Renal cortical mitochondrial aconitase is regulated in hypo- and hypercitraturia.
Renal cortical mitochondrial aconitase is regulated in hypo- and hypercitraturia.
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DOI：
10.1046/j.1523-1755.1998.00974.x
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发表时间：
1998-07
影响因子：
19.6
通讯作者：
J. Melnick;P. Preisig;O. Moe;P. Srere;R. Alpern
中科院分区：
文献类型：
--
作者：
J. Melnick;P. Preisig;O. Moe;P. Srere;R. Alpern
BACKGROUND Chronic metabolic acidosis and K+ deficiency increase, while alkali feeding decreases proximal tubule citrate absorption and metabolism. The present studies examined the regulation of mitochondrial aconitase (m-aconitase), the first step in mitochondrial citrate metabolism, in these conditions. METHODS Rats were fed appropriate diets, and m-aconitase activity and protein abundance measured. RESULTS In chronic metabolic acidosis and chronic K+ deficiency, renal cortical m-aconitase activity was increased 17% and 43%, respectively. This was associated with respective 90% and 221% increases in renal cortical m-aconitase protein abundance. With chronic alkali feeding, there was a 12% decrease in renal cortical m-aconitase activity, associated with a 35% decrease in m-aconitase protein abundance. Hepatic m-aconitase activity was not regulated in a similar manner. There was no regulation of citrate synthase, the enzyme responsible for mitochondrial citrate synthesis. CONCLUSIONS These studies demonstrate tissue specific chronic regulation of renal cortical m-aconitase activity and protein abundance, which likely contributes to the hypocitraturia and hypercitraturia seen in these conditions. As m-aconitase is the only step in citrate transport and metabolism found to be regulated in alkali feeding, its regulation likely plays a significant role in mediating the hypercitraturia seen in this condition.
