抄録
Brown adipose tissue is a thermogenic organ and plays important roles in maintenance of energy balance and body temperature. α1 adrenoceptor activation elicits IP3-induced Ca2+ release and store-operated Ca2+ entry (SOC) from the ER, while β3-receptor activity activates lipolysis and uncoupling proteins in mitochondria, producing heat. Uncoupling of mitochondrial respiration by FCCP activates mitochondrial Ca2+ release, non- SOC Ca2+ entry, Ca2+ release from the ER and SOC. We have studied how bile acid intake prevents obesity in high fat-fed mice. Changes in intracellular Ca2+ ([Ca2+]i), mitochondrial membrane potential and heat production were recorded by fluorometry and thermography. Mice were fed with high fat diet, high fat diet with cholic acids and chow for 7-9 weeks. Cholic acids diets prevented increases in body weight, white adipose tissue and whitish changes in brown adipose tissue caused by high fat diet. Cholic acids-fed mice showed greater FCCP-, noradrenaline- and isoprenaline-induced rises in [Ca2+]i in brown adipocytes than high fat diet- or chow-fed mice and produced smaller mitochondrial depolarization accompanying the initial rise in [Ca2+]i and greater heat production from brown adipose tissues. Thus, cholic acid intake prevents high fat diet-induced obesity by increasing energy expenditure as the result of increased responses of brown adipose tissues to sympathetic nerve activity. [J Physiol Sci. 2007;57 Suppl:S132]
