International Journal of Biological Sciences

Impact factor
3.873

ISSN 1449-2288

News feeds of IJBS published articles
My Manuscript
My Account

Journal of Biomedicinenew

Theranostics

International Journal of Medical Sciences

Journal of Cancer

Oncomedicine

Journal of Genomics

Journal of Bone and Joint Infection (JBJI)

Nanotheranostics

Journal of Genomics now in PubMed/PubMed Central. Submit manuscript...

PubMed Central Indexed in Journal Impact Factor

Int J Biol Sci 2016; 12(12):1544-1554. doi:10.7150/ijbs.16612

Research Paper

Signal transduction mechanism for glucagon-induced leptin gene expression in goldfish liver

Ai-fen Yan1, Ting Chen2,3,✉, Shuang Chen4, Dong-sheng Tang1, Fang Liu1, Xiao Jiang2, Wen Huang2, Chun-hua Ren2,3, Chao-qun Hu2,3

1. School of stomatology and medicine, Foshan University, Foshan 528000, China.
2. CAS Key Laboratory of Tropical Marine Bio-resources and Ecology (LMB)
Guangdong Provincial Key Laboratory of Applied Marine Biology (LAMB), South China Sea Institute of Oceanology, Chinese Academy of Sciences, Guangzhou 510301, China.
3. South China Sea Bio-Resource Exploitation and Utilization Collaborative Innovation Center, Guangzhou 510275, China.
4. School of Biomedical Sciences, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong, China.

Abstract

Leptin is a peripheral satiety hormone that also plays important roles in energy homeostasis in vertebrates ranging from fish to mammals. In teleost fish, however, the regulatory mechanism for leptin gene expression still remains unclear. In this study, we found that glucagon, a key hormone in glucose homeostasis, was effective at elevating the leptin-AI and leptin-AII transcript levels in goldfish liver via both in vivo intraperitoneal injection and in vitro cells incubation approaches. The responses of leptin-AI and leptin-AII mRNA to glucagon treatment were highly comparable. In contrast, blockade of local glucagon action could reduce the basal and induced leptin-AI and leptin-AII mRNA expression. The stimulation of leptin levels by glucagon was caused by the activation of adenylate cyclase (AC)/cyclic-AMP (cAMP)/ protein kinase A (PKA), and probably cAMP response element-binding protein (CREB) cascades. Our study described the effect and signal transduction mechanism of glucagon on leptin gene expression in goldfish liver, and may also provide new insight into leptin as a mediator in the regulatory network of energy metabolism in the fish model.

Keywords: leptin, glucagon, gene expression, signal transduction, goldfish.

This is an open access article distributed under the terms of the Creative Commons Attribution (CC BY-NC) License. See http://ivyspring.com/terms for full terms and conditions.
How to cite this article:
Yan Af, Chen T, Chen S, Tang Ds, Liu F, Jiang X, Huang W, Ren Ch, Hu Cq. Signal transduction mechanism for glucagon-induced leptin gene expression in goldfish liver. Int J Biol Sci 2016; 12(12):1544-1554. doi:10.7150/ijbs.16612. Available from http://www.ijbs.com/v12p1544.htm