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1 Group of Energy Metabolism, German Institute of Human Nutrition Potsdam-Rehbruecke, Nuthetal, Germany
2 DeveloGen AG, Gottingen, Germany
* To whom correspondence should be addressed. E-mail: klaus{at}mail.dife.de.
Skeletal muscle uncoupling by ectopic expression of mitochondrial uncoupling protein 1 (UCP1) has been shown to result in a lean phenotype in mice characterized by increased energy expenditure, resistance to diet induced obesity and improved glucose tolerance . Here we have investigated in detail the effect of ectopic UCP1 expression in skeletal muscle on thermoregulation and energy homeostasis in HSA-mUCP1 transgenic mice. Thermoneutrality was determined to be around 30°C for both wild-type (WT) and transgenic mice. Energy expenditure (EE), body temperature (Tb), activity and respiratory quotient (RQ) were then measured over 24h at ambient temperatures (Ta) of 30, 22 and 5°C. HSA-mUCP1 transgenic mice showed increased activity related energy expenditure (AEE) and heat loss, but similar basal metabolic rate as compared to WT. Tb at resting periods was progressively decreased with declining Ta in HSA-mUCP1 transgenic mice but not in WT. Compared to wild-type littermates the transgenic HSA-mUCP1mice displayed increased RQ levels during night time, indicative of increased overall glucose oxidation, and failed to decrease their RQ levels with declining Ta. Thus increased energy expenditure caused by skeletal muscle uncoupling is clearly due to a decreased muscle energy efficiency during activity combined with increased glucose oxidation and a compromised thermoregulation associated with increased overall heat loss. At ambient temperatures below thermoneutrality this puts increasing energy demands on the animals, whereas at thermoneutrality most differences in energy metabolism are not apparent any more.
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