Cholesterol and male fertility: what about orphans and adopted?

Mol Cell Endocrinol. 2013 Apr 10;368(1-2):30-46. doi: 10.1016/j.mce.2012.06.011. Epub 2012 Jul 3.

Abstract

The link between cholesterol homeostasis and male fertility has been clearly suggested in patients who suffer from hyperlipidemia and metabolic syndrome. This has been confirmed by the generation of several transgenic mouse models or in animals fed with high cholesterol diet. Next to the alteration of the endocrine signaling pathways through steroid receptors (androgen and estrogen receptors); "orphan" and "adopted" nuclear receptors, such as the Liver X Receptors (LXRs), the Proliferating Peroxisomal Activated Receptors (PPARs) or the Liver Receptor Homolog-1 (LRH-1), have been involved in this cross-talk. These transcription factors show distinct expression patterns in the male genital tract, explaining the large panel of phenotypes observed in transgenic male mice and highlighting the importance of lipid homesostasis and the complexity of the molecular pathways involved. Increasing our knowledge of the roles of these nuclear receptors in male germ cell differentiation could help in proposing new approaches to either treat infertile men or define new strategies for contraception.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Cholesterol / metabolism*
  • Fertility*
  • Gene Expression
  • Humans
  • Infertility, Male / metabolism
  • Leydig Cells / metabolism
  • Lipid Metabolism
  • Male
  • Organ Specificity
  • Orphan Nuclear Receptors / physiology*
  • Peroxisome Proliferator-Activated Receptors / physiology
  • Testis / metabolism
  • Testis / pathology
  • Testis / physiopathology

Substances

  • Orphan Nuclear Receptors
  • Peroxisome Proliferator-Activated Receptors
  • Cholesterol