UCP1 deficiency causes brown fat respiratory chain depletion and sensitizes mitochondria to calcium overload-induced dysfunction

Abstract

Significance We describe a physiological role for uncoupling protein 1 (UCP1) in the regulation of reactive oxygen species. Notably, the molecular differences between brown fat mitochondria from wild-type and UCP1 knockout (UCP1-KO) mice extend substantially beyond the deletion of UCP1 itself. Thus, caution must be taken when attributing a brown fat phenotype solely to UCP1 deletion when these animals are used. Given the wide utilization of the UCP1-KO mouse model, these data are of critical importance for the scientific communities studying obesity, thermogenesis and energy metabolism, and mitochondrial biology.