SYNTHESIS OF CITRATE FROM PHOSPHOENOLPYRUVATE AND ACETYLCARNITINE BY MITOCHONDRIA FROM RABBIT, PIGEON AND RAT-LIVER - IMPLICATIONS FOR LIPOGENESIS

Rabbit, pigeon and rat liver mitochondria convert exogenous phosphoeno lpyruvate and acetylcarnitine to citrate at rates of 14, 74 and 8 nmol /15 min/mg protein. Citrate formation is dependent on exogenous HCO3-, is increased consistently by exogenous nucleotides (GDP, IDP, CTP, AD P, ATP) and inhibited strongly by 3-mercaptopicolinate and 1,2,3-benze netricarboxylate. Citrate is not made from pyruvate alone or combined with acetylcarnitine. Pigeon and rat liver mitochondria make large amo unts of citrate from exogenous succinate, suggesting the Presence of a n endogenous source of acetyl units or a means of converting oxalaceta te to acetyl units. Citrate synthesis from succinate by pigeon and rab bit mitochondria is increased significantly by exogenous acetylcarniti ne. Pigeon and rat liver contain 80 and 15 times, respectively, more A TP:citrate lyase activity than does rabbit liver. Data suggest that mi tochondrial phosphoenolpyruvate carboxykinase in vivo could convert gl ycolysis-derived phosphoenolpyruvate to oxalacetate that, with acetyl CoA, could form citrate for export to support cytosolic lipogenesis as an activator of acetyl CoA carboxylase, a carbon source via ATP:citra te lyase and NADPH Via NADP:malate dehydrogenase or NADP:isocitrate de hydrogenase.