Apoptotic germ cells regulate fatty acid metabolism by activating PPARβ/δ in rat Sertoli cells

REGUEIRA M; RIERA MF; GALARDO MN; RINDONE GM ; PELLIZZARI EH ; CIGORRAGA SB ; MERONI SB

Grand Rapids, Michigan

Congreso; 47th Annual Meeting of the Society for the Study of Reproduction; 2014

Society for the Study of Reproduction

Sertoli cells (SC) provide the structural and nutritional support for germ cell development. Studies on SC glucose metabolism have shown that this cell type actively metabolizes glucose and converts it to lactate, which is the major source of energy for germ cells. Based on this particular metabolic strategy, it has been postulated that SC uses fatty acids (FA) as a source of energy. The transcriptional factor PPARβ/δ?member of the PPARs nuclear receptor family? is known to regulate the expression of genes involved in FA metabolism in many cells types. We have recently demonstrated that pharmacological activation of PPARβ/δ ?physiologically activated by FA or derivatives? increases mRNA levels of: FA transporter CD36 (FAT/CD36), carnitine palmitoyltransferase 1 (CPT1) and long- and medium-chain 3-hydroxyacyl-CoA dehydrogenases (LCAD, MCAD). The aim of this work was to analyze possible mechanisms which might be operating in the seminiferous tubules to regulate FA metabolism in SC. On the one hand, we evaluated if FA can regulate the levels of FA oxidation (β-oxidation) and the expression of the above-mentioned genes. For this purpose, SC cultures obtained from 20-day-old rats were maintained under basal (B) conditions or treated with palmitic acid for 48h (P, 500M), in the absence or presence of a PPARβ/δ inhibitor (20μM GSK3787; GSK). The β-oxidation assay was performed measuring 3H2O production from [9,10-3H(N)]-palmitic acid. CPT1 mRNA levels were analyzed by Northern Blot and FAT/CD36, LCAD and MCAD mRNA levels were analyzed by RQPCR. We observed that P increased β-oxidation (B: 1.9±0.1; P: 4.3±0.5* pmol P/h/g DNA, *p