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Significance of uncoupling protein 3 in mitochondrial function upon mid‐ and long‐term dietary high‐fat exposure
Author(s) -
Nabben Miranda,
Hoeks Joris,
Moonen-Kornips Esther,
van Beurden Denis,
Briedé Jacob J.,
Hesselink Matthijs K.C.,
Glatz Jan F.C.,
Schrauwen Patrick
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.2011.11.012
Subject(s) - ucp3 , uncoupling protein , mitochondrion , knockout mouse , biology , mitochondrial ros , medicine , endocrinology , microbiology and biotechnology , chemistry , biochemistry , gene , adipose tissue , brown adipose tissue
Uncoupling protein 3 (UCP3) may reduce mitochondrial ROS production, and thereby protect against mitochondrial dysfunction in skeletal muscle. UCP3 has been suggested to specifically fulfill this role under high‐fat conditions. Here we show that UCP3 knockout mice indeed have elevated mitochondrial ROS production after short‐term (8 weeks) high‐fat feeding. After 26 weeks of high‐fat feeding, UCP3 knockout mice exhibited reduced mitochondrial function as measured ex vivo in isolated mitochondria. In conclusion, these data suggest that UCP3 may have a role in the protection of mitochondria against lipid‐induced mitochondrial dysfunction, but only after long‐term exposure to high‐fat.