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Brain signaling systems in the Type 2 diabetes and metabolic syndrome: promising target to treat and prevent these diseases

The changes in the brain signaling systems play an important role in etiology and pathogenesis of Type 2 diabetes mellitus (T2DM) and metabolic syndrome (MS), being a possible cause of these diseases. Therefore, their restoration at the early stages of T2DM and MS can be regarded as a promising way...

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Detalles Bibliográficos
Autores principales: Shpakov, Alexander O, Derkach, Kira V, Berstein, Lev M
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Future Science Ltd 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5137856/
https://www.ncbi.nlm.nih.gov/pubmed/28031898
http://dx.doi.org/10.4155/fso.15.23
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author Shpakov, Alexander O
Derkach, Kira V
Berstein, Lev M
author_facet Shpakov, Alexander O
Derkach, Kira V
Berstein, Lev M
author_sort Shpakov, Alexander O
collection PubMed
description The changes in the brain signaling systems play an important role in etiology and pathogenesis of Type 2 diabetes mellitus (T2DM) and metabolic syndrome (MS), being a possible cause of these diseases. Therefore, their restoration at the early stages of T2DM and MS can be regarded as a promising way to treat and prevent these diseases and their complications. The data on the functional state of the brain signaling systems regulated by insulin, IGF-1, leptin, dopamine, serotonin, melanocortins and glucagon-like peptide-1, in T2DM and MS, are analyzed. The pharmacological approaches to restoration of these systems and improvement of insulin sensitivity, energy expenditure, lipid metabolism, and to prevent diabetic complications are discussed.
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spelling pubmed-51378562016-12-28 Brain signaling systems in the Type 2 diabetes and metabolic syndrome: promising target to treat and prevent these diseases Shpakov, Alexander O Derkach, Kira V Berstein, Lev M Future Sci OA Review The changes in the brain signaling systems play an important role in etiology and pathogenesis of Type 2 diabetes mellitus (T2DM) and metabolic syndrome (MS), being a possible cause of these diseases. Therefore, their restoration at the early stages of T2DM and MS can be regarded as a promising way to treat and prevent these diseases and their complications. The data on the functional state of the brain signaling systems regulated by insulin, IGF-1, leptin, dopamine, serotonin, melanocortins and glucagon-like peptide-1, in T2DM and MS, are analyzed. The pharmacological approaches to restoration of these systems and improvement of insulin sensitivity, energy expenditure, lipid metabolism, and to prevent diabetic complications are discussed. Future Science Ltd 2015-11-01 /pmc/articles/PMC5137856/ /pubmed/28031898 http://dx.doi.org/10.4155/fso.15.23 Text en © Shpakov AO, Derkach KV & Berstein LM This work is licensed under a Creative Commons Attribution 4.0 License (http://creativecommons.org/licenses/by/4.0/)
spellingShingle Review
Shpakov, Alexander O
Derkach, Kira V
Berstein, Lev M
Brain signaling systems in the Type 2 diabetes and metabolic syndrome: promising target to treat and prevent these diseases
title Brain signaling systems in the Type 2 diabetes and metabolic syndrome: promising target to treat and prevent these diseases
title_full Brain signaling systems in the Type 2 diabetes and metabolic syndrome: promising target to treat and prevent these diseases
title_fullStr Brain signaling systems in the Type 2 diabetes and metabolic syndrome: promising target to treat and prevent these diseases
title_full_unstemmed Brain signaling systems in the Type 2 diabetes and metabolic syndrome: promising target to treat and prevent these diseases
title_short Brain signaling systems in the Type 2 diabetes and metabolic syndrome: promising target to treat and prevent these diseases
title_sort brain signaling systems in the type 2 diabetes and metabolic syndrome: promising target to treat and prevent these diseases
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5137856/
https://www.ncbi.nlm.nih.gov/pubmed/28031898
http://dx.doi.org/10.4155/fso.15.23
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