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Titolo:
UCP3 and its putative function: consistencies and controversies
Autore:
Harper, ME; Dent, RM; Bezaire, V; Antoniou, A; Gauthier, A; Monemdjou, S; McPherson, R;
Indirizzi:
Univ Ottawa, Fac Med, Dept Biochem Microbiol & Immunol, Ottawa, ON K1H 8M5, Canada Univ Ottawa Ottawa ON Canada K1H 8M5 Immunol, Ottawa, ON K1H 8M5, Canada Univ Ottawa, Fac Med, Dept Psychiat, Ottawa, ON K1H 8M5, Canada Univ Ottawa Ottawa ON Canada K1H 8M5 Psychiat, Ottawa, ON K1H 8M5, Canada
Titolo Testata:
BIOCHEMICAL SOCIETY TRANSACTIONS
, volume: 29, anno: 2001,
parte:, 6
pagine: 768 - 773
SICI:
0300-5127(2001)29:<768:UAIPFC>2.0.ZU;2-H
Fonte:
ISI
Lingua:
ENG
Soggetto:
UNCOUPLING PROTEIN-3 GENE; MITOCHONDRIAL INNER MEMBRANE; SKELETAL-MUSCLE; PROTON LEAK; THYROID-HORMONE; METABOLIC-RATE; ENERGY-EXPENDITURE; PIMA-INDIANS; MICE; EXPRESSION;
Keywords:
fatty acid oxidation; muscle; proton leak; thermogenesis; uncoupling.;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
41
Recensione:
Indirizzi per estratti:
Indirizzo: Harper, ME Univ Ottawa, Fac Med, Dept Biochem Microbiol & Immunol, 451 Smyth Rd, Ottawa, ON K1H 8M5, Canada Univ Ottawa 451 Smyth Rd Ottawa ON CanadaK1H 8M5 H 8M5, Canada
Citazione:
M.E. Harper et al., "UCP3 and its putative function: consistencies and controversies", BIOCH SOC T, 29, 2001, pp. 768-773

Abstract

The physiological function of uncoupling protein 3 (UCP3) is as yet unknown. Based on its 57% homology to UCP1 whose physiologic function is uncoupling and thermogenesis, UCP3 was attributed with the function of mitochondrial uncoupling through proton-leak reactions. UCP3 is expressed selectively in muscle, a tissue in which it has been estimated that proton leak accountsfor approx. 50% of resting energy metabolism. Genetic linkage, associationand variant studies suggest a role for UCP3 in obesity and/or diabetes. Studies of the heterologous expression of UCP3 in yeast provide support for the idea that UCP3 can uncouple mitochondrial oxidative phosphorylation, butthe physiological relevance of these results is questionable. In vitro studies of mitochondria from Ucp3(--) - mice provide support, but there are nochanges in resting metabolic rate (RMR) of mice. In vivo studies demonstrate increased ATP synthesis, but estimates of substrate oxidation rate indicate no change. Mice that greatly overexpress Ucp3 in muscle have increased RMR. Inconsistent with the function of uncoupling are the observations thatfasting results in increased expression of UCP3, but no change in muscle proton leak. Moreover, fasting decreases energy expenditure in muscle. Expression patterns for Ucp3 and lipid-metabolism genes support a physiological role in fatty acid oxidation. Overall, findings support a role for Ucp3 in fatty acid metabolism that may have implications for obesity and/or Type IIdiabetes.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 14/07/20 alle ore 03:51:35