作者: J. Enrique Silva
DOI: 10.1002/1098-2299(200010)51:2<112::AID-DDR6>3.0.CO;2-Z
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摘要: The recently cloned uncoupling proteins 2 and 3 (UCP2, UCP3) cDNAs encode for with 57-59% homology brown adipose tissue protein (UCP1). As this latter, the novel UCPs can reduce proton motive force across inner membrane of mitochondria, but whether or not they function as uncouplers under physiological conditions has been unequivocally confirmed. Low resting energy expenditure difficulty oxidizing fat are potential risk factors development obesity, could potentially be affected by UCPs. However, studies largely focused on gene expression regulation do support a role level these in determining balance. Overall, information available suggests more complexity than anticipated many observations hard to reconcile simple dissipation. possibility that proteins, particularly ubiquitous UCP2, have unsuspected functions, some them cell-specific, remains open. One such reduction formation reactive oxygen species during mitochondrial respiration. It is necessary define cell how their activity regulated. Only when will we position determine targets pharmacological intervention treatment prevention perhaps influence other metabolic processes.