The Sensory Mechanisms of Nutrient-Induced GLP-1 Secretion

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The enteroendocrine system of the gut regulates energy homeostasis through the release of hormones. Of the gut-derived hormones, GLP-1 is particularly interesting, as analogs of the hormone have proven to be highly effective for the treatment of type 2 diabetes mellitus and obesity. Observations on increased levels of GLP-1 following gastric bypass surgery have enhanced the interest in endogenous hormone secretion and highlighted the potential of endogenous secretion in therapy. The macronutrients and their digestive products stimulate the secretion of GLP-1 through various mechanisms that we have only begun to understand. From findings obtained from different experimental models, we now have strong indications for a role for both Sodium-Glucose Transporter 1 (SGLT1) and the K+ATP channel in carbohydrate-induced GLP-1 secretion. For fat, the free fatty acid receptor FFA1 and the G-protein-coupled receptor GPR119 have been linked to GLP-1 secretion. For proteins, Peptide Transporter 1 (Pept1) and the Calcium-Sensing Receptor (CaSR) are thought to mediate the secretion. However, attempts at clinical application of these mechanisms have been unsuccessful, and more work is needed before we fully understand the mechanisms of nutrient-induced GLP-1 secretion.

OriginalsprogEngelsk
Artikelnummer420
TidsskriftMetabolites
Vol/bind12
Udgave nummer5
Antal sider15
ISSN2218-1989
DOI
StatusUdgivet - 2022

Bibliografisk note

Funding Information:
Acknowledgments: We thank Novo Nordisk Denmark for financial support given to Anna Pii Hjørne through the Novo Nordisk Scholarship Programme for master students enrolled at Danish Universities. Graphical abstract and figures are created with Biorender.com.

Funding Information:
Funding: This research was funded by the European Research Council, grant number 695069 and an unrestricted grant to Jens Juul Holst from the Novo Nordisk Foundation Center for Basic Metabolic Research (Novo Nordisk Foundation, Denmark).

Publisher Copyright:
© 2022 by the authors. Licensee MDPI, Basel, Switzerland.

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