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肝脏糖异生功能受损后大鼠肾脏糖异生能力的诱导

Induction of rat kidney gluconeogenic ability after impairment of liver gluconeogenesis.

作者信息

Sanchez-Medina F, Garcia-Ruiz J P, Lupiañez J A, Faus M J, Hortelano P

出版信息

Curr Probl Clin Biochem. 1977;8:310-7.

PMID:210998
Abstract

The renal gluconeogenic response to the inhibition of liver gluconeogenesis was studied in rats treated with CCl4. This treatment resulted in a generalized fall of hepatic gluconeogenic enzyme activities and a complete impairment of liver gluconeogenesis. On the contrary, an enhancement of renal phosphoenolpyruvate carboxykinase activity and gluconeogenic ability was found. This stimulation seemed to be not related to metabolic acidosis but mediated by glucocorticoids. On the other hand, the pattern of intermediate metabolites in kidney suggested that renal gluconeogenesis was operative in these conditions, probably playing a key role in glucose homeostasis.

摘要

在接受四氯化碳处理的大鼠中,研究了肾脏对肝脏糖异生抑制的反应。这种处理导致肝脏糖异生酶活性普遍下降以及肝脏糖异生完全受损。相反,发现肾脏磷酸烯醇式丙酮酸羧激酶活性和糖异生能力增强。这种刺激似乎与代谢性酸中毒无关,而是由糖皮质激素介导的。另一方面,肾脏中中间代谢产物的模式表明,在这些情况下肾脏糖异生起作用,可能在葡萄糖稳态中起关键作用。

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