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 of Megalobrama amblycephala fed 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.

中文翻译：

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烟酰胺可改善高碳水化合物饮食对钝嘴鲷的生长性能，中间代谢和葡萄糖稳态的影响

进行了为期12周的喂养试验，以评估烟酰胺对饲喂高碳水化合物饮食的钝口鼻的生长性能，葡萄糖和脂质代谢的影响。随机给鱼类喂食四种饮食，包括两种饮食中的碳水化合物水平（分别来自玉米淀粉的300和430 g / kg）和两种烟酰胺水平（0和31.0 mg / kg）。加入微晶纤维素以补偿所需的碳水化合物水平。高碳水化合物水平显着（p <.05）增加了肝体指数，腹膜内脂肪百分比，全身脂质和组织（包括肝脏，肌肉和脂肪组织）糖原和脂质的含量，血浆葡萄糖水平，糖化血清蛋白，高级糖化终产物，甘油三酸酯，丙酮酸和乳酸，以及过氧化物酶体增殖物激活受体γ（PPARγ），PPARα，葡萄糖转运蛋白2（GLUT2），葡萄糖激酶（GK），丙酮酸激酶（PK），糖原合酶（GS），葡萄糖的肝转录-6-磷酸脱氢酶，固醇调节元件结合蛋白-1，脂肪酸合酶（FAS），肉碱棕榈酰转移酶I（CPTI），乙酰-CoA羧化酶α，而肝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（SIRT1）蛋白水平以及SIRT1，叉头转录因子1（FOXO1），磷酸烯醇丙酮酸羧激酶，葡萄糖-6-磷酸酶（G6pase）和酰基-CoA氧化酶的转录（p  <.05）。此外，补充烟酰胺（p  <.05）显着增加了全身脂质和组织糖原含量，肝NAD ⁺含量和NAD ⁺ / NADH比值，肝SIRT1蛋白水平以及SIRT1共激活因子（PPARγ共激活因子-1α，FOXO1的转录） PPARα），GLUT2，GK，PK，G6pase，GS和CPTI，而其余指标则相反。此外，显著（p 在上述大多数参数中，还观察到了饮食碳水化合物水平与烟酰胺之间的相互作用（<0.05）。总体而言，烟酰胺的好处的葡萄糖和脂质代谢团头鲂饲喂高碳水化合物饮食通过介导SIRT1的转录和葡萄糖和脂质代谢有关的基因以及刺激葡萄糖运输，糖酵解，糖原，脂肪酸氧化，同时按压两个脂肪生成和糖异生。