Lipolysis in Brown Adipocytes Is Not Essential for Cold-Induced Thermogenesis in Mice

Publication date: 7 November 2017
Source:Cell Metabolism, Volume 26, Issue 5
Author(s): Hyunsu Shin, Yinyan Ma, Tatyana Chanturiya, Qiang Cao, Youlin Wang, Anil K.G. Kadegowda, Rachel Jackson, Dominic Rumore, Bingzhong Xue, Hang Shi, Oksana Gavrilova, Liqing Yu
Lipid droplet (LD) lipolysis in brown adipose tissue (BAT) is generally considered to be required for cold-induced nonshivering thermogenesis. Here, we show that mice lacking BAT Comparative Gene Identification-58 (CGI-58), a lipolytic activator essential for the stimulated LD lipolysis, have normal thermogenic capacity and are not cold sensitive. Relative to littermate controls, these animals had higher body temperatures when they were provided food during cold exposure. The increase in body temperature in the fed, cold-exposed knockout mice was associated with increased energy expenditure and with increased sympathetic innervation and browning of white adipose tissue (WAT). Mice lacking CGI-58 in both BAT and WAT were cold sensitive, but only in the fasted state. Thus, LD lipolysis in BAT is not essential for cold-induced nonshivering thermogenesis in vivo. Rather, CGI-58-dependent LD lipolysis in BAT regulates WAT thermogenesis, and our data uncover an essential role of WAT lipolysis in fueling thermogenesis during fasting.

Graphical abstract

Teaser

Lipolysis in brown fat is generally considered to be required for cold-induced thermogenesis. Shin et al. show that mice defective in brown fat lipolysis are not cold sensitive. These animals compensate for the defect by increasing white fat browning and combustion of fuels derived from diet or white fat lipolysis.


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