Alleviation of the Adverse Effect of Dietary Carbohydrate by Supplementation of Myo-Inositol to the Diet of Nile Tilapia (Oreochromis niloticus)

SIMPLE SUMMARY: Recently, the price escalation of fishmeal has made aquaculture nutritionists to consider using carbohydrate in aquafeed to spare the use of dietary protein. However, the high carbohydrate diet could induce lipid metabolism disorder, impair antioxidant capacity, reduce nonspecific immunity and decrease resistance to a pathogen in farmed fish. Myo-inositol is regarded as a vitamin-like essential nutrient for most aquatic animals. Previous studies have shown that dietary supplementation with myo-inositol can reduce lipid accumulation in tissues and decrease the chance of becoming a fatty liver. To explore the mechanism of myo-inositol on alleviating the adverse effect of the high carbohydrate diet in Nile tilapia, six diets contained either low carbohydrate (30%) or high carbohydrate (45%) with three levels of myo-inositol supplementation (0, 400 and 1200 mg/kg diet) to each level of the carbohydrate diet. After an 8-week trial, the result showed that additive myo-inositol in the diet could significantly improve the growth performance and increase the crude protein content of fish. The addition of myo-inositol could effectively decrease the lipid accumulation induced by the high carbohydrate diet by accelerating the transportation of cholesterol back to the liver and promoting the lipid decomposition. ABSTRACT: This study investigated the effect of dietary myo-inositol (MI) on alleviating the adverse effect of the high carbohydrate diet in Nile tilapia (Oreochromis niloticus). Six diets contained either low carbohydrate (LC 30%) or high carbohydrate (HC 45%) with three levels of MI supplementation (0, 400 and 1200 mg/kg diet) to each level of the carbohydrate diet. After an 8-week trial, the fish fed 400 mg/kg MI under HC levels had the highest weight gain and fatness, but the fish fed 1200 mg/kg MI had the lowest hepatosomatic index, visceral index and crude lipid in the HC group. The diet of 1200 mg/kg MI significantly decreased triglyceride content in the serum and liver compared with those fed the MI supplemented diets regardless of carbohydrate levels. Dietary MI decreased triglyceride accumulation in the liver irrespective of carbohydrate levels. The content of malondialdehyde decreased with increasing dietary MI at both carbohydrate levels. Fish fed 1200 mg/kg MI had the highest glutathione peroxidase, superoxide dismutase, aspartate aminotransferase and glutamic-pyruvic transaminase activities. The HC diet increased the mRNA expression of key genes involved in lipid synthesis (DGAT, SREBP, FAS) in the fish fed the diet without MI supplementation. Dietary MI significantly under expressed fatty acid synthetase in fish fed the HC diets. Moreover, the mRNA expression of genes related to lipid catabolism (CPT, ATGL, PPAR-α) was significantly up-regulated with the increase of dietary MI levels despite dietary carbohydrate levels. The gene expressions of gluconeogenesis, glycolysis and MI biosynthesis were significantly down-regulated, while the expression of the pentose phosphate pathway was up-regulated with the increase of MI levels. This study indicates that HC diets can interrupt normal lipid metabolism and tend to form a fatty liver in fish. Dietary MI supplement can alleviate lipid accumulation in the liver by diverging some glucose metabolism into the pentose phosphate pathway and enhance the antioxidant capacity in O. niloticus.