Format

Send to

Choose Destination
Nat Rev Endocrinol. 2016 Nov;12(11):633-645. doi: 10.1038/nrendo.2016.104. Epub 2016 Jul 22.

Skeletal muscle mitochondria as a target to prevent or treat type 2 diabetes mellitus.

Author information

1
Department of Human Biology and Human Movement Sciences, Maastricht University Medical Center, Universiteitsingel 50, 6229 ER, Maastricht, Netherlands.
2
NUTRIM, School for Nutrition and Translational Research in Metabolism, Maastricht University Medical Center, Universiteitsingel 50, 6229 ER, Maastricht, Netherlands.
3
Department of Radiology, Maastricht University Medical Center, P. Debyelaan 25, 6229 HX, Maastricht, Netherlands.

Abstract

Low levels of physical activity and the presence of obesity are associated with mitochondrial dysfunction. In addition, mitochondrial dysfunction has been associated with the development of insulin resistance and type 2 diabetes mellitus (T2DM). Although the evidence for a causal relationship between mitochondrial function and insulin resistance is still weak, emerging evidence indicates that boosting mitochondrial function might be beneficial to patient health. Exercise training is probably the most recognized promoter of mitochondrial function and insulin sensitivity and hence is still regarded as the best strategy to prevent and treat T2DM. Animal data, however, have revealed several new insights into the regulation of mitochondrial metabolism, and novel targets for interventions to boost mitochondrial function have emerged. Importantly, many of these targets seem to be regulated by factors such as nutrition, ambient temperature and circadian rhythms, which provides a basis for nonpharmacological strategies to prevent or treat T2DM in humans. Here, we will review the current evidence that mitochondrial function can be targeted therapeutically to improve insulin sensitivity and to prevent T2DM, focusing mainly on human intervention studies.

PMID:
27448057
DOI:
10.1038/nrendo.2016.104
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Nature Publishing Group
Loading ...
Support Center