Acadesine supplementation in a soybean oil-based diet remodels hepatic lipid and glucose metabolism in juvenile large yellow croaker (Larimichthys crocea)

Abstract

Dietary high soybean oil (SO) inclusion leads to excessive hepatic lipid accumulation and metabolism disorder in fish species. This study was conducted to investigate the effects of adenosine 5’-monophosphate-activated protein kinase (AMPK) pathway activation by acadesine (AICAR) on hepatic histology and metabolism-related gene expression of juvenile large yellow croakers (Larimichthys crocea) fed with SO-based diet. In this study, fish (initial body weight 3.89 ± 0.02 g) were fed fish oil (FO)-based, SO, or SOA (SO diet supplemented with 100 mg kg−1 AICAR) diets with three replicates of each treatment for 70 days. In general, the replacement of dietary FO with SO led to excessive hepatic lipid accumulation and a glucose metabolism disorder. Histological sections and biochemical analysis of hepatic tissue consistently revealed that AICAR supplementation could partly ameliorate SO-induced excessive hepatic lipid accumulation, probably by suppressing the expression of genes related to fatty acid uptake and lipogenesis while enhancing the expression of lipolysis-related genes. Nevertheless, AICAR regulated lipid metabolism in muscle tissue in an inverse pattern to that in hepatic tissue, indicating that muscle tissue could attempt to mitigate lipid accumulation by improving lipolysis in response to the dietary inclusion of SO. Dietary AICAR partly improved glucose metabolism by reducing the expression of genes related to gluconeogenesis in hepatic tissue while increasing the expression of genes related to glucose uptake and glycolysis in muscle tissue. Collectively, dietary AICAR mitigated excessive hepatic lipid accumulation and glucose metabolism disorder. The amelioration of hepatic lipid accumulation by AICAR is likely caused by increasing lipid catabolism and decreasing lipid anabolism. The improved glucose metabolism by AICAR may be ascribed to decreased hepatic gluconeogenesis, as well as increased muscle glucose uptake and utilization.