Search

Expensive and unsustainable fishmeal is increasingly being replaced with cheaper lipids and carbohydrates as sources of energy in aquaculture. Although it is known that the excess of lipids and carbohydrates has negative effects on nutrient utilization, growth, metabolic homeostasis, and health of fish, our current understanding of mechanisms behind these effects is limited. To improve the understanding of diet-induced metabolic disorders (both in fish and other vertebrates), we conducted an eight-week high-fat–high-carbohydrate diet feeding trial on blunt snout bream (Megalobrama amblycephala), and studied gene expression changes (transcriptome and qPCR) in the liver. Disproportionately large numbers of differentially expressed genes were associated with mitochondrial metabolism, neurodegenerative diseases (Alzheimer’s, Huntington’s, and Parkinson’s), and functional categories indicative of liver dysfunction. A high-fat–high-carbohydrate diet may have caused mitochondrial dysfunction, and possibly downregulated the mitochondrial biogenesis in the liver. While the relationship between diet and neurodegenerative disorders is well-established in mammals, this is the first report of this connection in fish. We propose that fishes should be further explored as a potentially promising model to study the mechanisms of diet-associated neurodegenerative disorders in humans.

Fish meal is the main protein source in fish diet, but due to its unsustainability, it has to be replaced with more sustainable protein sources, such as soybean meal (SBM), in fish feeds. A...

A high intake of carbohydrates, associated with obesity, is one of the major causes of fatty liver disease in humans. This study investigated how high carbohydrate intake induces fatty liver disease in Blunt snout bream (Megalobrama amblycephala). Blunt snout bream were fed a high-carbohydrate diet (HCBD) for 60 days. Their growth indices were evaluated, and the transcriptomes, metabolites, biochemistry, and histology of their blood and livers were analyzed. The final weight, weight gain, specific growth rate, and feed conversion ratio were all higher in the HCBD group than in the control group, but not significantly so (P > 0.05). The hepatosomatic index (HSI) differed significantly in the two groups (P < 0.05), and the metabolomics results showed that a high carbohydrate intake induced significant increases in plasma α/β-glucose, succinate, and tyrosine, which could increase hepatic glycogen and triglyceride. Low levels of betaine were also found in the livers of the HCBD group. The histology and blood biochemistry results suggested abnormal liver, with excessive lipid accumulation and liver damage. A transcriptome analysis and quantitative reverse transcription–PCR (RT–qPCR) indicated that the expression of the factors INSR, IRS, PI3K, PDK, AKT, ACC, IL6, AP1, ChREBP-MLX, PEPCK, and FBP in the insulin signaling pathway was significantly upregulated and that of SOCS3, GSK3β, and AMPK significantly downregulated in the HCBD. This pattern is associated with the nonalcoholic fatty liver disease (NAFLD) pathway. This study extends our understanding of how high carbohydrate causes increased fat deposition in the liver, enhanced glycolysis (α/β-glucose) in the plasma, and reduced betaine in the liver. This leads to activation of hepatocyte insulin resistance and lipogenesis by regulating the expression of genes related to fatty liver disease.

Introduction High-fat and high-carbohydrate diets cause a number of metabolic disorders in mammals. However, little is known about metabolomic changes caused by dietary imbalances in fish.