Steroid and thyroid hormones action

We have also noted that 24-hour urinary estrogens can be a sensitive monitor of liver detoxification capability. Elevated urinary estrogens in normally-cycling women may indicate a history of exposure to liver stresses such as excessive environmental organic chemicals. Interventions intended to improve liver function result in a gradual normalization of the abnormal estrogen levels. Thus, measurement of urinary estrogens can give insight into other aspects of physiology. This phenomenon is also noted in peri- or post-menopausal women who have previously taken Premarin, and have switched to triple-estrogen replacement with less-than-optimal symptom relief.

GR was the first receptor to be identified in mitochondria with this methodology (Fig. 2 A, Table 1 ). Specifically, GR was found in rat liver mitochondria of adrenalectomized animals, 15 min after dexamethasone administration, whereas in noninduced animals the mitochondria showed only traces of the receptor ( 45 ). GR was detected in mitochondria of HeLa cells ( 46 ), in cytoplasmic and synaptosomal mitochondria of rat brain ( 47 ), in mitochondria of Mueller glia cells of the Salamander retina ( 48 ) and of rat C6 glioma cells ( 49 ). GR was also located in HepG2 hepatocarcinoma and SaOS-2 osteosarcoma cell lines ( 42 ). Using specific antibodies to GRα and GRβ, it was shown that GRα was the isoform detected in mitochondria, in addition to its presence in the cytoplasm and the nucleus, whereas GRβ was confined solely to the nucleus, accumulating preferentially in the nucleoli ( 42 ). Two main bands, reacting with anti-GRα, of molecular weight 95 and 90 K were observed in Western blots, as well as smaller proteins, which could represent GR degradation products. Mitochondrial GR was described by Sionov et al. ( 50 ) in T-lymphocytes, in relation to glucocorticoid induced apoptosis (see “ Role of Mitochondrial Steroid Hormone Receptors in Apoptosis ” section).

Cells of the zona fasciculata and zona reticularis lack aldosterone synthase (CYP11B2) that converts corticosterone to aldosterone, and thus these tissues produce only the weak mineralocorticoid corticosterone. However, both these zones do contain the CYP17A1 missing in zona glomerulosa and thus produce the major glucocorticoid, cortisol. Zona fasciculata and zona reticularis cells also contain CYP17A1, whose 17,20-lyase activity is responsible for producing the androgens, dehydroepiandosterone (DHEA) and androstenedione. Thus, fasciculata and reticularis cells can make corticosteroids and the adrenal androgens, but not aldosterone.

AB - Thyroid function is modulated by genetic and environmental causes as well as other illnesses and medications such as gonadal or sex steroids. The latter class of drugs (sex steroids) modulates thyroid function. Gonadal steroids exert their influence on thyroid function primarily by altering the clearance of thyroxine-binding globulin (TBG). While oestrogen administration causes an increase in serum TBG concentration, androgen therapy results in a decrease in this binding protein. These effects of gonadal steroids on TBG clearance and concentration are modulated by the chemical structure of the steroid being used, its dose and the route of administration. Despite the gonadal steroids-induced changes in serum TBG concentrations, subjects with normal thyroid glands maintain clinical and biochemical euthyroidism without changes in their serum free thyroxine (T4) or thyroid-stimulating hormone (TSH) levels. In contrast, the administration of gonadal steroids to patients with thyroid diseases causes significant biochemical and clinical alterations requiring changes in the doses of thyroid medications. Similarly, gonadal steroid therapy might unmask thyroid illness in previously undiagnosed subjects. It would be prudent to assess thyroid function in subjects with thyroid disease 6-8 weeks after gonadal steroid administration or withdrawal.

Steroid and thyroid hormones action

steroid and thyroid hormones action

AB - Thyroid function is modulated by genetic and environmental causes as well as other illnesses and medications such as gonadal or sex steroids. The latter class of drugs (sex steroids) modulates thyroid function. Gonadal steroids exert their influence on thyroid function primarily by altering the clearance of thyroxine-binding globulin (TBG). While oestrogen administration causes an increase in serum TBG concentration, androgen therapy results in a decrease in this binding protein. These effects of gonadal steroids on TBG clearance and concentration are modulated by the chemical structure of the steroid being used, its dose and the route of administration. Despite the gonadal steroids-induced changes in serum TBG concentrations, subjects with normal thyroid glands maintain clinical and biochemical euthyroidism without changes in their serum free thyroxine (T4) or thyroid-stimulating hormone (TSH) levels. In contrast, the administration of gonadal steroids to patients with thyroid diseases causes significant biochemical and clinical alterations requiring changes in the doses of thyroid medications. Similarly, gonadal steroid therapy might unmask thyroid illness in previously undiagnosed subjects. It would be prudent to assess thyroid function in subjects with thyroid disease 6-8 weeks after gonadal steroid administration or withdrawal.

Media:

steroid and thyroid hormones actionsteroid and thyroid hormones actionsteroid and thyroid hormones actionsteroid and thyroid hormones actionsteroid and thyroid hormones action

http://buy-steroids.org