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Bile acid supplementation decreases body mass gain in C57BL/6J but not 129S6/SvEvTac mice without increasing energy expenditure

机译:补充胆汁酸可降低C57BL / 6J的体重增加但不会降低129S6 / SvEvTac小鼠的体重而不会增加能量消耗

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摘要

Supplementation of cholate to a high fat diet can protect mice from diet-induced, increased body mass gain. It has been hypothesized that uncoupling protein 1 dependent, non-shivering thermogenesis in brown adipocytes provides the mechanism of increased energy expenditure to counteract excessive energy intake. We scrutinized this conjecture in wildtype mice and mice genetically devoid of a functional uncoupling protein 1 gene (C57BL/6J) as well as mice of the 129S6/SvEvTac strain that, in comparison, display an extraordinary capacity to recruit ectopic brown adipocytes. Protection from diet-induced, increased body mass gain by cholate supplementation was absent in 129S6/SvEvTac mice, a consequence of much lower bile acid absorption and spillover in this strain. Conversely, Ucp1-KO mice did not differ from C57BL/6J wildtype controls in any parameter assessed. Daily energy expenditure and resting metabolic rate of C57BL/6J mice remained unaffected by cholate supplementation. We conclude that protection of mice from diet-induced, increased body mass gain by cholate supplementation depends on the specific genetic background of C57BL/6J mice, does not involve increased energy expenditure and is independent of uncoupling protein 1 dependent non-shivering thermogenesis.
机译:在高脂饮食中补充胆酸盐可以保护小鼠免受饮食诱导的体重增加。已经假设,解耦棕色脂肪细胞中依赖蛋白1的,非颤抖的生热作用提供了增加能量消耗以抵消过多能量摄入的机制。我们在野生型小鼠和遗传上缺乏功能性解偶联蛋白1基因(C57BL / 6J)的小鼠以及129S6 / SvEvTac菌株的小鼠中仔细检查了这个猜想,相比之下,它们显示出异常的募集异位棕色脂肪细胞的能力。 129S6 / SvEvTac小鼠缺乏通过饮食补充胆固醇引起的饮食诱导的体重增加的保护,这是该菌株中胆汁酸吸收和溢出低得多的结果。相反,Ucp1-KO小鼠在任何评估参数方面均与C57BL / 6J野生型对照无差异。 C57BL / 6J小鼠的每日能量消耗和静息代谢率不受补充胆酸盐的影响。我们得出的结论是,通过添加胆酸盐来保护小鼠免受饮食诱导的体重增加的依赖取决于C57BL / 6J小鼠的具体遗传背景,不涉及能量消耗的增加,并且独立于解偶联蛋白1的非颤抖生热作用。

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