Now we know—for sure.
Adding to a growing literature on the role of metabolic enzymes and ATP production in sperm function, it is now shown that one lactate dehydrogenase family member, LDHC, is required for male fertility. Several decades of work on this glycolytic enzyme had shown that it is expressed primarily in testis, but its functional significance had been only speculative. In an article on p. 26 Odet et al. report that male mice homozygous for a targeted disruption of Ldhc are severely impaired in fertility, whereas females are fertile. The fertility defects include impaired sperm motility, reduction of capacitation-related protein phosphorylation, and fertilization defects—all probably due to compromised ATP production. Thus, LDHC is required for glycolysis and ATP production in the sperm tail, and this finding may lead to new insights into infertility in men.
Fanny Odet, Chongwen Duan, William D. Willis, Eugenia H.
Goulding, Aisha Kung, Edward M. Eddy, and Erwin Goldberg.
Expression of the Gene for Mouse Lactate Dehydrogenase C
(Ldhc) Is Required for Male Fertility.
Biol Reprod
2008; 79:36-34. Published online in BOR-Papers in Press
on 26 March 2008; DOI 10.1095/biolreprod.108.068353
http://www.biolreprod.org/cgi/content/abstract/79/1/36?etoc
Prenatal programming.
Polycystic ovary syndrome, or PCOS, is among the most common causes of infertility, conservatively affecting 6-8% of women. Increasing evidence suggests symptoms of PCOS arise during the pubertal process; however, the cause or causes of PCOS remain unclear. Although genetic predispositions likely exist, environmental causes have also been suggested. In an article on p. 154 of this issue, Abbott and coworkers provide evidence in a primate model that prenatal exposure to androgens, which are elevated in women with PCOS during late gestation, provides an endocrine environment that leads to increased gonadotropin release both prenatally and postnatally, as well as leading to increased androgen levels in female infants. While these changes occurred in the absence of elevations of estrogen levels in the fetuses—suggesting androgen-mediated prenatal programming may be one of the factors that can contribute to the constellation of symptoms that define PCOS—local tissue conversion of androgen to estrogen may provide additional programming.
David H. Abbott, Deborah K. Barnett, Jon E. Levine, Vasantha
Padmanabhan, Daniel A. Dumesic, Steve Jacoris, and Alice F.
Tarantal.
Endocrine Antecedents of Polycystic Ovary Syndrome
in Fetal and Infant Prenatally Androgenized Female Rhesus
Monkeys.
Biol Reprod 2008; 79: 154-163. Published online in
BOR-Papers in Press on 2 April 2008;
DOI 10.1095/biolreprod.108.067702
http://www.biolreprod.org/cgi/content/abstract/79/1/154?etoc
Journal
Biology of Reproduction