Renal cortical mitochondrial aconitase is regulated in hypo- and hypercitraturia

Joel Z. Melnick, Patricia A. Preisig, Orson W. Moe, Paul Srere, Robert J. Alpern

Research output: Contribution to journalArticlepeer-review

47 Scopus citations

Abstract

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 mithochondrial aconitase (m-aconitase), the first step in mithochondrial citrate metabolism, in these conditions. Methods. Rats were fed appropriate diets, and m- aconitase activity and protein abundance measured. Results. In chronic metabolic acidosis anf 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 witlh 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 mithochondrial 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.

Original languageEnglish (US)
Pages (from-to)160-165
Number of pages6
JournalKidney international
Volume54
Issue number1
DOIs
StatePublished - 1998

ASJC Scopus subject areas

  • Nephrology

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