"The mechanism by which prolactin regulates prostate citrate production has recently been addressed. Studies with rat lateral prostate epithelial cells revealed that prolactin stimulates mAAT gene expression and mAAT biosynthesis [6, 32,34–36] and stimulates PDHE1a expression, PDHE1a levels, and pyruvate oxidation [23,37]. In contrast to the stimulatory effect on mAAT and PDH, prolactin inhibits the gene expression of m-aconitase and the level of m-aconitase resulting in decreased citrate oxidation [27, 38]."
Deletion of prolactin reduce glycolysis, pyruvate dehydrogenase whilst increasing fatty acid oxidation.
Though the massive reduction in fatty acid synthase and SCD2 is interesting. But invivo > vitro
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