State Key Laboratory of Freshwater Ecology and Biotechnology, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan430072, China.
College of Advanced Agricultural Sciences, University of Chinese Academy of Sciences, Beijing100049, China.
Br J Nutr. 2021 Jun 14;125(11):1215-1229. doi: 10.1017/S0007114520003608. Epub 2020 Sep 14.
Previous nutritional studies have shown that insulin regulation is different between DT and A strains of gibel carp. As leptin plays a pivotal role in the effects of insulin, we hypothesised that leptin regulation of glucose and lipid metabolism would differ between the two strains. To test our hypothesis, recombinant human leptin was injected into two strains. The results showed that leptin activated the phosphatidylinositol 3-kinase (PI3K)-protein kinase B (AKT), AMP-activated protein kinase-acetyl coenzyme A carboxylase and Janus kinase 2 (JAK2)-signal transducer and activator of transcription (STAT) signalling pathways in both strains. Hypoglycaemia induced by leptin might be due to higher glucose uptake by the liver and muscles together with enhanced glycolytic potential and reduced gluconeogenic potential. Decreased lipogenesis and up-regulated fatty acid oxidation were induced by leptin. In terms of genotype, the PI3K-AKT signalling pathway was more strongly activated by leptin in the muscle tissue of the A strain, as reflected by the heightened phosphorylation of AKT. Furthermore, glycogen content, glycolytic enzyme activity and gluconeogenic capability were higher in the A strain than the DT strain. Strain A had higher levels of fatty acid synthesis and lipolytic capacity in the liver than the DT strain, but the opposite was true in white muscle. Regarding leptin-genotype interactions, the DT strain displayed stronger regulation of glucose metabolism in the liver by leptin as compared with the A strain. Moreover, a more active JAK2-STAT signalling pathway accompanied by enhanced inhibition of fatty acid synthesis by leptin was observed in the DT strain. Overall, the regulation of glucose and lipid metabolism by leptin differed between the two strains, as expected.
先前的营养研究表明,胰岛素调节在吉富罗非鱼 DT 品系和 A 品系之间存在差异。由于瘦素在胰岛素作用中起着关键作用,我们假设瘦素对葡萄糖和脂质代谢的调节在这两个品系之间会有所不同。为了验证我们的假设,我们向两个品系注射重组人瘦素。结果表明,瘦素激活了 PI3K-蛋白激酶 B (AKT)、AMP 激活的蛋白激酶-乙酰辅酶 A 羧化酶和 Janus 激酶 2 (JAK2)-信号转导和转录激活因子 (STAT) 信号通路。瘦素引起的低血糖可能是由于肝脏和肌肉摄取的葡萄糖增加,同时增强了糖酵解能力和降低了糖异生能力。瘦素诱导了脂肪生成减少和脂肪酸氧化增加。就基因型而言,与 DT 品系相比,瘦素在 A 品系肌肉组织中更强烈地激活了 PI3K-AKT 信号通路,这反映在 AKT 的磷酸化水平升高上。此外,A 品系的肝糖原含量、糖酵解酶活性和糖异生能力均高于 DT 品系。A 品系的肝脏脂肪酸合成和脂解能力高于 DT 品系,但白色肌肉的情况则相反。关于瘦素-基因型相互作用,与 A 品系相比,DT 品系的肝脏对瘦素的葡萄糖代谢调节更强。此外,在 DT 品系中观察到更活跃的 JAK2-STAT 信号通路,伴随着瘦素对脂肪酸合成的抑制增强。总的来说,正如预期的那样,瘦素对葡萄糖和脂质代谢的调节在这两个品系之间存在差异。