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.

中文翻译：

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在尼罗罗非鱼（Oreochromis niloticus）的饮食中补充肌醇可减轻饮食中碳水化合物的不良影响

这项研究调查了饮食的影响肌上减轻尼罗罗非鱼的高碳水化合物饮食的不利影响肌醇（MI）（尼罗罗非鱼）。六种饮食中分别含有低碳水化合物（LC 30％）或高碳水化合物（HC 45％），并且每水平都需要补充三水平的MI（0、400和1200 mg / kg饮食）。经过8周的试验，以HC水平饲喂400 mg / kg MI的鱼增重和脂肪最高，但是以HC组饲喂1200 mg / kg MI的鱼的肝体指数，内脏指数和粗脂质最低。与饲喂MI补充饮食的人相比，无论碳水化合物水平如何，1200 mg / kg MI的饮食都显着降低了血清和肝脏中甘油三酸酯的含量。饮食MI减少了肝脏中甘油三酸酯的积累，而与碳水化合物水平无关。在两种碳水化合物水平下，丙二醛的含量均随着饮食中MI的增加而降低。饲喂1200 mg / kg MI的鱼的谷胱甘肽过氧化物酶最高，超氧化物歧化酶，天冬氨酸转氨酶和谷氨酸-丙酮酸转氨酶活性。HC饮食增加了参与脂质合成的关键基因的mRNA表达（鱼中的DGAT，SREBP，FAS）饲喂不添加MI的饮食。饲喂HC日粮的鱼的日粮MI明显低于表达的脂肪酸合成酶。此外，与脂质分解代谢相关的基因（CPT，ATGL，PPAR-α）的mRNA表达尽管饮食中的碳水化合物水平较高，但随着饮食中MI含量的增加，β显着上调。糖原异生，糖酵解和心肌梗死生物合成的基因表达明显下调，而磷酸戊糖途径的表达则随着心肌梗死水平的增加而上调。这项研究表明，高碳饮食可以中断正常的脂质代谢，并倾向于在鱼类中形成脂肪肝。膳食MI补充剂通过使葡萄糖代谢进入戊糖磷酸途径来减轻肝脏中脂质的积累，增强尼罗罗非鱼的抗氧化能力。