UCP3 regulates cardiac efficiency and mitochondrial coupling in high fat-fed
mice but not in leptin-deficient mice.
Authors Boudina S, Han YH, Pei S, Tidwell TJ, Henrie B, Tuinei J, Olsen C, Sena S, Abel
Submitted By E. Dale Abel on 3/4/2015
Status Published
Journal Diabetes
Year 2012
Date Published 12/1/2012
Volume : Pages 61 : 3260 - 3269
PubMed Reference 22912419
Abstract These studies investigate the role of uncoupling protein 3 (UCP3) in cardiac
energy metabolism, cardiac O(2) consumption (MVO(2)), cardiac efficiency (CE),
and mitochondrial uncoupling in high fat (HF)-fed or leptin-deficient mice.
UCP3KO and wild-type (WT) mice were fed normal chow or HF diets for 10 weeks.
Substrate utilization rates, MVO(2), CE, and mitochondrial uncoupling were
measured in perfused working hearts and saponin-permeabilized cardiac fibers,
respectively. Similar analyses were performed in hearts of ob/ob mice lacking
UCP3 (U3OB mice). HF increased cardiac UCP3 protein. However, fatty acid (FA)
oxidation rates were similarly increased by HF diet in WT and UCP3KO mice. By
contrast, MVO(2) increased in WT, but not in UCP3KO with HF, leading to
increased CE in UCP3KO mice. Consistent with increased CE, mitochondrial
coupling was increased in the hearts of HF-fed UCP3KO mice. Unexpectedly, UCP3
deletion in ob/ob mice reduced FA oxidation but had no effect on MVO(2) or CE.
In addition, FA-induced mitochondrial uncoupling was similarly enhanced in U3OB
compared with ob/ob hearts and was associated with elevated mitochondrial
thioesterase-1 protein content. These studies show that although UCP3 may
mediate mitochondrial uncoupling and reduced CE after HF feeding, it does not
mediate uncoupling in leptin-deficient states.

Investigators with authorship
E. Dale AbelUniversity of Iowa