Abstract

Our previous research found that excessive accumulation of adipose tissue is an important factor that reduces fish tolerance and utilization of high-energy feeds and limits the development of high-energy feeds in the aquaculture industry. However, the pathological characteristics and molecular mechanisms of fish adipose tissue remodeling caused by high-energy diet were still unclear. In this study, using histopathological observation, we found that restricted adipocyte hyperplasia, adipocyte hypertrophy, inflammation, and fibrosis are the main characteristics of pathological remodeling of fish adipose tissue induced by high-fat diet (HFD) and high-carbohydrate diet (HCD). Besides, this study further analyzed the molecular mechanisms and key marker proteins invovled in pathological remodeling of adipose tissue induced by HFD and HCD through comparative proteomics. The results found: (1) Inhibition of the differentiation of preadipocytes may be the main pathway through which both HCD and HFD inhibited adipocyte hyperplasia in grass carp; (2) Although both HFD and HCD induce adipocyte hypertrophy by increasing the de novo lipogenesis (DNL) pathway and promoting triglycerides (TG) synthesis. But the difference is that HFD increases fatty acid transport, while HCD increases glycolysis; (3) The inhibitory effect of HCD on glucose transporter type 4 (Glut4) may be an important cause of carbohydrate intolerance in fish; (4) Both HFD and HCD increase lactate production by promoting the expression of lactate dehydrogenase (Ldh), which may be the molecular mechanism of high-energy diet-induced adipose tissue hypoxia; (5) Interleukin-8 (Il-8) can be used as a pro-inflammatory marker for identifying HFD and HCD induced adipose tissue inflammation. This study aims to incestigate the reasons why HFD and HCD have negative effects on fish from the perspective of pathological remodeling of adipose tissue, and provide new underlying regulatory targets for improving the tolerance and utilization of HCD or HFD in farmed fish.

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