Journal article
UCP3 Regulates Cardiac Efficiency and Mitochondrial Coupling in High Fat―Fed Mice but Not in Leptin-Deficient Mice
Diabetes (New York, N.Y.), Vol.61(12), pp.3260-3269
2012
DOI: 10.2337/db12-0063
PMCID: PMC3501860
PMID: 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.
Details
- Title: Subtitle
- UCP3 Regulates Cardiac Efficiency and Mitochondrial Coupling in High Fat―Fed Mice but Not in Leptin-Deficient Mice
- Creators
- Sihem BOUDINA - Division of Endocrinology, Metabolism, and Diabetes and Program in Molecular Medicine, University of Utah School of Medicine, Salt Lake City, Utah, United StatesYong Hwan Han - Division of Endocrinology, Metabolism, and Diabetes and Program in Molecular Medicine, University of Utah School of Medicine, Salt Lake City, Utah, United StatesShaobo PEI - Division of Endocrinology, Metabolism, and Diabetes and Program in Molecular Medicine, University of Utah School of Medicine, Salt Lake City, Utah, United StatesTimothy J TIDWELL - Division of Endocrinology, Metabolism, and Diabetes and Program in Molecular Medicine, University of Utah School of Medicine, Salt Lake City, Utah, United StatesBrandon HENRIE - Division of Endocrinology, Metabolism, and Diabetes and Program in Molecular Medicine, University of Utah School of Medicine, Salt Lake City, Utah, United StatesJoseph TUINEI - Division of Endocrinology, Metabolism, and Diabetes and Program in Molecular Medicine, University of Utah School of Medicine, Salt Lake City, Utah, United StatesCurtis OLSEN - Division of Endocrinology, Metabolism, and Diabetes and Program in Molecular Medicine, University of Utah School of Medicine, Salt Lake City, Utah, United StatesSandra SENA - Division of Endocrinology, Metabolism, and Diabetes and Program in Molecular Medicine, University of Utah School of Medicine, Salt Lake City, Utah, United StatesE Dale Abel - Division of Endocrinology, Metabolism, and Diabetes and Program in Molecular Medicine, University of Utah School of Medicine, Salt Lake City, Utah, United States
- Resource Type
- Journal article
- Publication Details
- Diabetes (New York, N.Y.), Vol.61(12), pp.3260-3269
- Publisher
- American Diabetes Association; Alexandria, VA
- DOI
- 10.2337/db12-0063
- PMID
- 22912419
- PMCID
- PMC3501860
- ISSN
- 0012-1797
- eISSN
- 1939-327X
- Language
- English
- Date published
- 2012
- Academic Unit
- Roy J. Carver Department of Biomedical Engineering; Biochemistry and Molecular Biology; Internal Medicine
- Record Identifier
- 9984025300202771
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