Nicotinamide improves the growth performance, intermediary metabolism and glucose homeostasis of blunt snout bream Megalobrama amblycephala fed high-carbohydrate diets
Nicotinamide improves the growth performance, intermediary metabolism and glucose homeostasis of blunt snout bream Megalobrama amblycephala fed high-carbohydrate diets
复制标题
烟酰胺改善高碳水化合物饮食的团头鲂的生长性能、中间代谢和葡萄糖稳态
DOI：
10.1111/anu.13088
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发表时间：
2020
影响因子：
3.5
通讯作者：
Liu Wenbin
中科院分区：
文献类型：
--
作者：
Shi Hua-Juan;Li Xiang-Fei;Xu Chao;Zhang Dingdong;Zhang Li;Xia Si-Lei;Liu Wenbin
通过为期12周的饲养试验，研究了烟酰胺对高碳水化合物饲料中团头鱼生长性能、糖脂代谢的影响。随机饲喂四种饲料，包括两种碳水化合物水平(300和430微克/公斤，来自玉米淀粉)和两种烟酰胺水平(0和31.0微克/公斤)。加入微晶纤维素是为了补偿所需的碳水化合物水平。高碳水化合物水平显著(p<；增加肝体指数、腹膜脂肪百分比、全身脂肪和组织(包括肝脏、肌肉和脂肪组织)糖原和脂肪含量、血浆葡萄糖、糖化血清蛋白、糖基化终末产物、甘油三酯、丙酮酸和乳酸水平，以及肝脏中过氧化体增殖物激活受体γ(PPARγ)、PPARα、葡萄糖转运蛋白2(GLUT2)、葡萄糖激酶(GK)、丙酮酸激酶(PK)、糖原合成酶(GS)、葡萄糖-6-磷酸脱氢酶(GDP)、固醇调节元件结合蛋白-1、脂肪酸合成酶(Fas)、卡尼汀棕榈酰转移酶(CPTI)、乙酰辅酶A羧基酶α，而肝脏烟酰胺腺嘌呤二核苷酸(NAD+)、烟酰胺腺嘌呤二核苷酸磷酸(NADH)和肝sirtuin-1蛋白水平以及Sirt1、叉头转录因子1(FOXO1)、磷酸烯醇式丙酮酸羧酸激酶、葡萄糖-6-磷酸酶(G6pase)和酰辅酶A氧化酶(p<)的转录水平则相反；(05)。此外，添加烟酰胺显著提高了整体脂肪和组织糖原含量、肝脏NAD+含量和NAD+/NADH比值、肝脏SIRT1蛋白水平和SIRT1辅活化子(PPARγ辅活化子-1α、FOXO1PPARα)、GLUT2、GK、PK、G6pase、GS和CPTI的转录水平，而其余指标则相反。此外，在上述大多数参数中，膳食碳水化合物水平和烟酰胺之间也观察到了显著的(p<；0.05)交互作用。总体而言，烟酰胺通过介导SIRT1和糖脂代谢相关基因的转录，刺激葡萄糖转运、糖酵解、糖生成、脂肪酸氧化，同时抑制脂肪生成和糖异生，从而有利于团头鲨高碳水化合物饲料的糖脂代谢。
A 12‐week feeding trial was conducted to evaluate the effects of nicotinamide on the growth performance, glucose and lipid metabolism of blunt snout bream fed high‐carbohydrate diets. Fish were randomly fed four diets including two dietary carbohydrate levels (300 and 430 g/kg, deriving from corn starch) and two nicotinamide levels (0 and 31.0 mg/kg). Microcrystalline cellulose was incorporated to compensate for the carbohydrate levels required. High‐carbohydrate levels significantly (p< .05) increased the hepatosomatic index, intraperitoneal fat percentage, the contents of whole‐body lipid and tissues (including liver, muscle and adipose tissue) glycogen and lipid, plasma levels of glucose, glycated serum protein, advanced glycation end products, triglyceride, pyruvate and lactic acid, as well as the hepatic transcriptions of peroxisome proliferator‐activated receptor γ (PPARγ), PPARα, glucose transporter 2 (GLUT2), glucokinase (GK), pyruvate kinase (PK), glycogen synthase (GS), glucose‐6‐phosphate dehydrogenase, sterol regulatory element‐binding protein‐1, fatty acid synthase (FAS), carnitine palmitoyl transferase I (CPTI), acetyl‐CoA carboxylase α, whereas the opposite was found for hepatic nicotinamide adenine dinucleotide (NAD+), nicotinamide adenine dinucleotide phosphate (NADH) and hepatic sirtuin‐1 (SIRT1) protein level and the transcriptions of SIRT1, forkhead transcription factor 1(FOXO1), phosphoenolpyruvate carboxykinase, glucose‐6‐phosphatase (G6pase) and acyl‐CoA oxidase (p< .05). Additionally, nicotinamide supplementation significantly (p< .05) increased whole‐body lipid and tissues glycogen contents, hepatic NAD+content and the NAD+/NADH ratio, hepatic SIRT1 protein level and the transcriptions of SIRT1 coactivators (PPARγ coactivator‐1α, FOXO1 PPARα), GLUT2, GK, PK, G6pase, GS and CPTI, while the opposite was found for the remaining indicators. Furthermore, a significant (p< .05) interaction between dietary carbohydrate levels and nicotinamide was also observed in most parameters aforementioned. Overall, nicotinamide benefits the glucose and lipid metabolism ofMegalobrama amblycephalafed high‐carbohydrate diets by mediating the transcriptions of SIRT1 and glucose and lipid metabolism‐related genes as well as stimulating glucose transportation, glycolysis, glycogenesis, fatty acid oxidation, while depressing both lipogenesis and gluconeogenesis.