The diabetic feature limits the utilization of dietary carbohydrates in carnivorous fish, and excessive dietary carbohydrate usually cause negative effects on health and growth of these fish. In this study, a 9-weeks' feeding experiment was conducted to figure out the influence of dietary metformin (MET), an effective agent for diabetes in mammals, supplementation on largemouth bass, a typical carnivorous fish, feeding high dietary carbohydrates. Compared with the low dietary carbohydrates (LC) group, high dietary carbohydrates (HC) impaired growth performance, which was improved by the inclusion of MET in HC diets. Meanwhile, compared with the HC group, dietary MET supplementation significantly reduced hepatic glycogen and serum glucose contents. Additionally, on the transcriptional level, HC repressed the insulin pathway and induced imbalanced regulation of glycolysis and glycogenesis compared with LC group. However, the MET supplementation significantly enhanced the genes' expression involved in insulin pathway (, , , , ) followed by the activated expression of glycolysis (, and ) and inhibited expression of glycogenesis ( and ). HC significantly reduced antioxidant capacity compared with the LC group, which was reversed with MET supplementation at both transcriptional and enzymatic levels. Additionally, high dietary carbohydrates inhibited apoptosis, which was activated with the inclusion of MET with the inhibition of / ratio and the activation of apoptosis-promoting genes ( and ). In summary, dietary MET inclusion in high carbohydrate diet improved glucose utilization via activating the insulin pathway, and further enhance the growth performance and antioxidant capacity.

中文翻译：

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二甲双胍对高膳食碳水化合物喂养的大口黑鲈（Micropterus salmoides）的生长性能、葡萄糖利用率、抗氧化能力和细胞凋亡的有益影响

糖尿病的特征限制了肉食性鱼类对膳食碳水化合物的利用，过量的膳食碳水化合物通常会对这些鱼类的健康和生长造成负面影响。在这项研究中，进行了为期 9 周的喂养实验，以找出膳食二甲双胍（MET）（一种治疗哺乳动物糖尿病的有效药物）对大口黑鲈（一种典型的肉食性鱼类）喂养高膳食碳水化合物的影响。与低膳食碳水化合物 (LC) 组相比，高膳食碳水化合物 (HC) 会损害生长性能，但通过在 HC 日粮中添加 MET 可以改善生长性能。同时，与HC组相比，膳食补充MET显着降低了肝糖原和血糖含量。此外，在转录水平上，与LC组相比，HC抑制了胰岛素通路并诱导糖酵解和糖原生成的不平衡调节。然而，补充 MET 显着增强了胰岛素途径相关基因的表达 (, , , , )，随后激活了糖酵解的表达 (, 和 ) 并抑制了糖原生成 ( 和 ) 的表达。与 LC 组相比，HC 组的抗氧化能力显着降低，而补充 MET 在转录和酶水平上可逆转这一情况。此外，高膳食碳水化合物会抑制细胞凋亡，通过加入 MET 来激活细胞凋亡，抑制 / 比例并激活细胞凋亡促进基因 ( 和 )。综上所述，高碳水化合物饮食中的膳食MET通过激活胰岛素途径提高了葡萄糖利用率，并进一步增强了生长性能和抗氧化能力。