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FEBS Lett. 2011 Feb 18;585(4):677-82. doi: 10.1016/j.febslet.2011.01.031. Epub 2011 Jan 27.

Cyclophilin D deficiency prevents diet-induced obesity in mice.

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  • 1Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, NE 68198-5850, USA.

Abstract

Mitochondrial coupling efficiency is pivotal in thermogenesis and energy homeostasis. Here we show that deletion of cyclophilin D (CypD), a key modulator of the mitochondrial permeability transition pore, demonstrated resistance to diet-induced obesity (DIO) in both male and female mice, due to increased basal metabolic rate, heat production, total energy expenditure and expenditure of fat energy, despite increased food consumption. Absorption of fatty acids is not altered between CypD(-/-) and wild-type mice. Adult CypD(-/-) developed hyperglycemia, insulin resistance and glucose intolerance albeit resistant to DIO. These data demonstrate that inhibition of CypD function could protect from HFD-IO by increasing energy expenditure in both male and female mice. Inhibition of CypD may offer a novel target to modulate metabolism.

PMID:
21276794
DOI:
10.1016/j.febslet.2011.01.031
[PubMed - indexed for MEDLINE]
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