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Details for phenotype: negative regulation of steroid hormone biosynthetic

EndoNet ID: ENP00398

Name

negative regulation of steroid hormone biosynthetic

General information

This phenotype is not pathologic

Links to other resources

GO
MeSH term 68013256

Phenotype triggers

  • normal activity of BMP receptor type II
    in adrenal_cortex
    • In contrast to BMP-6, it recently could be demonstrated that both BMP-2 and BMP-5 are able to overall suppress forskolin-induced steroidogenesis in NCIh295R cells. [1]
    • Specifically, secretion of aldosterone, cortisol, and dehydroepiandrosterone-sulphate, was reduced by BMP-2 and BMP-5 in a dose-dependent manner. [1]
  • normal activity of leptin receptor
    in granulosa_cell
    • Leptin inhibited insulin-induced steroidogenesis by bovine granulosa cells. [2]
    • Leptin, at physiologic concentrations, directly affects insulin-induced steroidogenesis of granulosa cells. Normally fluctuating concentrations of leptin in blood may play an important role in communicating the metabolic status of the animal to the reproductive system. [2]
    • Leptin significantly suppresses LH-induced estradiol production. This is consistent with an endocrine action of leptin on the human ovary, with possible implications for female reproduction in health and disease. [3]
    • High dose of leptin suppressed LH-stimulated estradiol production in human granulosa cells. [3]
  • normal activity of leptin receptor
    in theca_cell
    • Leptin inhibited steroidogenesis by bovine theca cells. [4]
    • Leptin, at physiologic concentrations, directly affects steroidogenesis of thecal cells. Normally fluctuating concentrations of leptin in blood may play an important role in communicating the metabolic status of the animal to the reproductive system. [4]
    • In cultured theca cells, leptin did not alter androstenedione production, alone or in the presence of LH. Leptin caused a concentration-related inhibition of the IGF-I augmentation of LH-stimulated androstenedione production. Leptin can directly inhibit IGF-I action in ovarian theca at concentrations commonly present in obese women. [5]
Reference