Format

Send to

Choose Destination
See comment in PubMed Commons below
Int J Biochem Cell Biol. 2011 Sep;43(9):1257-62. doi: 10.1016/j.biocel.2011.05.006. Epub 2011 May 14.

Mitochondria and endoplasmic reticulum: mitochondria-endoplasmic reticulum interplay in type 2 diabetes pathophysiology.

Author information

1
INSERM U1060, CarMeN laboratory, Lyon 1 University, F-69921 Oullins, France. jennifer.rieusset@univ-lyon1.fr

Abstract

Mitochondria and endoplasmic reticulum (ER) are two important metabolic organelles for the maintenance of cellular homeostasis and their functional defects are suspected to participate to the aetiology of type 2 diabetes (T2D). Particularly, excessive lipid intake and/or ectopic lipid accumulation in tissues (referred as lipotoxicity) are involved in alterations of both organelles and are closely linked to peripheral insulin resistance and defective insulin secretion. Since, mitochondria and ER are physically and functionally interconnected, their respective alterations during T2D could be interrelated. However, the mechanisms that coordinate the interplay between mitochondrial dysfunction and ER stress, and its relevance in the control of glucose homeostasis are unknown. Among these mechanisms, we will discuss on the potential role of altered mitochondria/ER crosstalk in organelle dysfunctions and in T2D pathophysiology.

PMID:
21605696
DOI:
10.1016/j.biocel.2011.05.006
[Indexed for MEDLINE]
Free full text
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science Icon for HAL archives ouvertes
    Loading ...
    Support Center