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Titolo:
REGULATION OF THE 3RD MEMBER OF THE UNCOUPLING PROTEIN FAMILY, UCP3, BY COLD AND THYROID-HORMONE
Autore:
LARKIN S; MULL E; MIAO W; PITTNER R; ALBRANDT K; MOORE C; YOUNG A; DENARO M; BEAUMONT K;
Indirizzi:
AMYLIN PHARMACEUT INC,DEPT PHARMACOL,9373 TOWNE CTR DR SAN DIEGO CA 92121 AMYLIN PHARMACEUT INC,DEPT PHARMACOL SAN DIEGO CA 92121 AMYLIN PHARMACEUT INC,DEPT PHYSIOL SAN DIEGO CA 92121
Titolo Testata:
Biochemical and biophysical research communications
fascicolo: 1, volume: 240, anno: 1997,
pagine: 222 - 227
SICI:
0006-291X(1997)240:1<222:ROT3MO>2.0.ZU;2-0
Fonte:
ISI
Lingua:
ENG
Soggetto:
BROWN ADIPOSE-TISSUE; INDUCED THERMOGENESIS; SKELETAL-MUSCLE; MESSENGER-RNA; MITOCHONDRIA; ADIPOCYTES; METABOLISM; GENE; RATS; T3;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
37
Recensione:
Indirizzi per estratti:
Citazione:
S. Larkin et al., "REGULATION OF THE 3RD MEMBER OF THE UNCOUPLING PROTEIN FAMILY, UCP3, BY COLD AND THYROID-HORMONE", Biochemical and biophysical research communications, 240(1), 1997, pp. 222-227

Abstract

Uncoupling protein (UCP1) is a transmembrane proton transporter present in the mitochondria of brown adipose tissue (BAT), a specialized tissue which functions in temperature homeostasis and energy balance (Nicholls, D. G., and Locke, R. M. (1984) Physiol. Rev. 64, 2-40; Lowell,D. D., and Flier, J. S. (1997) Annu. Rev. Med.). UCP1 mediates the thermogenesis that is characteristic of BAT by uncoupling mitochondrial oxidation of substrates from ATP synthesis. Recently, two proteins related to UCP1 have been identified and designated UCP2 (Fleury, C., et al. (1997) Nature Genetics 15, 269-272) or UCP homolog (UCPH) (Gimeno,R. E., et al. (1997) Diabetes 46, 900-906) and UCP3 (Boss, O., et al. (1997) FEES Lett. 408, 39-42; Vidal-Puig, A., et al. (1997) Biochem. Biophys. Res. Commun. 235, 79-82). We investigated the regulation in rats of UCP3, which is expressed primarily in skeletal muscle and BAT. Expression of rat UCP3 mRNA in BAT was upregulated by in vivo treatment with triiodothyronine (T-3) and by exposure to cold, suggesting thatUCP3 is active in thermogenesis and energy expenditure. In skeletal muscle, UCP3 mRNA was also upregulated by T-3 but, surprisingly, not bycold exposure. A hypothesis is proposed to account for this differential regulation. (C) 1997 Academic Press.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/12/20 alle ore 16:36:26