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Cell Death Dis. 2018 Mar 9;9(3):388. doi: 10.1038/s41419-018-0416-1.

The role of endoplasmic reticulum-mitochondria contact sites in the control of glucose homeostasis: an update.

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1
Laboratoire CarMeN, Unité Mixte de Recherche INSERM U-1060 et INRA U-1397, Université Lyon 1, Oullins, 69600, France. jennifer.rieusset@univ-lyon1.fr.

Abstract

The contact sites that the endoplasmic reticulum (ER) forms with mitochondria, called mitochondria-associated membranes (MAMs), are a hot topic in biological research, and both their molecular determinants and their numerous roles in several signaling pathways are is continuously evolving. MAMs allow the exchange between both organelles of lipids, calcium (Ca2+), and likely reactive oxygen species, allowing adaptations of both cellular bioenergetics and cell fate depending of cellular needs or stresses. Therefore, it is not surprising that MAMs affect cellular metabolism. Nevertheless, recent arguments suggest that MAMs could also act as key hub of hormonal and/or nutrient signaling in several insulin-sensitive tissues, pointing a specific role of MAMs in the control of glucose homeostasis. Here, I provide a brief review and update on current key signaling roles of the MAMs in the control of glucose homeostasis in both health and metabolic diseases. Particularly, the relevance of ER-mitochondria miscommunication in the disruption of glucose homeostasis is analyzed in details in the liver, skeletal muscle, adipose tissue, and beta cells of the pancreas.

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