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首页> 外文期刊>Journal of Lipid Research >Thioredoxin-interacting protein deficiency disrupts the fasting-feeding metabolic transition
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Thioredoxin-interacting protein deficiency disrupts the fasting-feeding metabolic transition

机译：硫氧还蛋白相互作用蛋白缺乏会破坏空腹喂养的代谢转变

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摘要

Through a positional cloning approach, the thioredoxin-interacting protein gene (Txnip) was recently identified as causal for a form of combined hyperlipidemia in mice (Bodnar, J. S., A. Chatterjee, L. W. Castellani, D. A. Ross, J. Ohmen, J. Cavalcoli, C. Wu, K. M. Dains, J. Catanese, M. Chu, S. S. Sheth, K. Charugundla, P. Demant, D. B. West, P. de Jong, and A. J. Lusis. 2002. Positional cloning of the combined hyperlipidemia gene Hyplip1. Nat. Genet. 30: 110-116). We now show that Txnip-deficient mice in the fed state exhibit a metabolic profile similar to fasted mice, including increased levels of plasma ketone bodies and free fatty acids, decreased glucose, and increased hepatic expression of peroxisome proliferator-activated receptor-gamma coactivator-lot, phosphoenolpyruvate carboxykinase, glucose-6-phosphatase, and acyl-CoA oxidase. Dramatic differences in the expression of key metabolic enzymes were also observed in other tissues, and the fat-to-muscle ratio of Txnip-deficient mice was increased by similar to40%. We demonstrate an effect of Txnip on the redox status, as the Txnip-deficient mice in the fed state had a significant increase in the ratio of NADH to NAD(+). Surprisingly, we observed that Txnip-deficient mice and wild-type mice had similar levels of thioredoxin activity, suggesting that the effects of Txnip deficiency may be mediated in part by other interactions. These results indicate a role for Txnip in the metabolic response to feeding and the maintenance of the redox status.
机译：通过位置克隆方法，最近与硫氧还蛋白相互作用的蛋白基因（Txnip）被确定为小鼠合并高脂血症形式的病因（Bodnar，JS，A. Chatterjee，LW Castellani，DA Ross，J. Ohmen，J. Cavalcoli ，C。Wu，KM Dains，J。Catanese，M。Chu，SS Sheth，K。Charugundla，P。Demant，DB West，P。de Jong和AJ Lusis。2002年。高脂血症基因Hyplip1的位置克隆。 Nat.Genet.30：110-116）。我们现在显示，处于饲喂状态的Txnip缺陷小鼠表现出与禁食小鼠相似的代谢特征，包括血浆酮体和游离脂肪酸水平增加，葡萄糖减少以及过氧化物酶体增殖物激活的受体-γ共激活子的肝表达增加。磷酸烯醇丙酮酸羧激酶，葡萄糖6磷酸酶和酰基辅酶A氧化酶。在其他组织中也观察到关键代谢酶表达的显着差异，Txnip缺陷小鼠的脂肪/肌肉比率增加了约40％。我们证明了Txnip对氧化还原状态的影响，因为处于进食状态的Txnip缺陷小鼠的NADH与NAD（+）的比例显着增加。令人惊讶地，我们观察到Txnip缺陷小鼠和野生型小鼠具有相似水平的硫氧还蛋白活性，这表明Txnip缺陷的影响可能部分地由其他相互作用介导。这些结果表明Txnip在进食代谢反应和维持氧化还原状态中的作用。

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