Stanniocalcin2 acts as an anorectic factor through activation of STAT3 pathway
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Yang Jiao1,*, Jiejie Zhao1,*, Guojun Shi1,*, Xing Liu2, Xuelian Xiong2, Xiaoying Li1,2, Huijie Zhang3, Qinyun Ma1 and Yan Lu1,2
1Department of Endocrine and Metabolic Diseases, Shanghai Clinical Center for Endocrine and Metabolic Diseases, Shanghai Institute of Endocrinology and Metabolism, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China
2Department of Endocrinology, Fudan Institute for Metabolic Diseases, Zhongshan Hospital, Fudan University, Shanghai 200032, China
3Department of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China
*These authors contributed equally to this work
Qinyun Ma, email: email@example.com
Yan Lu, email: firstname.lastname@example.org
Keywords: appetite, body weight, stanniocalcin 2, STAT3
Received: January 26, 2017 Accepted: July 12, 2017 Published: July 20, 2017
The regulation of food intake and body weight has been hotly investigated. In the present study, we show that stanniocalcin2 (STC2), a cytokine ubiquitously expressed and especially upregulated in many types of human cancers, has a regulatory role in food intake and weight loss. Systemic treatment of C57BL/6 mice with recombinant STC2 protein resulted in decreased food intake and body weight, whereas energy expenditure was not affected. Similarly, STC2 treatment also induced anorexia in hyperphagic leptin-deficient mice, leading to a significant reduction in body weight and improvement of blood glucose levels. Furthermore, intracerebroventricular administration of STC2 to mice led to an acute decrease in food intake, which was mediated, at least in part, by activation of STAT3 pathway. Taken together, our results revealed the importance of STC2 in the regulation of feeding behavior as well as body weight.
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