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Abstract

Follicle-stimulating hormone and leukemia inhibitory factor regulate Sertoli cell retinol metabolism (PDF) (HTML) 
Guo,Xiajia; Morris,Patricia L.; Gudas,Lorraine J..
Endocrinology 142(3): 1024-1032
Publication date: 2001

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Sertoli cells, the somatic epithelial cells of the seminiferous tubules,provide both structural and biochemical support for developing malegerm cells. The Sertoli cells are targets of retinoid actionin the testis. We have found that FSH, (Bu)cAMP, and leukemia inhibitoryfactor elicit substantial changes in the metabolism of [H]retinol(vitamin A) in primary cultures of purified rat Sertoli cells.Addition of (Bu)cAMP for 2 h or FSH for 6 h results in a 3-foldincrease in the metabolism of [H]retinol to [H]retinoic acid ([H]RA);the esterification of [H]retinol to [H]retinyl esters, especially [H]retinylpalmitate, is also increased by approximately 5-fold. The additionof 1 µM all-trans-RA also elicits changes in [H]retinolmetabolism, but in this case the metabolism of [H]retinol to [H]RAis inhibited, whereas the metabolism of [H]retinol to [H]retinylesters is increased by over 50-fold. Leukemia inhibitory factorincreases the esterification of [H]retinol by 2- to 3-fold.FSH leads to a reduction in the level of cellular retinol bindingprotein I transcripts, whereas RA increases the cellular retinolbinding protein I messenger RNA level by about 2-fold at approximately24 h. Levels of AHD-2 (aldehyde dehydrogenase-2) and RALDH-2 (retinaldehydedehydrogenase-2) messenger RNAs, which encode enzymes that convert[H]retinaldehyde to [H]RA, are increased by about 2-fold byFSH, whereas no change in CYP26 (RA hydroxylase) expressionis seen. Our results suggest that one function of FSH (and/or(Bu)cAMP) in Sertoli cells is to increase the metabolism ofretinol to the biologically active metabolite RA and to retinylesters.

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