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Details for phenotype: sebaceous gland development

EndoNet ID: ENP00710

Name

sebaceous gland development

General information

This phenotype is not pathologic

Links to other resources

GO

Phenotype triggers

  • normal activity of AR
    in sebaceous_glands
    • The development of the sebaceous gland depends on androgens. The administration of testosterone to castrated males, children or postmenopausal women in whom sebaceous secretion is normally low results in significant increase in sebaceous gland activity. Thus, the sebaqueous gland is an androgen target-organ. [1]
  • more activity (high ligand concentration, overexpression) of ER-alpha
    in sebaceous_glands
    • Systematically administered estrogen elicits a reduction in the size and secretion of sebaceous glands both in men and women, but this effect is usually achieved only with doses that exceed the physiologic requirement of women and produce feminization in men. [1]
  • more activity (high ligand concentration, overexpression) of ER-beta
    in sebaceous_glands
    • Systematically administered estrogen elicits a reduction in the size and secretion of sebaceous glands both in men and women, but this effect is usually achieved only with doses that exceed the physiologic requirement of women and produce feminization in men. [1]
  • normal activity of PR B
    in sebaceous_glands
    • Progesterone could increase the size of sebaceous glands in spayed rats. [2]
    • But this hormone is not responsible for maintaining sebaceous gland secretion. [1]
  • normal activity of progesterone receptor A
    in sebaceous_glands
    • Progesterone could increase the size of sebaceous glands in spayed rats. [2]
    • But this hormone is not responsible for maintaining sebaceous gland secretion. [1]
  • normal activity of melanocortin receptor 5
    in sebaceous_glands
    • Adrenal androgens may contribute significantly in sebaceous gland development. If neither estrogen nor ACTH has any directly supressive or stimulating effect respectively on the sebaqueous gland, the negative response to ACTH stimulation may mean either that endogenous androgens from the adrenal cortex are not sebum stimulating or that the estrogen together with pituitary-gonadal hormones supresses the adrenal gland directly. [1]
Reference