Response of g6p homologous genes in Chinese perch to high-carbohydrate diets

• Main Authors: Yanpeng Zhang, Zhen Zhang, Xu-Fang Liang, Shan He, Ling Li, Jing Xu, Jiao Li, Muhammad Shoaib Alam
• Format: Article
• Language: English
• Published: Elsevier 2021-03-01
• Series: Aquaculture Reports
• Subjects: g6p homologous genes; DNA methylation; High-carbohydrate diets; Glucose metabolism; Gene expression
• Online Access: http://www.sciencedirect.com/science/article/pii/S2352513420306748

Glucose-6-phosphatase (g6p) plays a crucial role in glucose homeostasis by completing the final step of gluconeogenesis in mammals. Multiple g6p homologous genes were identified in fish due to whole genome replication. However, the g6p homologous genes closely related to glucose metabolism have not been systematically screened and the DNA methylation of g6p homologous genes induced by dietary carbohydrates is also poorly explored in fish. In this study, g6p homologous genes from different species were compared and analyzed. The tissue expression profiles of g6p homologous genes were identified. Then, two diets with different starch levels (0%, 20 %) were fed to Chinese perch for 8 weeks to evaluate the relative mRNA levels and DNA methylation levels of g6p homologous genes in liver. Results showed that g6pcb2 was lost in genome of Chinese perch. g6pca and g6pcb1 were mainly expressed in liver. g6pc2 and g6pc3 showed extremely low expression levels in liver. Moreover, compared with 0% starch group, 20 % starch group exhibited the significant decrease in relative mRNA levels of g6pca and g6pcb1, no difference in relative mRNA levels of g6pc2 and g6pc3, and the significant increase in DNA methylation of g6pca. Our results suggested that g6pca and g6pcb1 might coordinate to regulate the gluconeogenesis pathway and high-carbohydrate diet might up-regulate the DNA methylation level of g6pca to inhibit the mRNA expression level of g6pca, thereby down-regulating the gluconeogenesis pathway. g6pc2 and g6pc3 might not be related to the post meal regulation of glucose metabolism.