Abstract:
:Although mitochondrial dysfunction, endoplasmic reticulum (ER) stress, and disrupted lipid and calcium (Ca2+) homeostasis are classically associated with both insulin resistance and β-cell dysfunction in type 2 diabetes mellitus (T2DM), the interplay between these metabolic stresses is less known. Both organelles interact through contact points known as mitochondria-associated membranes (MAM), in order to exchange both lipids and Ca2+ and regulate cellular homeostasis. Recent evidences suggest that MAM could be an important hub for hormonal and nutrient signaling in the liver and that ER-mitochondria miscommunication could participate to hepatic insulin resistance, highlighting the importance of MAM in the control of glucose homeostasis. Here, we specifically discuss the role of MAM in hormonal and nutrient-regulated signaling pathways supporting a role in the control of glucose homeostasis and analyze the evidences pointing a role of ER-mitochondria miscommunication in T2DM. Collectively, these data suggest that targeting MAM structure and function might be a novel strategy for the treatment of T2DM.
journal_name
Adv Exp Med Bioljournal_title
Advances in experimental medicine and biologyauthors
Rieusset Jdoi
10.1007/978-981-10-4567-7_13subject
Has Abstractpub_date
2017-01-01 00:00:00pages
171-186eissn
0065-2598issn
2214-8019journal_volume
997pub_type
杂志文章,评审abstract::Anumber of observations have lent support to a model in which thermal stress is transduced into a signal at the level of the cellular membranes. Our alternative, but not exclusive, approach is based on the concept that the initial stress-sensing events are associated with the physical state and lipid composition of ce...
journal_title:Advances in experimental medicine and biology
pub_type: 杂志文章,评审
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pub_type: 临床试验,杂志文章
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