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Expression of uncoupling protein 1 in skeletal muscle decreases muscle energy efficiency and affects thermoregulation and substrate oxidation

¹ German Institute of Human Nutrition Potsdam-Rehbruecke, Group of Energy Metabolism, Nuthetal, Germany
² DeveloGen AG, Göttingen, Germany

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 (EE), resistance to diet-induced obesity, and improved glucose tolerance. Here, we 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 30°C for both wild-type (WT) and transgenic mice. EE, body temperature (T_b), activity, and respiratory quotient (RQ) were then measured over 24 h at ambient temperatures (T_a) of 30, 22, and 5°C. HSA-mUCP1 transgenic mice showed increased activity-related EE and heat loss but similar basal metabolic rate compared with WT. T_b at resting periods was progressively decreased with declining T_a in HSA-mUCP1 transgenic mice but not in WT. Compared with WT littermates, the transgenic HSA-mUCP1 mice displayed increased RQ levels during night time, indicative of increased overall glucose oxidation, and failed to decrease their RQ levels with declining T_a. Thus increased EE 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 T_as below thermoneutrality, this puts increasing energy demands on the animals, whereas at thermoneutrality most differences in energy metabolism are not apparent any more.

mitochondrial uncoupling; brown adipose tissue; skeletal muscle metabolism; thermal conductance

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