Ablation of Galectin-12 Results in Enhanced Lipolysis and Reduced Adiposity in Mice
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- Department of Dermatology, School of Medicine, University of California, Davis
- Mouse Biology Program, School of Veterinary Medicine, University of California, Davis
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- Received 06 May 2009 00:30 UTC; Posted 06 May 2009
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- Molecular Cell Biology
- Abstract:
Aside from leptin, galectin-12 is the only other gene exclusively expressed in mouse adipose tissue, suggesting an important role in energy homeostasis. The breakdown of triglycerides, or lipolysis, is a tightly controlled process to tailor fat mobilization according to the body’s energy status. Lipolysis is stimulated by hormones that signal energy demand, and suppressed the satiety hormone insulin. However, much still remains to be learned about the intracellular control of lipolytic signaling in adipocytes. Here we show that galectin-12 functions as an intrinsic negative regulator of lipolysis by modulating cyclic adenosine monophosphate (cAMP) levels. Galectin-12 deficiency reduced adiposity of mice on regular chow, alleviated obesity in old ob/ob mice, and accelerated fasting-induced fat mobilization in mice that had been fed a high-fat diet. This study identifies a critical intracellular function for galectin-12 in lipid metabolism that could have important implications for future research of galectins and human metabolic disorders.
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- This document is licensed to the public under the Creative Commons Attribution 3.0 License
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Yang, Ri-Yao, Yu, Lan, Hsu, Daniel, Lloyd, K. C. Kent, and Liu, Fu-Tong. Ablation of Galectin-12 Results in Enhanced Lipolysis and Reduced Adiposity in Mice. Available from Nature Precedings <http://hdl.handle.net/10101/npre.2009.3224.1> (2009)
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