Our objective is to study the low metabolic utilization of dietary carbohydrates in fish. The regulation of key enzymes involved in glucose and lipid metabolism in the common carp (Cyprinus carpio L.), known to be relatively tolerant to dietary carbohydrates, were assessed. We performed intraperitoneal (i.p.) administration of insulin and glucagon to common carp and also subjected common carp primary hepatocytes to insulin or glucagon. The results showed that insulin administration induced hypoglycaemia through up-regulation of the expression of the glycolysis genes glucokinase (GK) and hexose kinase (HK), coupled with increased gene expression of fatty acid synthase (FAS), acetyl-CoA carboxylase-1 (ACC-1), sterol-regulator element-binding protein-1 (SREBP-1). Insulin also limited the expression of the gluconeogenesis genes phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6Pase), coupled with decreased gene expression of lipoprotein lipase (LPL) and carnitine palmitoyl transferase I (CPT-1). However, glucagon had the opposite effect. The results showed that glucagon induced hyperglycemia with increased expression of PEPCK and G6Pase and increased lipolytic capacity as indicated by lower mRNA levels of SREBP-1. Glucagon (i.p.) significantly increased the activity of PEPCK and LPL in hepatopancreas. In addition, the mRNA expression of HK showed an up-regulated trend and the mRNA expression of PEPCK and G6Pase showed a down-regulated trend in the group of glucose (i.p.). This study demonstrates that insulin and glucagon possess the intrinsic ability to regulate hepatic energy metabolism in common carp, the regulation of which seems to be similar to that of the mammals at least at the molecular level.

我们的目标是研究鱼中膳食碳水化合物的低代谢利用。评估了已知对饮食碳水化合物相对耐受的鲤鱼（Cyprinus carpio L.）中参与葡萄糖和脂质代谢的关键酶的调节。我们对鲤鱼进行了腹膜内（ip）胰岛素和胰高血糖素给药，并对鲤鱼的原代肝细胞进行了胰岛素或胰高血糖素治疗。结果表明，胰岛素给药可通过上调糖酵解基因葡萄糖激酶（GK）和己糖激酶（HK）的表达而诱导低血糖症，同时增加脂肪酸合酶（FAS），乙酰辅酶A羧化酶1（FAS）的基因表达。ACC-1），固醇调节因子结合蛋白1（SREBP-1）。胰岛素还限制了糖原异生基因磷酸烯醇丙酮酸羧激酶（PEPCK）和葡萄糖-6-磷酸酶（G6Pase）的表达，同时脂蛋白脂肪酶（LPL）和肉碱棕榈酰转移酶I（CPT-1）的基因表达降低。然而，胰高血糖素具有相反的作用。结果表明，胰高血糖素可导致高血糖，PEPCK和G6Pase的表达增加，脂解能力增加，SREBP-1的mRNA水平较低。胰高血糖素（IP）显着增加了肝胰腺中PEPCK和LPL的活性。此外，在葡萄糖（ip）组中，HK的mRNA表达呈上调趋势，而PEPCK和G6Pase的mRNA表达呈下调趋势。这项研究表明，胰岛素和胰高血糖素具有调节鲤鱼肝脏能量代谢的内在能力，至少在分子水平上，其调节作用似乎与哺乳动物相似。