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Cyclophilin D deficiency prevents diet‐induced obesity in mice
Author(s) -
Devalaraja-Narashimha Kishor,
Diener Alicia M.,
Padanilam Babu J.
Publication year - 2011
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2011.01.031
Subject(s) - thermogenesis , medicine , endocrinology , mitochondrion , insulin resistance , basal metabolic rate , mitochondrial permeability transition pore , obesity , biology , homeostasis , metabolism , chemistry , biochemistry , apoptosis , programmed cell death
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.