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Physiol Rep. 2017 Apr;5(7). pii: e13247. doi: 10.14814/phy2.13247.

Cycling our way to fit fat.

Author information

1
Department of Human Health and Nutritional Science, University of Guelph, Guelph, Canada.
2
Department of Human Health and Nutritional Science, University of Guelph, Guelph, Canada dcwright@uoguelph.ca.

Abstract

Adipose tissue is increasingly being recognized as a key regulator of whole body carbohydrate and lipid metabolism. In conditions of obesity and insulin resistance mitochondrial content in this tissue is reduced, while treatment with insulin sensitizing drugs such as thiazolidinediones (TZDs) increase mitochondrial content. It has been known for decades that exercise increases mitochondrial content in skeletal muscle and now several laboratories have shown similar effects in adipose tissue. To date the specific mechanisms mediating this effect have not been fully identified. In this review we highlight recent work suggesting that increases in lipolysis and subsequently fatty acid re-esterification trigger the activation of 5' AMP-activated protein kinase (AMP) activated protein kinase and ultimately the induction of mitochondrial biogenesis. It is our current view that this pathway could be a unifying mechanism linking numerous systemic factors (catecholamines, interleukin-6, meteorin-like) to induction of mitochondrial biogenesis following exercise.

KEYWORDS:

AMPK ; Adipose Tissue; PGC‐1α; exercise; mitochondria

PMID:
28404813
PMCID:
PMC5392531
DOI:
10.14814/phy2.13247
[Indexed for MEDLINE]
Free PMC Article

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