes remission in patients with type 2 diabetes. Surgery is also associated with dramatic increases in the secretion of the gut hormones, glucagon-like peptide-1 (GLP-1) and peptide YY (PYY), both of which regulate appetite and food intake, while GLP-1 in addition functions as an incretin hormone, stimulating insulin secretion. It has been possible to probe the role of GLP-1 for the diabetes resolution after gastric bypass using a GLP-1 receptor antagonist, and it is clear that the enhanced beta cell sensitivity to glucose which underlies the enhanced insulin secretion in the patients after the operation depends critically on the increased GLP-1 secretion. Both hormones seem to contribute importantly to the reduction in food intake after bypass and, therefore, to the weight loss. Currently, there are no data to indicate that decreased secretion of the hormones is involved in the pathogenesis of obesity and/or diabetes, but impaired secretion generally observed in obesity (and hence also in diabetes) may contribute to the development. Because of these effects receptor agonists for both hormones are currently being developed for the treatment of obesity and diabetes.

AB - Gastric bypass surgery is associated with a major weight loss and often causes remission in patients with type 2 diabetes. Surgery is also associated with dramatic increases in the secretion of the gut hormones, glucagon-like peptide-1 (GLP-1) and peptide YY (PYY), both of which regulate appetite and food intake, while GLP-1 in addition functions as an incretin hormone, stimulating insulin secretion. It has been possible to probe the role of GLP-1 for the diabetes resolution after gastric bypass using a GLP-1 receptor antagonist, and it is clear that the enhanced beta cell sensitivity to glucose which underlies the enhanced insulin secretion in the patients after the operation depends critically on the increased GLP-1 secretion. Both hormones seem to contribute importantly to the reduction in food intake after bypass and, therefore, to the weight loss. Currently, there are no data to indicate that decreased secretion of the hormones is involved in the pathogenesis of obesity and/or diabetes, but impaired secretion generally observed in obesity (and hence also in diabetes) may contribute to the development. Because of these effects receptor agonists for both hormones are currently being developed for the treatment of obesity and diabetes.

KW - Bariatric Surgery

KW - Diabetes Mellitus, Type 2

KW - Eating

KW - Enteroendocrine Cells

KW - Gastrointestinal Hormones

KW - Gastrointestinal Tract

KW - Humans

KW - Obesity

U2 - 10.1016/j.coph.2013.09.014

DO - 10.1016/j.coph.2013.09.014

M3 - Journal article

C2 - 24161809

VL - 13

SP - 983

EP - 988

JO - Current Opinion in Pharmacology

JF - Current Opinion in Pharmacology

SN - 1471-4892

IS - 6

ER -

ID: 117853223