The role of ACTH in the pathogenesis of polycystic ovarian syndrome in rats: hormonal profiles and ovarian morphology

Physiol Res. 2007;56(1):67-78. doi: 10.33549/physiolres.930870. Epub 2006 Feb 23.

Abstract

Numerous hypotheses have been proposed about the pathogenesis of the polycystic ovarian syndrome (PCOS). However, hormonal control of persistent follicles has not been established. The objective of the present study was to compare the follicular structure and hormonal profiles of rats treated with the adrenocorticotrophic hormone (ACTH) with two experimental models of PCOS. ACTH-treated animals were compared with those exposed to continuous light, those treated with estradiol valerate, and with control (in proestrous and diestrous). Serum hormone levels, histomorphometrical changes, and immunoexpression of vimentin, cytokeratins, cadherins, and proliferating cell nuclear antigen (PCNA) were examined. Treatment with ACTH resulted in an elevation of corticosterone secretion with LH reduction but without changes in ovarian morphology. Although stress (or ACTH) stimulation may be only one of pathophysiological mechanisms involved in follicular cyst pathogenesis in other species, we do not have important evidence to suppose that this would happen in rats.

MeSH terms

  • Adrenocorticotropic Hormone / physiology*
  • Animals
  • Cadherins / blood
  • Cell Proliferation
  • Corticosterone / blood
  • Estrous Cycle / physiology
  • Female
  • Gonadal Steroid Hormones / blood
  • Hormones / blood*
  • Image Processing, Computer-Assisted
  • Immunohistochemistry
  • Keratins / metabolism
  • Ovarian Follicle / pathology
  • Ovary / pathology*
  • Polycystic Ovary Syndrome / pathology*
  • Polycystic Ovary Syndrome / physiopathology*
  • Proliferating Cell Nuclear Antigen / blood
  • Rats
  • Rats, Wistar
  • Vimentin / metabolism

Substances

  • Cadherins
  • Gonadal Steroid Hormones
  • Hormones
  • Proliferating Cell Nuclear Antigen
  • Vimentin
  • Keratins
  • Adrenocorticotropic Hormone
  • Corticosterone