PROLACTIN SPECIFICALLY INCREASES PYRUVATE-DEHYDROGENASE E1-ALPHA IN RAT LATERAL PROSTATE EPITHELIAL-CELLS

Prolactin is an important regulator of prostate citrate production. In rats this regulatory effect of prolactin is specific for lateral pros tate, and has no effect on either ventral or dorsal prostate. The mech anisms by which prolactin regulates prostate citrate production have n ot been elucidated. Two key regulatory enzymes involved in citrate syn thesis by prostate epithelial cells are mitochondrial aspartate aminot ransferase (mAAT) which provides oxalacetate, and PDH E1 alpha (pyruva te dehydrogenase) which provides acetyl CoA for citrate synthesis. Our previous studies demonstrated that prolactin regulates mAAT. However, an increase in citrate synthesis would require an increase in both ox alacetate and acetyl CoA. Therefore, we investigated the possibility t hat prolactin might also regulate PDH E1 alpha in LP epithelial cells. The present studies demonstrate that prolactin administration (1 mg/r at) to rats resulted in an increased level of E1 alpha in LP epithelia l cells within 6 hr, but had no effect on the E1 alpha level of VP epi thelial cells. In vitro studies demonstrated that exposure of freshly prepared LP epithelial cells to prolactin (0.1-1.0 mu g/ml) resulted i n increased levels of E1 alpha. Prolactin had no effect on either VP o r DP epithelial cells. The stimulatory effect of prolactin on E1 alpha was inhibited by actinomycin and cycloheximide, thereby indicating th at prolactin stimulated the biosynthesis of E1 alpha. The studies reve al that prolactin specifically stimulates E1 alpha levels of LP epithe lial cells, whereas testosterone specifically stimulates E1 alpha leve ls of VP epithelial cells. At this time, we propose that the effects o f prolactin and testosterone involve increased expression of the E1 al pha gene of LP and VP epithelial cells, respectively. (C) 1995 Wiley-L iss, Inc.