Effects of insulin and its related signaling pathways on lipid metabolism in the yellow catfish Pelteobagrus fulvidraco.

J Exp Biol

Key Laboratory of Freshwater Animal Breeding, Ministry of Agriculture of PRC, Fishery College, Huazhong Agricultural University, Wuhan 430070, China Freshwater Aquaculture Collaborative Innovative Centre of Hubei Province, Wuhan 430070, China.

Published: October 2015

AI Article Synopsis

  • - The study investigates how insulin affects lipid metabolism in yellow catfish (Pelteobagrus fulvidraco), focusing on hepatic lipid accumulation and the activity of key enzymes and transcription factors involved in this process.
  • - Insulin seems to boost liver lipid levels and increase lipogenic enzyme activity, particularly affecting mRNA levels of PPARα and PPARγ, while also showing that specific activators and inhibitors can modulate these insulin effects via different signaling pathways.
  • - The findings enhance our understanding of insulin's role in fish hepatic metabolism, highlighting the involvement of PPARα and PPARγ pathways in regulating lipid accumulation influenced by insulin.

Article Abstract

The influence of insulin on hepatic metabolism in fish is not well understood. The present study was therefore conducted to investigate the effects of insulin on lipid metabolism, and the related signaling pathways, in the yellow catfish Pelteobagrus fulvidraco. Hepatic lipid and intracellular triglyceride (TG) content, the activity and expression levels of several enzymes and the mRNA expression of transcription factors (PPARα and PPARγ) involved in lipid metabolism were determined. Troglitazone, GW6471, fenofibrate and wortmannin were used to explore the signaling pathways by which insulin influences lipid metabolism. Insulin tended to increase hepatic lipid accumulation, the activity of lipogenic enzymes (6PGD, G6PD, ME, ICDH and FAS) and mRNA levels of FAS, G6PD, 6PGD, CPT IA and PPARγ, but down-regulated PPARα mRNA level. The insulin-induced effect could be stimulated by the specific PPARγ activator troglitazone or reversed by the PI3 kinase/Akt inhibitor wortmannin, demonstrating that signaling pathways of PPARγ and PI3 kinase/Akt were involved in the insulin-induced alteration of lipid metabolism. The specific PPARα pathway activator fenofibrate reduced insulin-induced TG accumulation, down-regulated the mRNA levels of FAS, G6PD and 6PGD, and up-regulated mRNA levels of CPT IA, PPARα and PPARγ. The specific PPARα pathway inhibitor GW6471 reduced insulin-induced changes in the expression of all the tested genes, indicating that PPARα mediated the insulin-induced changes of lipid metabolism. The present results contribute new knowledge on the regulatory role of insulin in hepatic metabolism in fish.

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http://dx.doi.org/10.1242/jeb.124271DOI Listing

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