Research Paper Volume 7, Issue 10 pp 869—881
Mitochondrial Hormesis links nutrient restriction to improved metabolism in fat cell
- 1 Department of Biology, University of Rome “Tor Vergata”, 00133 Rome, Italy
- 2 Università Telematica San Raffaele Roma, 00166, Rome, Italy
- 3 IRCCS San Raffaele Roma, 00163, Rome, Italy
received: September 3, 2015 ; accepted: October 5, 2015 ; published: October 28, 2015 ;https://doi.org/10.18632/aging.100832
How to Cite
Fasting promotes longevity by reprogramming metabolic and stress resistance pathways. However, although the impact on adipose tissue physiology through hormonal inputs is well established, the direct role of fasting on adipose cells is poorly understood. Herein we show that white and beige adipocytes, as well as mouse epididymal and subcutaneous adipose depots, respond to nutrient scarcity by acquiring a brown-like phenotype. Indeed, they improve oxidative metabolism through modulating the expression of mitochondrial-and nuclear-encoded oxidative phosphorylation genes as well as mitochondrial stress defensive proteins (UCP1, SOD2). Such adaptation is placed in a canonical mitohormetic response that proceeds via mitochondrial reactive oxygen species (mtROS) production and redistribution of FoxO1 transcription factor into nucleus. Nuclear FoxO1 (nFoxO1) mediates retrograde communication by inducing the expression of mitochondrial oxidative and stress defensive genes. Collectively, our findings describe an unusual white/beige fat cell response to nutrient availability highlighting another health-promoting mechanism of fasting.