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ER–Mitochondria Contacts and Insulin Resistance Modulation through Exercise Intervention

The endoplasmic reticulum (ER) makes physical contacts with mitochondria at specific sites, and the hubs between the two organelles are called mitochondria-associated ER membranes (MAMs). MAMs are known to play key roles in biological processes, such as intracellular Ca(2+) regulation, lipid traffic...

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Detalles Bibliográficos
Autores principales: Sun, Yi, Ding, Shuzhe
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7765572/
https://www.ncbi.nlm.nih.gov/pubmed/33339212
http://dx.doi.org/10.3390/ijms21249587
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author Sun, Yi
Ding, Shuzhe
author_facet Sun, Yi
Ding, Shuzhe
author_sort Sun, Yi
collection PubMed
description The endoplasmic reticulum (ER) makes physical contacts with mitochondria at specific sites, and the hubs between the two organelles are called mitochondria-associated ER membranes (MAMs). MAMs are known to play key roles in biological processes, such as intracellular Ca(2+) regulation, lipid trafficking, and metabolism, as well as cell death, etc. Studies demonstrated that dysregulation of MAMs significantly contributed to insulin resistance. Alterations of MAMs’ juxtaposition and integrity, impaired expressions of insulin signaling molecules, disruption of Ca(2+) homeostasis, and compromised metabolic flexibility are all actively involved in the above processes. In addition, exercise training is considered as an effective stimulus to ameliorate insulin resistance. Although the underlying mechanisms for exercise-induced improvement in insulin resistance are not fully understood, MAMs may be critical for the beneficial effects of exercise.
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spelling pubmed-77655722020-12-27 ER–Mitochondria Contacts and Insulin Resistance Modulation through Exercise Intervention Sun, Yi Ding, Shuzhe Int J Mol Sci Review The endoplasmic reticulum (ER) makes physical contacts with mitochondria at specific sites, and the hubs between the two organelles are called mitochondria-associated ER membranes (MAMs). MAMs are known to play key roles in biological processes, such as intracellular Ca(2+) regulation, lipid trafficking, and metabolism, as well as cell death, etc. Studies demonstrated that dysregulation of MAMs significantly contributed to insulin resistance. Alterations of MAMs’ juxtaposition and integrity, impaired expressions of insulin signaling molecules, disruption of Ca(2+) homeostasis, and compromised metabolic flexibility are all actively involved in the above processes. In addition, exercise training is considered as an effective stimulus to ameliorate insulin resistance. Although the underlying mechanisms for exercise-induced improvement in insulin resistance are not fully understood, MAMs may be critical for the beneficial effects of exercise. MDPI 2020-12-16 /pmc/articles/PMC7765572/ /pubmed/33339212 http://dx.doi.org/10.3390/ijms21249587 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Sun, Yi
Ding, Shuzhe
ER–Mitochondria Contacts and Insulin Resistance Modulation through Exercise Intervention
title ER–Mitochondria Contacts and Insulin Resistance Modulation through Exercise Intervention
title_full ER–Mitochondria Contacts and Insulin Resistance Modulation through Exercise Intervention
title_fullStr ER–Mitochondria Contacts and Insulin Resistance Modulation through Exercise Intervention
title_full_unstemmed ER–Mitochondria Contacts and Insulin Resistance Modulation through Exercise Intervention
title_short ER–Mitochondria Contacts and Insulin Resistance Modulation through Exercise Intervention
title_sort er–mitochondria contacts and insulin resistance modulation through exercise intervention
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7765572/
https://www.ncbi.nlm.nih.gov/pubmed/33339212
http://dx.doi.org/10.3390/ijms21249587
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