Key result
UCP3 deletion prevented increased cardiac O2 consumption and improved cardiac efficiency in high fat-fed mice, but did not mediate mitochondrial uncoupling in leptin-deficient states.
Population
UCP3 knockout (UCP3KO) and wild-type (WT) mice, as well as ob/ob mice lacking UCP3 (U3OB mice) and ob/ob mice
Comparison
High fat diet for 10 weeks or UCP3 deletion in… vs Normal chow diet or ob/ob mice with intact UCP3
Design
Preclinical
Follow-up
10 weeks
Authors
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UCP3 effects on cardiac efficiency are model-specific; hypothesis-generating for selective targeting and leaves open distinct mechanisms in diet vs genetic obesity.
UCP3 mediates mitochondrial uncoupling and reduced cardiac efficiency after high-fat feeding, but does not mediate uncoupling in leptin-deficient states.
Boudina et al. (2012) studied High fat diet-induced obesity and leptin deficiency. UCP3 deletion and high-fat diet vs. Wild-type mice and normal chow was evaluated on Cardiac O2 consumption (MVO2), cardiac efficiency (CE), and mitochondrial uncoupling. UCP3 deletion prevented increased cardiac O2 consumption and improved cardiac efficiency in high fat-fed mice, but did not mediate mitochondrial uncoupling in leptin-deficient states.
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