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Magnesium stimulates renal phosphate reabsorption

机译:镁刺激肾磷酸盐重吸收

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摘要

magnesium (Mg~(2+)) is the second most abundant intracellular cation in vertebrates. It interacts with calcium (Ca~(2+)) and phosphate (Pi) homeostasis in different ways. Mg~(2+) activates like Ca~(2+) the Ca~(2+)-sensing receptor (CaSR) of the parathyroid glands (2). Activation of the CaSR results in decreased parathyroid hormone (PTH) secretion. Although Mg~(2+) is less potent than Ca~(2+) in stimulating the CaSR, genetic diseases caused by mutations in the CaSR gene suggest that CaSR serves as an Mg~(2+) sensor in vivo. Individuals with autosomal-dominant hypoparathyroidism (ADH) due to activating mutations of the CaSR show, besides hypercalciuric hypocalcemia, tendencies toward hypomagnesemia and hyperphosphatemia (10). Heterozygous inactivating mutations of the CaSR cause familial hypocalciuric hypercalcemia (FHH), which is characterized by hypocalciuric hypercalcemia often associated with hypomagnesiuric hypermagnesemia (26).
机译:镁(Mg〜(2+))是脊椎动物中最丰富的细胞内阳离子。 它以不同方式与钙(Ca〜(2+))和磷酸盐(PI)稳态相互作用。 Mg〜(2+)如Ca〜(2+)如甲状旁腺(2)的Ca〜(2+)感应受体(CasR)激活。 CASR的激活导致甲状旁腺激素(PTH)分泌减少。 虽然Mg〜(2+)比CA〜(2+)在刺激CASR时较少,但CASR基因突变引起的遗传疾病表明CASR用作体内Mg〜(2+)传感器。 具有常染色体显性性低羟基甲醛的个体(ADH)由于CASR的激活突变显示,除了过高钙血症的低钙血症之外,趋势患者血症和高磷血症(10)。 杂基的杂合突变引起家族性低核酸高钙血症(FHH),其特征在于常见与低钙血症高钙血症(26)相关的低视野血尿病。

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