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Leptin, diabetes, and the brain
Diabetes is a major worldwide problem. Despite some progress in the development of new antidiabetic agents, the ability to maintain tight glycemic control in order to prevent renal, retinal, and neuropathic complications of diabetes without adverse complications still remains a challenge. Recent evi...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Medknow Publications & Media Pvt Ltd
2012
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3602981/ https://www.ncbi.nlm.nih.gov/pubmed/23565487 http://dx.doi.org/10.4103/2230-8210.105568 |
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author | Meek, Thomas H. Morton, Gregory J. |
author_facet | Meek, Thomas H. Morton, Gregory J. |
author_sort | Meek, Thomas H. |
collection | PubMed |
description | Diabetes is a major worldwide problem. Despite some progress in the development of new antidiabetic agents, the ability to maintain tight glycemic control in order to prevent renal, retinal, and neuropathic complications of diabetes without adverse complications still remains a challenge. Recent evidence suggests, however, that in addition to playing a key role in the regulation of energy homeostasis, the adiposity hormone leptin also plays an important role in the control of glucose metabolism via its actions in the brain. This review examines the role of leptin action in the central nervous system and the mechanisms whereby leptin mediates its effects to regulate glucose metabolism. These findings suggest that defects or dysfunction in leptin signaling may contribute to the etiology of diabetes and raise the possibility that either leptin or downstream targets of leptin may have therapeutic potential for the treatment of diabetes. |
format | Online Article Text |
id | pubmed-3602981 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | Medknow Publications & Media Pvt Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-36029812013-04-05 Leptin, diabetes, and the brain Meek, Thomas H. Morton, Gregory J. Indian J Endocrinol Metab Review Article Diabetes is a major worldwide problem. Despite some progress in the development of new antidiabetic agents, the ability to maintain tight glycemic control in order to prevent renal, retinal, and neuropathic complications of diabetes without adverse complications still remains a challenge. Recent evidence suggests, however, that in addition to playing a key role in the regulation of energy homeostasis, the adiposity hormone leptin also plays an important role in the control of glucose metabolism via its actions in the brain. This review examines the role of leptin action in the central nervous system and the mechanisms whereby leptin mediates its effects to regulate glucose metabolism. These findings suggest that defects or dysfunction in leptin signaling may contribute to the etiology of diabetes and raise the possibility that either leptin or downstream targets of leptin may have therapeutic potential for the treatment of diabetes. Medknow Publications & Media Pvt Ltd 2012-12 /pmc/articles/PMC3602981/ /pubmed/23565487 http://dx.doi.org/10.4103/2230-8210.105568 Text en Copyright: © Indian Journal of Endocrinology and Metabolism http://creativecommons.org/licenses/by-nc-sa/3.0 This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Article Meek, Thomas H. Morton, Gregory J. Leptin, diabetes, and the brain |
title | Leptin, diabetes, and the brain |
title_full | Leptin, diabetes, and the brain |
title_fullStr | Leptin, diabetes, and the brain |
title_full_unstemmed | Leptin, diabetes, and the brain |
title_short | Leptin, diabetes, and the brain |
title_sort | leptin, diabetes, and the brain |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3602981/ https://www.ncbi.nlm.nih.gov/pubmed/23565487 http://dx.doi.org/10.4103/2230-8210.105568 |
work_keys_str_mv | AT meekthomash leptindiabetesandthebrain AT mortongregoryj leptindiabetesandthebrain |