Leptin expression in mandarin fish Siniperca chuatsi (Basilewsky): Regulation by postprandial and short-term fasting treatment

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• 作者：Xiaochen Yuan^a ; ^b ; ¹ ; Aixuan Li^a ; ^b ; ¹ ; Xu-Fang Liang^a ; ^b ; ^{xufang_liang@hotmail.com" class="auth_mail" title="E-mail the corresponding author} ; Wei Huang^a ; ^b ; Yi Song^a ; ^b ; Shan He^a ; ^b ; Wenjing Cai^a ; ^b ; Ya-xiong Tao^c
• 关键词：Gene structure ; Intron loss ; Tissue expression ; Postprandial ; Energy regulation
• 刊名：Comparative Biochemistry and Physiology - Part A: Molecular & Integrative Physiology
• 出版年：2016
• 出版时间：April 2016
• 年：2016
• 卷：194
• 期：Complete
• 页码：8-18
• 全文大小：2086 K

文摘

Most fish species possess duplicate leptin genes (LEP). Mandarin fish (Siniperca chuatsi) leptin A gene (sLEP-A) have been cloned in the previous study. In the present study, we cloned and characterized leptin B gene (sLEP-B) in mandarin fish, including a 471 bp open reading frame (ORF) encoding a 158-amino acid protein. The three-dimensional (3D) structural model of sLEP-B protein showed a highly conserved of tertiary structure similar to that of other vertebrates. Genomic sequencing results indicated that sLEP-B possessed only one intron. This is the first report of the loss of an intron in LEP-B in Perciformes. The different distribution patterns of sLEPs suggest different physiological roles of these two genes. The presence of HNF3β, a liver-enriched transcription factor, only in sLEP-A indicated abundant expression and metabolic function of sLEP-A in the liver. In an in vivo experiment, the expressions of brain sLEP-A and sLEP-B were observed to increase after a meal. During the short-term fasting, the expressions of sLEPs in mandarin fish brain were decreased significantly. A persistent and significant increase in hepatic sLEP-A expression supported a relationship between leptin and food intake in mandarin fish. These results suggest that sLEP-A plays an important role in the regulation of energy homeostasis in this carnivorous fish, and sLEP-B is probably a specialized gene responsible for the central nervous system (CNS) control of energy regulation.