Abstract
Food intake of carnivorous fish decreases after feeding on a carbohydrate-rich diet. However, the molecular mechanism underlying the anorexia caused by high-carbohydrate diets has remained elusive. We domesticated the mandarin fish to feed on carbohydrate-rich (8%) diets. After 61 days of feeding, several fish (Group A) fed well on artificial diets during the whole feeding period; the other fish (Group B) fed well on artificial diets at the beginning of the feeding period, with their food intake then decreasing to half (anorexia) and then to zero for 5 days; and, finally, a negative control (Group C) fed on live prey fish throughout the experimental process. The plasma glucose was significantly higher in the mandarin fish of Group B than in those of Group A, whereas levels of hepatic glycogen and plasma triglyceride were significantly lower. Using transcriptome sequencing, we investigated the differentially expressed genes between Groups A and B and excluded the genes that were not differentially expressed between Groups A and C. The activation of mTOR and Jak/STAT pathways were found in the mandarin fish with anorexia, which was consistent with the higher expression levels of pepck and pomc genes. We found a higher expression of histone methyltransferase setd1b gene and an increased histone H3 tri-methylated at lysine 4 (H3K4me3) in the fish of Group B. Furthermore, using ChIP assay and inhibitor treatment, we found that the up-regulated H3K4me3 could activate pepck expression, which might have contributed to the hyperglycemia and anorexia in the mandarin fish that fed on carbohydrate-rich diets. Our study initially indicated a link between histone methylation and pepck expression, which might be a novel regulatory mechanism of fish who are fed a carbohydrate-rich diet.
Highlights
In aquaculture, carbohydrates are added to artificial diets as the energy source to save protein [1, 2]
To uncover the molecular mechanism of anorexia in mandarin fish after feeding on carbohydrate-rich diets, we examined the levels of plasma glucose, hepatic glycogen, muscle glycogen, plasma insulin, and plasma triglyceride
The decreased hepatic glycogen and plasma triglyceride levels were found in the fish of Group B, and the muscle glycogen and plasma insulin levels showed no differences
Summary
Carbohydrates are added to artificial diets as the energy source to save protein [1, 2]. Carbohydrates could be an efficient inhibitor of appetite; food intake decreases after feeding a carbohydrate-rich diet in mammals and carnivorous fish [4, 5]. Previous research shows that hyperglycemia could contribute to a decreased food intake in mammals after feeding on high-carbohydrate diets [6,7,8]. High-carbohydrate diets (10.5%) reduce the food intake by changing the parameters of glucose-sensing, such as the increased levels of glucose, glucose 6-phosphate, and glycogen [9, 10]. The regulation of food intake is mediated by a neuronal circuit that integrates orexigenic and anorexigenic signals such as NPY/AGRP and POMC/CART [12]. Little is known about the regulatory mechanisms of hyperglycemia on anorexia induced by highcarbohydrate diets in fish
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