1. Academic Validation
  2. Tumour necrosis factor-α inhibits hepatic lipid deposition through GSK-3β/β-catenin signaling in juvenile turbot (Scophthalmus maximus L.)

Tumour necrosis factor-α inhibits hepatic lipid deposition through GSK-3β/β-catenin signaling in juvenile turbot (Scophthalmus maximus L.)

  • Gen Comp Endocrinol. 2016 Mar 1;228:1-8. doi: 10.1016/j.ygcen.2015.12.027.
Dongwu Liu 1 Kangsen Mai 1 Yanjiao Zhang 1 Wei Xu 1 Qinghui Ai 2
Affiliations

Affiliations

  • 1 Key Laboratory of Aquaculture Nutrition and Feed (Ministry of Agriculture) and the Key Laboratory of Mariculture (Education Ministry of China), Ocean University of China, Qingdao 266003, PR China.
  • 2 Key Laboratory of Aquaculture Nutrition and Feed (Ministry of Agriculture) and the Key Laboratory of Mariculture (Education Ministry of China), Ocean University of China, Qingdao 266003, PR China. Electronic address: qhai@ouc.edu.cn.
Abstract

In this study, the mechanism that TNFα inhibits lipid deposition through GSK-3β/β-catenin signaling was investigated in the liver of juvenile turbot (Scophthalmus maximus L.) by injection of TNFα or TNFα inhibitor pomalidomide (POM). It was found that TNFα inhibited the expression of GSK-3β and induced β-catenin expression. TNFα inhibited the expression of Peroxisome Proliferator-activated Receptor γ (PPARγ) and CCAAT/enhancer binding protein α (C/EBPα), as well as the activity of lipoprotein Lipase (LPL) and fatty acid synthetase (FAS). In addition, the level of triglyceride (TG), total Cholesterol (TC), nonesterified fatty acid (NEFA), and glycerol was decreased by TNFα treatment in the liver. In the plasma, the level of TG, TC, low density lipoprotein Cholesterol (LDL-C), NEFA, and glycerol was decreased, but high density lipoprotein Cholesterol (HDL-C) was increased by TNFα treatment. However, compared to TNFα, POM had the opposite effect on the biochemical indexes and genes related to lipid deposition in the liver. The results indicated that TNFα may regulate hepatic lipid metabolism and fat distribution through GSK-3β/β-catenin signaling as well as transcription factors PPARγ and C/EBPα in juvenile turbot.

Keywords

GSK-3β; Juvenile turbot; Lipid deposition; Liver; Tumour necrosis factor-α; β-Catenin.

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