Oral Presentation The Annual Scientific Meeting of the Endocrine Society of Australia and the Society for Reproductive Biology 2013

Adaptive thermogenesis in models of diet-induced obesity and genetic obesity (#201)

Rachael Loughnan 1 , Iain J Clarke , Belinda A Henry
  1. Monash University, Clayton, Vic, Australia

Adaptive thermogenesis is one component of energy expenditure. We aimed to characterize the effects on thermogenesis of altered adiposity, caused by either diet-manipulation or genetic selection. Female sheep were meal-fed to entrain post-prandial thermogenesis and dataloggers were used to measure temperature in retroperitioneal and sternal adipose tissue and skeletal muscle. Dietary manipulation was used to produce either obese (79±3.7kg) or lean (32±1.5Kg) ovariectomised ewes (5/group). In lean animals, thermogenesis was reduced in skeletal muscle (P=0.002), sternal fat (P=0.01) and (P<0.05) retroperitoneal fat. Tissue temperatures were similar in the normal and obese animals. In the muscle of lean animals, reduced thermogenesis was associated with lowered uncoupling protein (UCP) 1 and UCP3 gene expression, as well as altered mitochondrial function with a reduction in uncoupled respiration and total respiratory capacity. Sarco/endoplasmic reticulum calcium-dependent ATPase (SERCA1) was also lowered indicating impaired calcium cycling. In contrast to the result in muscle, UCP3 expression in the sternal fat was higher (P<0.01) in lean sheep. There was no effect of altered adiposity on expression of other UCP in retroperitoneal and sternal fat. In genetically lean and obese ewes (5-6/group), we measured post-prandial thermogenesis in muscle and retroperitoneal fat. Thermogenesis was significantly (P=0.01) lower in the retroperitoneal fat of genetically fat animals than in genetically lean animals and this was associated with parallel changes in UCP1 expression (P=0.028). Thermogenic profiles and UCP gene expression in skeletal muscle were similar in genetically lean and obese animals.

We conclude that reduced adiposity caused by food-restriction, reduces thermogenesis, which may be a compensatory mechanism. Conversely, reduced UCP1 expression and reduced thermogenesis in genetically fat animals may contribute to their increased adiposity in animals genetically predisposed to obesity. Thus, alterations in adiposity that occur by either dietary manipulation or genetic selection are accompanied by adaptive changes in thermogenesis.