Ablation of Sam68 in adult mice increases thermogenesis and energy expenditure

成年小鼠中 Sam68 的消融可增加产热作用和能量消耗

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作者:Aijun Qiao, Wenxia Ma, Jianxin Deng, Junlan Zhou, Chaoshan Han, Eric Zhang, Chan Boriboun, Shiyue Xu, Chunxiang Zhang, Chunfa Jie, Jeong-A Kim, Kirk M Habegger, Hongyu Qiu, Ting C Zhao, Jianyi Zhang, Gangjian Qin

Abstract

Genetic deletion of Src associated in mitosis of 68kDa (Sam68), a pleiotropic adaptor protein prevents high-fat diet-induced weight gain and insulin resistance. To clarify the role of Sam68 in energy metabolism in the adult stage, we generated an inducible Sam68 knockout mice. Knockout of Sam68 was induced at the age of 7-10 weeks, and then we examined the metabolic profiles of the mice. Sam68 knockout mice gained less body weight over time and at 34 or 36 weeks old, had smaller fat mass without changes in food intake and absorption efficiency. Deletion of Sam68 in mice elevated thermogenesis, increased energy expenditure, and attenuated core-temperature drop during acute cold exposure. Furthermore, we examined younger Sam68 knockout mice at 11 weeks old before their body weights deviate, and confirmed increased energy expenditure and thermogenic gene program. Thus, Sam68 is essential for the control of adipose thermogenesis and energy homeostasis in the adult.

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