Effect of prolactin on testicular lipid metabolism in pubertal rats.
Prolactin administration for 7 day to pubertal rats resulted in marked depletion of total lipids, phospholipids and particularly phosphatidyl choline and phosphatidyl ethanolamine. There was a concomitant increase in total cholesterol and cholesterol ester with a fall in free cholesterol. The increase in total cholesterol in the testis of prolactin-treated animals appears not to be due to its increased synthesis, as the hormonal treatment had no significant effect on HMG-Co A reductase, the rate limiting enzyme of sterol synthesis. Prolactin also had no significant effect on the enzymes glucose-6-phosphate dehydrogenase, malic- and isocitrate dehydrogenases reported to generate NADPH required for active steroidogenesis. Thus, it appears that the fall observed in testicular phospholipids and free cholesterol with concurrent increases in total cholesterol and cholesterol ester after prolactin administration is not due to prolactin's effect directly on testicular lipid metabolism in pubertal rats.
D000818:Animals; D002784:Cholesterol / Q000378:metabolism; D005954:Glucosephosphate Dehydrogenase / Q000378:metabolism; D005989:Glycerides / Q000378:metabolism; D006903:Hydroxymethylglutaryl CoA Reductases / Q000378:metabolism; D007521:Isocitrate Dehydrogenase / Q000378:metabolism; D050356:Lipid Metabolism; D008291:Malate Dehydrogenase / Q000378:metabolism; D008297:Male; D010743:Phospholipids / Q000378:metabolism; D011388:Prolactin / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D012741:Sexual Maturation; D013737:Testis / Q000201:enzymology / Q000378:metabolism*; D014280:Triglycerides / Q000378:metabolism
D005989:Glycerides; D010743:Phospholipids; D014280:Triglycerides; D011388:Prolactin; D002784:Cholesterol; D006903:Hydroxymethylglutaryl CoA Reductases; D008291:Malate Dehydrogenase; D007521:Isocitrate Dehydrogenase; D005954:Glucosephosphate Dehydrogenase