Uncoupling protein homologs: emerging views of physiological function.
J Nutr
; 130(4): 711-4, 2000 Apr.
Article
en En
| MEDLINE
| ID: mdl-10736318
ABSTRACT
The widespread occurrence of excess weight and related diseases demands that efforts be made to understand energy expenditure from the gene to the whole animal. For some time, it has been understood that mitochondrial oxidation of fuels generates an electrochemical gradient via outward pumping of protons by the electron transport chain. ATP production via F(1)F(0) ATP synthase is then facilitated by the inward flux of protons down the gradient. There is a growing appreciation that a significant portion of the metabolic rate of endotherms is attributable to counteracting "proton leak" (uncoupling), wherein a flux of protons down the electrochemical gradient generates heat independently of ATP production. Proton leak is especially apparent in thermogenic brown adipose tissue, which expresses a tissue-specific uncoupling protein (UCP1). The recent discovery of widely expressed putative UCP1 homologs [UCP2, UCP3, UCP4, UCP5/brain mitochondrial carrier protein-1 (BMCP1)] raised the possibility that innate proton leak and metabolic rate are regulated by UCP1-like proteins. On the basis of current published data, one may not exclude the possibility that UCP homologs influence metabolic rate.
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Base de datos:
MEDLINE
Asunto principal:
Proteínas Portadoras
/
Proteínas de la Membrana
Tipo de estudio:
Prognostic_studies
Idioma:
En
Revista:
J Nutr
Año:
2000
Tipo del documento:
Article