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Acute Homeostatic Responses to Increased Fat Consumption in MCH1R Knockout Mice
Melanin-concentrating hormone (MCH) is a hypothalamic neuropeptide which has been shown to regulate energy homeostasis. Using genetic knockout mice lacking the MCH1 receptor (MCH1R), we investigated how these mice adapt to metabolic changes caused by excessive caloric consumption. We show that the M...
Autores principales: | , , , |
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Formato: | Texto |
Lenguaje: | English |
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Humana Press Inc
2010
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2955453/ https://www.ncbi.nlm.nih.gov/pubmed/20411353 http://dx.doi.org/10.1007/s12031-010-9358-5 |
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author | Chung, Shinjae Wong, Timothy Nagasaki, Hiroshi Civelli, Olivier |
author_facet | Chung, Shinjae Wong, Timothy Nagasaki, Hiroshi Civelli, Olivier |
author_sort | Chung, Shinjae |
collection | PubMed |
description | Melanin-concentrating hormone (MCH) is a hypothalamic neuropeptide which has been shown to regulate energy homeostasis. Using genetic knockout mice lacking the MCH1 receptor (MCH1R), we investigated how these mice adapt to metabolic changes caused by excessive caloric consumption. We show that the MCH system is one of the players mediating behavioral and metabolic responses upon increased caloric consumption. MCH1R knockout mice showed decreased tendency of food intake upon exposure to a high-fat diet. They also are resistant to gain weight upon high-fat diet by increasing fat metabolism. Therefore, the MCH system is important in regulating metabolic responses upon various environmental stimuli such as high-fat diet. |
format | Text |
id | pubmed-2955453 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2010 |
publisher | Humana Press Inc |
record_format | MEDLINE/PubMed |
spelling | pubmed-29554532010-10-29 Acute Homeostatic Responses to Increased Fat Consumption in MCH1R Knockout Mice Chung, Shinjae Wong, Timothy Nagasaki, Hiroshi Civelli, Olivier J Mol Neurosci Article Melanin-concentrating hormone (MCH) is a hypothalamic neuropeptide which has been shown to regulate energy homeostasis. Using genetic knockout mice lacking the MCH1 receptor (MCH1R), we investigated how these mice adapt to metabolic changes caused by excessive caloric consumption. We show that the MCH system is one of the players mediating behavioral and metabolic responses upon increased caloric consumption. MCH1R knockout mice showed decreased tendency of food intake upon exposure to a high-fat diet. They also are resistant to gain weight upon high-fat diet by increasing fat metabolism. Therefore, the MCH system is important in regulating metabolic responses upon various environmental stimuli such as high-fat diet. Humana Press Inc 2010-04-22 2010 /pmc/articles/PMC2955453/ /pubmed/20411353 http://dx.doi.org/10.1007/s12031-010-9358-5 Text en © The Author(s) 2010 https://creativecommons.org/licenses/by-nc/4.0/ This article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited. |
spellingShingle | Article Chung, Shinjae Wong, Timothy Nagasaki, Hiroshi Civelli, Olivier Acute Homeostatic Responses to Increased Fat Consumption in MCH1R Knockout Mice |
title | Acute Homeostatic Responses to Increased Fat Consumption in MCH1R Knockout Mice |
title_full | Acute Homeostatic Responses to Increased Fat Consumption in MCH1R Knockout Mice |
title_fullStr | Acute Homeostatic Responses to Increased Fat Consumption in MCH1R Knockout Mice |
title_full_unstemmed | Acute Homeostatic Responses to Increased Fat Consumption in MCH1R Knockout Mice |
title_short | Acute Homeostatic Responses to Increased Fat Consumption in MCH1R Knockout Mice |
title_sort | acute homeostatic responses to increased fat consumption in mch1r knockout mice |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2955453/ https://www.ncbi.nlm.nih.gov/pubmed/20411353 http://dx.doi.org/10.1007/s12031-010-9358-5 |
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