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Roles of Vitamin A Metabolism in the Development of Hepatic Insulin Resistance

The increase in the number of people with obesity- and noninsulin-dependent diabetes mellitus has become a major public health concern. Insulin resistance is a common feature closely associated with human obesity and diabetes. Insulin regulates metabolism, at least in part, via the control of the ex...

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Autor principal: Chen, Guoxun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4890907/
https://www.ncbi.nlm.nih.gov/pubmed/27335827
http://dx.doi.org/10.1155/2013/534972
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author Chen, Guoxun
author_facet Chen, Guoxun
author_sort Chen, Guoxun
collection PubMed
description The increase in the number of people with obesity- and noninsulin-dependent diabetes mellitus has become a major public health concern. Insulin resistance is a common feature closely associated with human obesity and diabetes. Insulin regulates metabolism, at least in part, via the control of the expression of the hepatic genes involved in glucose and fatty acid metabolism. Insulin resistance is always associated with profound changes of the expression of hepatic genes for glucose and lipid metabolism. As an essential micronutrient, vitamin A (VA) is needed in a variety of physiological functions. The active metablite of VA, retinoic acid (RA), regulates the expression of genes through the activation of transcription factors bound to the RA-responsive elements in the promoters of RA-targeted genes. Recently, retinoids have been proposed to play roles in glucose and lipid metabolism and energy homeostasis. This paper summarizes the recent progresses in our understanding of VA metabolism in the liver and of the potential transcription factors mediating RA responses. These transcription factors are the retinoic acid receptor, the retinoid X receptor, the hepatocyte nuclear factor 4α, the chicken ovalbumin upstream promoter-transcription factor II, and the peroxisome proliferator-activated receptor β/δ. This paper also summarizes the effects of VA status and RA treatments on the glucose and lipid metabolism in vivo and the effects of retinoid treatments on the expression of insulin-regulated genes involved in the glucose and fatty acid metabolism in the primary hepatocytes. I discuss the roles of RA production in the development of insulin resistance in hepatocytes and proposes a mechanism by which RA production may contribute to hepatic insulin resistance. Given the large amount of information and progresses regarding the physiological functions of VA, this paper mainly focuses on the findings in the liver and hepatocytes and only mentions the relative findings in other tissues and cells.
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spelling pubmed-48909072016-06-22 Roles of Vitamin A Metabolism in the Development of Hepatic Insulin Resistance Chen, Guoxun ISRN Hepatol Review Article The increase in the number of people with obesity- and noninsulin-dependent diabetes mellitus has become a major public health concern. Insulin resistance is a common feature closely associated with human obesity and diabetes. Insulin regulates metabolism, at least in part, via the control of the expression of the hepatic genes involved in glucose and fatty acid metabolism. Insulin resistance is always associated with profound changes of the expression of hepatic genes for glucose and lipid metabolism. As an essential micronutrient, vitamin A (VA) is needed in a variety of physiological functions. The active metablite of VA, retinoic acid (RA), regulates the expression of genes through the activation of transcription factors bound to the RA-responsive elements in the promoters of RA-targeted genes. Recently, retinoids have been proposed to play roles in glucose and lipid metabolism and energy homeostasis. This paper summarizes the recent progresses in our understanding of VA metabolism in the liver and of the potential transcription factors mediating RA responses. These transcription factors are the retinoic acid receptor, the retinoid X receptor, the hepatocyte nuclear factor 4α, the chicken ovalbumin upstream promoter-transcription factor II, and the peroxisome proliferator-activated receptor β/δ. This paper also summarizes the effects of VA status and RA treatments on the glucose and lipid metabolism in vivo and the effects of retinoid treatments on the expression of insulin-regulated genes involved in the glucose and fatty acid metabolism in the primary hepatocytes. I discuss the roles of RA production in the development of insulin resistance in hepatocytes and proposes a mechanism by which RA production may contribute to hepatic insulin resistance. Given the large amount of information and progresses regarding the physiological functions of VA, this paper mainly focuses on the findings in the liver and hepatocytes and only mentions the relative findings in other tissues and cells. Hindawi Publishing Corporation 2013-09-30 /pmc/articles/PMC4890907/ /pubmed/27335827 http://dx.doi.org/10.1155/2013/534972 Text en Copyright © 2013 Guoxun Chen. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Chen, Guoxun
Roles of Vitamin A Metabolism in the Development of Hepatic Insulin Resistance
title Roles of Vitamin A Metabolism in the Development of Hepatic Insulin Resistance
title_full Roles of Vitamin A Metabolism in the Development of Hepatic Insulin Resistance
title_fullStr Roles of Vitamin A Metabolism in the Development of Hepatic Insulin Resistance
title_full_unstemmed Roles of Vitamin A Metabolism in the Development of Hepatic Insulin Resistance
title_short Roles of Vitamin A Metabolism in the Development of Hepatic Insulin Resistance
title_sort roles of vitamin a metabolism in the development of hepatic insulin resistance
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4890907/
https://www.ncbi.nlm.nih.gov/pubmed/27335827
http://dx.doi.org/10.1155/2013/534972
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