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Regulation of Energy Homeostasis by GPR41

Imbalances in energy regulation lead to metabolic disorders such as obesity and diabetes. Diet plays an essential role in the maintenance of body energy homeostasis by acting not only as energy source but also as a signaling modality. Excess energy increases energy expenditure, leading to a consumpt...

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Autores principales: Inoue, Daisuke, Tsujimoto, Gozoh, Kimura, Ikuo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4033597/
https://www.ncbi.nlm.nih.gov/pubmed/24904531
http://dx.doi.org/10.3389/fendo.2014.00081
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author Inoue, Daisuke
Tsujimoto, Gozoh
Kimura, Ikuo
author_facet Inoue, Daisuke
Tsujimoto, Gozoh
Kimura, Ikuo
author_sort Inoue, Daisuke
collection PubMed
description Imbalances in energy regulation lead to metabolic disorders such as obesity and diabetes. Diet plays an essential role in the maintenance of body energy homeostasis by acting not only as energy source but also as a signaling modality. Excess energy increases energy expenditure, leading to a consumption of it. In addition to glucose, mammals utilize short-chain fatty acids (SCFAs), which are produced by colonic bacterial fermentation of dietary fiber, as a metabolic fuel. The roles of SCFAs in energy regulation have remained unclear, although the roles of glucose are well-studied. Recently, a G-protein-coupled receptor deorphanizing strategy successfully identified GPR41 (also called free fatty acid receptor 3 or FFAR3) as a receptor for SCFAs. GPR41 is expressed in adipose tissue, gut, and the peripheral nervous system, and it is involved in SCFA-dependent energy regulation. In this mini-review, we focus on the role of GPR41 in host energy regulation.
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spelling pubmed-40335972014-06-05 Regulation of Energy Homeostasis by GPR41 Inoue, Daisuke Tsujimoto, Gozoh Kimura, Ikuo Front Endocrinol (Lausanne) Endocrinology Imbalances in energy regulation lead to metabolic disorders such as obesity and diabetes. Diet plays an essential role in the maintenance of body energy homeostasis by acting not only as energy source but also as a signaling modality. Excess energy increases energy expenditure, leading to a consumption of it. In addition to glucose, mammals utilize short-chain fatty acids (SCFAs), which are produced by colonic bacterial fermentation of dietary fiber, as a metabolic fuel. The roles of SCFAs in energy regulation have remained unclear, although the roles of glucose are well-studied. Recently, a G-protein-coupled receptor deorphanizing strategy successfully identified GPR41 (also called free fatty acid receptor 3 or FFAR3) as a receptor for SCFAs. GPR41 is expressed in adipose tissue, gut, and the peripheral nervous system, and it is involved in SCFA-dependent energy regulation. In this mini-review, we focus on the role of GPR41 in host energy regulation. Frontiers Media S.A. 2014-05-26 /pmc/articles/PMC4033597/ /pubmed/24904531 http://dx.doi.org/10.3389/fendo.2014.00081 Text en Copyright © 2014 Inoue, Tsujimoto and Kimura. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Endocrinology
Inoue, Daisuke
Tsujimoto, Gozoh
Kimura, Ikuo
Regulation of Energy Homeostasis by GPR41
title Regulation of Energy Homeostasis by GPR41
title_full Regulation of Energy Homeostasis by GPR41
title_fullStr Regulation of Energy Homeostasis by GPR41
title_full_unstemmed Regulation of Energy Homeostasis by GPR41
title_short Regulation of Energy Homeostasis by GPR41
title_sort regulation of energy homeostasis by gpr41
topic Endocrinology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4033597/
https://www.ncbi.nlm.nih.gov/pubmed/24904531
http://dx.doi.org/10.3389/fendo.2014.00081
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