Luteinizing hormone in testicular descent

Mol Cell Endocrinol. 2007 Apr 15;269(1-2):34-7. doi: 10.1016/j.mce.2006.10.021. Epub 2007 Feb 13.

Abstract

A proper hypothalamus-pituitary-testis axis with normal androgen synthesis and action is a prerequisite for normal testicular descent. Various defects in this axis may result in cryptorchidism but endocrine abnormalities are rarely detected. Androgens regulate testicular descent but androgen action alone is not sufficient for normal testicular descent. The regulation of androgen production is influenced both by placental human chorionic gonadotropin (hCG) and pituitary luteinizing hormone (LH). There is evidence that the longer pregnancy continues, the more important role pituitary LH may have. Insulin-like hormone-3 (INSL3) is suggested to be the main regulator of gubernacular development and therefore an apparent regulator of testicular descent. INSL3 production is also related to LH, and reduced INSL3 action is a possible cause for cryptorchidism. Cryptorchid boys have normal testosterone levels with slightly but significantly elevated LH levels as compared to healthy boys. This high gonadotropin drive may compensate for mild Leydig cell dysfunction in cryptorchidism.

Publication types

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

MeSH terms

  • Animals
  • Chorionic Gonadotropin / physiology
  • Cryptorchidism / etiology
  • Cryptorchidism / genetics
  • Humans
  • Insulin / genetics
  • Insulin / physiology
  • Luteinizing Hormone / pharmacology
  • Luteinizing Hormone / physiology*
  • Male
  • Models, Biological
  • Proteins / genetics
  • Proteins / physiology
  • Testis / drug effects
  • Testis / embryology*

Substances

  • Chorionic Gonadotropin
  • Insulin
  • Leydig insulin-like protein
  • Proteins
  • Luteinizing Hormone