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通过在尼罗罗非鱼()日粮中添加肌醇来减轻日粮碳水化合物的不良影响。

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

作者信息

Zhu Jiahua, Pan Jingyu, Wang Xiaodan, Huang Yuxing, Qin Chuanjie, Qiao Fang, Qin Jianguang, Chen Liqiao

机构信息

Laboratory of Aquaculture Nutrition and Environmental Health, School of Life Sciences, East China Normal University, Shanghai 200241, China.

Key Laboratory of Sichuan Province for Fishes Conservation and Utilization in the Upper Reaches of the Yangtze River, Neijiang Normal University, Neijiang 641100, China.

出版信息

Animals (Basel). 2020 Nov 23;10(11):2190. doi: 10.3390/ani10112190.

DOI:10.3390/ani10112190
PMID:33238508
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7700398/
Abstract

This study investigated the effect of dietary -inositol (MI) on alleviating the adverse effect of the high carbohydrate diet in Nile tilapia (). 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 () 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 () 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 .

摘要

本研究调查了日粮肌醇(MI)对减轻尼罗罗非鱼高碳水化合物日粮不良影响的作用。六种日粮分别含有低碳水化合物(LC 30%)或高碳水化合物(HC 45%),并向每种碳水化合物日粮水平补充三个肌醇水平(0、400和1200毫克/千克日粮)。经过8周的试验,在高碳水化合物水平下,饲喂400毫克/千克肌醇的鱼体重增加和肥满度最高,但在高碳水化合物组中,饲喂1200毫克/千克肌醇的鱼肝体指数、脏体指数和粗脂肪含量最低。与饲喂补充肌醇日粮的鱼相比,无论碳水化合物水平如何,1200毫克/千克肌醇日粮均显著降低了血清和肝脏中的甘油三酯含量。日粮肌醇可降低肝脏中甘油三酯的积累,而与碳水化合物水平无关。在两种碳水化合物水平下,丙二醛含量均随日粮肌醇的增加而降低。饲喂1200毫克/千克肌醇的鱼谷胱甘肽过氧化物酶、超氧化物歧化酶、天冬氨酸转氨酶和谷丙转氨酶活性最高。高碳水化合物日粮增加了未补充肌醇日粮的鱼中参与脂质合成()关键基因的mRNA表达。日粮肌醇显著下调了高碳水化合物日粮鱼中脂肪酸合成酶的表达。此外,尽管日粮碳水化合物水平不同,但与脂质分解代谢()相关基因的mRNA表达随日粮肌醇水平的增加而显著上调。随着肌醇水平的增加,糖异生、糖酵解和肌醇生物合成的基因表达显著下调,而磷酸戊糖途径的表达上调。本研究表明,高碳水化合物日粮会干扰鱼类正常的脂质代谢并倾向于形成脂肪肝。日粮补充肌醇可通过将部分葡萄糖代谢转向磷酸戊糖途径来减轻肝脏中的脂质积累,并增强尼罗罗非鱼的抗氧化能力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efec/7700398/f2d1a9252258/animals-10-02190-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efec/7700398/4e7a32e59e97/animals-10-02190-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efec/7700398/082a130fc63c/animals-10-02190-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efec/7700398/f8840f39adb3/animals-10-02190-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efec/7700398/f2d1a9252258/animals-10-02190-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efec/7700398/4e7a32e59e97/animals-10-02190-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efec/7700398/082a130fc63c/animals-10-02190-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efec/7700398/f8840f39adb3/animals-10-02190-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efec/7700398/f2d1a9252258/animals-10-02190-g004.jpg

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