The protective role of conjugated linoleic acid in excessive hepatic lipid deposition in juvenile black seabream (Acanthopagrus schlegelii) fed a high-fat diet

To investigate the regulatory pathways by which dietary conjugated linoleic acid (CLA) alleviates hepatic lipid deposition, endoplasmic reticulum stress (ERS), inflammatory response and apoptosis in marine fish. In vivo and in vitro high fat diet (HFD) models were constructed using black seabream ( Acanthopagrus schlegelii ). In vivo study, an eight-week feeding experiment was conducted in A. schlegelii with an initial weight of 1.25 ± 0.10 g. Three experimental diets were used: a control normal fat diet (Control), a high-fat diet (HFD), and an HFD containing 1.37 % CLA (HFD+CLA). Results showed that hepatic lipid content significantly decreased, and liver staining analysis showed a decline in the vacuolization area of lipid droplets and an increase in nuclear crumpling in the HFD+CLA, preliminarily suggesting that CLA could reduce HFD-induced hepatic lipid deposition in A. schlegelii . HFD+CLA inhibited hepatic lipid deposition by activating peroxisome proliferators-activated receptors ( pparα ) expression and inducing it to undergo nuclear translocation, which then up-regulated lipolysis-related genes and protein expression, while downregulating lipogensis-related genes and protein expression. Meanwhile, CLA alleviated ERS by downregulating ER marker genes, thereby reducing ER swelling and irregular distribution. CLA supplementation significantly decreased the expression of nuclear factor kappa-B ( nf-κb ), inhibited its nuclear translocation and suppressed the expression of related pro-inflammatory factors, thereby alleviating HFD-induced hepatic inflammatory response. HFD+CLA significantly inhibited the expression of c-Jun N-terminal kinase ( jnk ), thereby dampening the expression of pro-apoptotic factors in the downstream pathway and reducing the rate of hepatocyte apoptosis. In vitro HFD model, CLA can activate the expression of Pparα, relieve fat deposition, and slow down the inflammatory and apoptosis of hepatocytes by inhibiting the expression of Nf-κb p65 and Jnk. In sum, the study showed that CLA supplementation can serve as a feed additive to alleviate excessive hepatic lipid deposition in HFD-fed A. schlegelii by regulating the activation of the Pparα/ Sterol-regulatory element binding proteins (Srebp-1c) pathway, and attenuate inflammatory via inhibition of the Nf-kb and Jnk pathways. • Conjugated linoleic acid (CLA) supplementation reduces lipid accumulation in liver/hepatocyte. • CLA regulates lipid metabolism by activation of Pparα/Srebp-1c pathway. • CLA alleviate ERS by reducing swelling and irregular distribution of ER. • CLA relieves inflammatory and apoptosis by the inhibition of the Nf-κb and Jnk pathways.