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Research Paper|Volume 7, Issue 10|pp 869—881

Mitochondrial Hormesis links nutrient restriction to improved metabolism in fat cell

Daniele Lettieri Barbato1, Giuseppe Tatulli2, Katia Aquilano1,3, Maria R. Ciriolo1
  • 1Department of Biology, University of Rome “Tor Vergata”, 00133 Rome, Italy
  • 2Università Telematica San Raffaele Roma, 00166, Rome, Italy
  • 3IRCCS San Raffaele Roma, 00163, Rome, Italy

* * Equal contribution

Received: September 3, 2015Accepted: October 5, 2015Published: October 28, 2015
https://doi.org/10.18632/aging.100832

Copyright: © 2015 Barbato et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

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.