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Submitted on September 22, 2005
Accepted on January 30, 2006
Pennington Biomedical Research Center, Louisiana State University, 6400 Perkins Road., Baton Rouge, Louisiana, 70808, USA
* To whom correspondence should be addressed. E-mail: kozaklp{at}pbrc.edu.
We investigated the role of leptin in regulating energy metabolism through induction of UCP1-based brown fat thermogenesis by comparing phenotypes of energy balance in ob/ob and double mutant ob/ob.Ucp1-/- mice. Measurements of adiposity and lean body mass (NMR), energy expenditure (indirect calorimetry), body weight, food intake and core body temperature were determined in the two mutant stocks of 3-month-old mice maintained at an initial ambient temperature of 28°C for 21 days, then at 21°C for 16 days and finally with leptin administration for 8 days at 21°C. No phenotypic differences between ob/ob and ob/ob.Ucp1-/- mice were detected suggesting that UCP1-based thermogenesis is not essential for the regulation of adiposity in ob/ob mice at temperatures between 21 and 28°C. Although both Ucp1-/- and ob/ob mice can survive in extreme cold at 4°C, provided they are adapted to the cold by gradually lowering ambient temperature, ob/ob.Ucp1-/- mice could not adapt and survive at temperatures <12°C, unless they were administered leptin. As the ambient temperature was reduced from 20 to 16°C ob/ob.Ucp1-/- mice treated with leptin have elevated levels of circulating T3 that correlate with elevated SERCA 2a mRNA levels in gastrocnemius muscle. Furthermore, ob/ob.Ucp1-/- mice, treated with T3, were able to maintain body temperature and stimulate SERCA 2a expression when the ambient temperature was gradually reduced to 4°C. Thus, in the absence of UCP1, leptin-induced thermogenesis protects body temperature in part through its action on the thyroid hormone axis.
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