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Could there be a fine-tuning role for brain-derived adipokines in the regulation of bodyweight and prevention of obesity?

Obesity is one of the most prevalent medical conditions, often associated with several negative stereotypes. Although it is true that weight gain occurs when food intake exceeds energy expenditure, it is important to note that even a 1% mismatch between the two can lead to a substantial weight gain...

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Detalles Bibliográficos
Autor principal: Brown, Russell E.
Formato: Texto
Lenguaje:English
Publicado: McGill University 2008
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2582659/
https://www.ncbi.nlm.nih.gov/pubmed/19148319
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author Brown, Russell E.
author_facet Brown, Russell E.
author_sort Brown, Russell E.
collection PubMed
description Obesity is one of the most prevalent medical conditions, often associated with several negative stereotypes. Although it is true that weight gain occurs when food intake exceeds energy expenditure, it is important to note that even a 1% mismatch between the two can lead to a substantial weight gain after only a few years. Further, the body appears to balance energy metabolism via an endogenous lipostatic loop in which adipose stores send hormonal signals (e.g. adipokines such as leptin) to the hypothalamus in order to reduce appetite and increase energy expenditure. However, the brain is also a novel site of expression of many of these adipokine genes. This led to the hypothesis that hypothalamic-derived adipokines might also be involved in bodyweight regulation by exerting some effect on the control of appetite or hypothalamic function. When RNA interference (RNAi) was used to specifically silence adipokine gene expression in various in vitro models, this led to increases in cell death, modification of the expression of key signaling genes (i.e. suppressor of cytokine signaling-3; SOCS-3), and modulation of the activation of cellular energy sensors (i.e. adenosine monophosphate-activated protein kinase; AMPK). Subsequently, when RNAi was used to inhibit the expression of brain-derived leptin in adult rats this resulted in minor increases in weight gain in addition to modifying the expression of other adipokine genes (eg. resistin). In summary, although adipokines secreted by adipose tissue appear to the main regulator of lipostatic loop, this review shows that the fine tuning that is required to maintain a stable bodyweight by this system might be accomplished by hypothalamic-derived adipokines. Perturbations in this central adipokine system could lead to alterations in normal hypothalamic function which leads to unintended weight gain.
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spelling pubmed-25826592009-01-15 Could there be a fine-tuning role for brain-derived adipokines in the regulation of bodyweight and prevention of obesity? Brown, Russell E. Mcgill J Med Review Articles Obesity is one of the most prevalent medical conditions, often associated with several negative stereotypes. Although it is true that weight gain occurs when food intake exceeds energy expenditure, it is important to note that even a 1% mismatch between the two can lead to a substantial weight gain after only a few years. Further, the body appears to balance energy metabolism via an endogenous lipostatic loop in which adipose stores send hormonal signals (e.g. adipokines such as leptin) to the hypothalamus in order to reduce appetite and increase energy expenditure. However, the brain is also a novel site of expression of many of these adipokine genes. This led to the hypothesis that hypothalamic-derived adipokines might also be involved in bodyweight regulation by exerting some effect on the control of appetite or hypothalamic function. When RNA interference (RNAi) was used to specifically silence adipokine gene expression in various in vitro models, this led to increases in cell death, modification of the expression of key signaling genes (i.e. suppressor of cytokine signaling-3; SOCS-3), and modulation of the activation of cellular energy sensors (i.e. adenosine monophosphate-activated protein kinase; AMPK). Subsequently, when RNAi was used to inhibit the expression of brain-derived leptin in adult rats this resulted in minor increases in weight gain in addition to modifying the expression of other adipokine genes (eg. resistin). In summary, although adipokines secreted by adipose tissue appear to the main regulator of lipostatic loop, this review shows that the fine tuning that is required to maintain a stable bodyweight by this system might be accomplished by hypothalamic-derived adipokines. Perturbations in this central adipokine system could lead to alterations in normal hypothalamic function which leads to unintended weight gain. McGill University 2008-11 /pmc/articles/PMC2582659/ /pubmed/19148319 Text en Copyright © 2008 by MJM
spellingShingle Review Articles
Brown, Russell E.
Could there be a fine-tuning role for brain-derived adipokines in the regulation of bodyweight and prevention of obesity?
title Could there be a fine-tuning role for brain-derived adipokines in the regulation of bodyweight and prevention of obesity?
title_full Could there be a fine-tuning role for brain-derived adipokines in the regulation of bodyweight and prevention of obesity?
title_fullStr Could there be a fine-tuning role for brain-derived adipokines in the regulation of bodyweight and prevention of obesity?
title_full_unstemmed Could there be a fine-tuning role for brain-derived adipokines in the regulation of bodyweight and prevention of obesity?
title_short Could there be a fine-tuning role for brain-derived adipokines in the regulation of bodyweight and prevention of obesity?
title_sort could there be a fine-tuning role for brain-derived adipokines in the regulation of bodyweight and prevention of obesity?
topic Review Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2582659/
https://www.ncbi.nlm.nih.gov/pubmed/19148319
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