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[血磷调节与低磷血症]

[Regulation of phosphatemia and hypophosphatemia].

作者信息

Essig M, Friedlander G

机构信息

INSERM U 426, Faculté Xavier-Bichat, Paris.

出版信息

Rev Prat. 1998 Jun 1;48(11):1218-25.

PMID:9781175
Abstract

Phosphate is an essential element for cellular metabolism and bone mineralization. The kidney regulates phosphate homeostasis by modulating the proximal reabsorption of phosphate. This regulation is mediated by hormonal or autocrine/paracrine factors. Recent results concerning the molecular structure of phosphate transport systems have clarified the mechanisms underlying the effects of these mediators. Hypophosphatemia is a frequent biological finding which results either from an intracellular shift of phosphate, or from a defect in the intestinal absorption or a renal leak. The decrease in phosphate leads to a depletion in cellular ATP (which accounts for neurological and muscular symptoms), to bone demineralization and to renal lithiasis when a renal leak exists.

摘要

磷酸盐是细胞代谢和骨矿化的必需元素。肾脏通过调节近端肾小管对磷酸盐的重吸收来维持磷酸盐稳态。这种调节由激素或自分泌/旁分泌因子介导。最近关于磷酸盐转运系统分子结构的研究结果阐明了这些介质作用的潜在机制。低磷血症是一种常见的生物学现象,其原因要么是磷酸盐向细胞内转移,要么是肠道吸收缺陷或肾脏漏磷。磷酸盐减少会导致细胞内三磷酸腺苷(ATP)耗竭(这会引发神经和肌肉症状),导致骨质脱矿,并且在存在肾脏漏磷的情况下会导致肾结石。

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