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Crosstalk between autophagy and insulin resistance: evidence from different tissues
Insulin is a critical hormone that promotes energy storage in various tissues, as well as anabolic functions. Insulin resistance significantly reduces these responses, resulting in pathological conditions, such as obesity and type 2 diabetes mellitus (T2DM). The management of insulin resistance requ...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10599071/ https://www.ncbi.nlm.nih.gov/pubmed/37876013 http://dx.doi.org/10.1186/s40001-023-01424-9 |
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author | Sadeghi, Asie Niknam, Maryam Momeni-Moghaddam, Mohammad Amin Shabani, Maryam Aria, Hamid Bastin, Alireza Teimouri, Maryam Meshkani, Reza Akbari, Hamed |
author_facet | Sadeghi, Asie Niknam, Maryam Momeni-Moghaddam, Mohammad Amin Shabani, Maryam Aria, Hamid Bastin, Alireza Teimouri, Maryam Meshkani, Reza Akbari, Hamed |
author_sort | Sadeghi, Asie |
collection | PubMed |
description | Insulin is a critical hormone that promotes energy storage in various tissues, as well as anabolic functions. Insulin resistance significantly reduces these responses, resulting in pathological conditions, such as obesity and type 2 diabetes mellitus (T2DM). The management of insulin resistance requires better knowledge of its pathophysiological mechanisms to prevent secondary complications, such as cardiovascular diseases (CVDs). Recent evidence regarding the etiological mechanisms behind insulin resistance emphasizes the role of energy imbalance and neurohormonal dysregulation, both of which are closely regulated by autophagy. Autophagy is a conserved process that maintains homeostasis in cells. Accordingly, autophagy abnormalities have been linked to a variety of metabolic disorders, including insulin resistance, T2DM, obesity, and CVDs. Thus, there may be a link between autophagy and insulin resistance. Therefore, the interaction between autophagy and insulin function will be examined in this review, particularly in insulin-responsive tissues, such as adipose tissue, liver, and skeletal muscle. |
format | Online Article Text |
id | pubmed-10599071 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-105990712023-10-26 Crosstalk between autophagy and insulin resistance: evidence from different tissues Sadeghi, Asie Niknam, Maryam Momeni-Moghaddam, Mohammad Amin Shabani, Maryam Aria, Hamid Bastin, Alireza Teimouri, Maryam Meshkani, Reza Akbari, Hamed Eur J Med Res Review Insulin is a critical hormone that promotes energy storage in various tissues, as well as anabolic functions. Insulin resistance significantly reduces these responses, resulting in pathological conditions, such as obesity and type 2 diabetes mellitus (T2DM). The management of insulin resistance requires better knowledge of its pathophysiological mechanisms to prevent secondary complications, such as cardiovascular diseases (CVDs). Recent evidence regarding the etiological mechanisms behind insulin resistance emphasizes the role of energy imbalance and neurohormonal dysregulation, both of which are closely regulated by autophagy. Autophagy is a conserved process that maintains homeostasis in cells. Accordingly, autophagy abnormalities have been linked to a variety of metabolic disorders, including insulin resistance, T2DM, obesity, and CVDs. Thus, there may be a link between autophagy and insulin resistance. Therefore, the interaction between autophagy and insulin function will be examined in this review, particularly in insulin-responsive tissues, such as adipose tissue, liver, and skeletal muscle. BioMed Central 2023-10-25 /pmc/articles/PMC10599071/ /pubmed/37876013 http://dx.doi.org/10.1186/s40001-023-01424-9 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Review Sadeghi, Asie Niknam, Maryam Momeni-Moghaddam, Mohammad Amin Shabani, Maryam Aria, Hamid Bastin, Alireza Teimouri, Maryam Meshkani, Reza Akbari, Hamed Crosstalk between autophagy and insulin resistance: evidence from different tissues |
title | Crosstalk between autophagy and insulin resistance: evidence from different tissues |
title_full | Crosstalk between autophagy and insulin resistance: evidence from different tissues |
title_fullStr | Crosstalk between autophagy and insulin resistance: evidence from different tissues |
title_full_unstemmed | Crosstalk between autophagy and insulin resistance: evidence from different tissues |
title_short | Crosstalk between autophagy and insulin resistance: evidence from different tissues |
title_sort | crosstalk between autophagy and insulin resistance: evidence from different tissues |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10599071/ https://www.ncbi.nlm.nih.gov/pubmed/37876013 http://dx.doi.org/10.1186/s40001-023-01424-9 |
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