PI3KR1 and AKT1 in largemouth bass (Micropterus salmoides): molecular cloning, characterization, and its involvement in the alleviation of hepatic glycogen deposition caused by insulin inclusion in vitro.
Autor: | Li Y; International Research Centre for Food and Health, College of Food Science and Technology, Shanghai Ocean University, Shanghai, 201306, China., Chen S; Research Centre of the Ministry of Agriculture and Rural Affairs On Environmental Ecology and Fish Nutrition, Shanghai Ocean University, Shanghai, 201306, China., Liu Y; Research Centre of the Ministry of Agriculture and Rural Affairs On Environmental Ecology and Fish Nutrition, Shanghai Ocean University, Shanghai, 201306, China., Liu P; International Research Centre for Food and Health, College of Food Science and Technology, Shanghai Ocean University, Shanghai, 201306, China., Li S; Research Centre of the Ministry of Agriculture and Rural Affairs On Environmental Ecology and Fish Nutrition, Shanghai Ocean University, Shanghai, 201306, China. slli@shou.edu.cn., Liu N; International Research Centre for Food and Health, College of Food Science and Technology, Shanghai Ocean University, Shanghai, 201306, China. nliu@shou.edu.cn.; Marine Biomedical Science and Technology Innovation Platform of Lin-Gang Special Area, Shanghai, 201306, China. nliu@shou.edu.cn.; Shanghai Engineering Research Center of Aquatic-Product Processing & Preservation, Shanghai, 201306, China. nliu@shou.edu.cn. |
---|---|
Jazyk: | angličtina |
Zdroj: | Fish physiology and biochemistry [Fish Physiol Biochem] 2024 Dec; Vol. 50 (6), pp. 2373-2388. Date of Electronic Publication: 2024 Aug 16. |
DOI: | 10.1007/s10695-024-01379-6 |
Abstrakt: | In this study, the full-length cDNA sequences of the phosphatidylinositol-3-kinase p85 alpha (PI3KR1) and serine/threonine kinase 1 (AKT1) genes in largemouth bass (Micropterus salmoides) were obtained using the rapid amplification of cDNA ends (RACE) method. Sequence analysis revealed that the cloned sequences of PI3KR1 and AKT1 are 4170 bp and 3672 bp in length, with open reading frames (ORFs) of 1389 bp and 1422 bp encoding 462 and 473 amino acids, respectively. Sequence alignment and evolutionary tree analysis indicated their close relationship to other teleosts, especially those with similar feeding habits. Tissue distribution demonstrated widespread distribution of both genes in various tissues, with the highest abundance in the liver. Further results found that the upregulation of the expression of p-PI3KR1, p-AKT1, p-FoxO1, and GLUT2 proteins by insulin, while suppressing the expression of the total FoxO1 protein, effectively triggers a significant activation of the PI3KR1-AKT1 insulin signaling pathway. Meanwhile, the mRNA levels of the key glycolytic genes, including glucokinase (gk), pyruvate kinase (pk), and phosphofructokinase liver type (pfkl), have been enhanced evidently. In contrast, the expression of gluconeogenic genes such as phosphoenolpyruvate carboxykinase (pepck), glucose-6-phosphatase catalytic subunit (g6pc), and fructose-1,6-bisphosphatase-1 (fbp1) has been notably down-regulated. In addition, insulin treatment promoted the phosphorylation of glycogen phosphorylase (PYGL) and the dephosphorylation of glycogen synthase (GS), and the glycogen content in the insulin-treated group was remarkably reduced compared to the control group. Overall, our study indicates that the activation of PI3KR1-AKT1 insulin signaling pathway represses the hepatic glycogen deposition via the regulation of glycolysis and gluconeogenesis, which provides some new insights into nutritional strategy to effectively regulate the glucose metabolism in carnivorous fish. Competing Interests: Declarations Ethics approval The animal study was reviewed and approved by the Animal Care and Use Committee of the Shanghai Ocean University. Consent for publication All authors review and approve the manuscript for publication. Competing interests The authors declare no competing interests. (© 2024. The Author(s), under exclusive licence to Springer Nature B.V.) |
Databáze: | MEDLINE |
Externí odkaz: |