Yan Ai-Fen, Chen Ting, Chen Shuang, Tang Dong-Sheng, Liu Fang, Jiang Xiao, Huang Wen, Ren Chun-Hua, Hu Chao-Qun
School of stomatology and medicine, Foshan University, Foshan 528000, China.
CAS Key Laboratory of Tropical Marine Bio-resources and Ecology (LMB); South China Sea Bio-Resource Exploitation and Utilization Collaborative Innovation Center, Guangzhou 510275, China.
Int J Biol Sci. 2016 Dec 6;12(12):1544-1554. doi: 10.7150/ijbs.16612. eCollection 2016.
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 -AI and -AII transcript levels in goldfish liver via both intraperitoneal injection and cells incubation approaches. The responses of -AI and -AII mRNA to glucagon treatment were highly comparable. In contrast, blockade of local glucagon action could reduce the basal and induced -AI and -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.
瘦素是一种外周饱腹感激素，在从鱼类到哺乳动物的脊椎动物的能量平衡中也起着重要作用。然而，在硬骨鱼中，瘦素基因表达的调控机制仍不清楚。在本研究中，我们发现胰高血糖素作为葡萄糖稳态中的关键激素，通过腹腔注射和细胞孵育两种方法，均能有效提高金鱼肝脏中-AI和-AII转录本水平。-AI和-AII mRNA对胰高血糖素处理的反应高度相似。相反，阻断局部胰高血糖素作用可降低基础和诱导的-AI和-AII mRNA表达。胰高血糖素对瘦素水平的刺激是由腺苷酸环化酶（AC）/环磷酸腺苷（cAMP）/蛋白激酶A（PKA），可能还有cAMP反应元件结合蛋白（CREB）级联反应的激活引起的。我们的研究描述了胰高血糖素对金鱼肝脏中瘦素基因表达的影响和信号转导机制，也可能为瘦素作为鱼类模型能量代谢调控网络中的介质提供新的见解。
