Sex hormone synthesis, regulation, and function ; ..

Increased glycogenesis is part of the androgen receptor-mediated cellular response and blockage of glycogenolysis by the GP inhibitor CP-91149 further increased glycogenesis. The combined use of a GP inhibitor with hormone therapy may increase the efficacy of hormone treatment by decreasing the survival of prostate cancer cells and thereby reducing the chance of cancer recurrence.

Sex hormone effects; Sex hormone synthesis, regulation, and function

Androgens Ppt | Androgen | Testosterone

20/11/2008 · Androgens Ppt - Download as ..

Testosterone is converted to two other important hormones. It is reduced to dihydrotestosterone in specific tissues like the skin and the prostate and it is oxidized to estradiol. In men this oxidation mainly takes place in adipose tissue and in the testes. In women the biosynthesis of estradiol takes place in the ovaria.

Ppt Androgen | Powerpoint Presentations and Slides » …

Much research has been devoted to unravel the biosynthesis of steroid hormones, because promising medical applications were expected. Many reviews have appeared in the literature about the biosynthetis of the male and female sex hormones [1][2]. The main features of the biosynthetic pathways of testosterone, dihydrotestosterone, estrone and estradiol are know today as they are depicted in Schemes 1 and 2.


Breastfeeding and Autism and Childhood Cancer

In this paper we describe the effect of androgen on glycogen metabolism in different prostate cancers. We used PC3-AR-V and PC3-AR-E7 cells, which ectopically expresses AR and in case of PC3-AR-E7 the HPV-E7 protein. Additionally, LNCaP, which maintains a functional AR, was tested for glycogen content and its correlation to the number of cells. The PC3-AR-V and PC3-AR-E7 cell lines demonstrated a response to androgen leading to G1 arrest with a corresponding increase in the glycogen content (2 to 5 fold). PC3 cells lacking AR did not increase glycogen content in response to androgen. PC3 (AR-) cells demonstrate that intracellular glycogen content corresponds with the growth and/or survival of cells harbouring a functional AR. Intracellular stores of glycogen correlated inversely with the cell number: when cell numbers are low the glycogen content is high. This inverse relationship suggests that glycogenesis participates in growth arrest. However, glycogenesis is most likely not sufficient to induce ATP-dependent apoptosis, as the inhibition of glycogenolysis with the GP inhibitor CP-91149 does not induce cell death in these prostate cell lines. Glycogen content normalized to the number of cells is about 50% higher in PC3-AR cells treated with R1881 than treated with CP-91149. The additional increase in glycogen content of R1881-treated PC3-AR-V/E7 cells upon CP-91149 treatment further results in a reduction of cell number by growth inhibition and reduction in cell viability, which suggests that a certain intracellular glycogen content has to be reached to affect cell viability. Alternatively, certain effects of hormone treatment on cell survival may be enhanced by inhibition of glycogenolysis using CP-91149. Similarly, LNCaP cells responded with glycogen accumulation and growth arrest upon androgen removal, which was further enhanced by the GP inhibitor CP-91149.

Steroid Hormone Synthesis In Adrenal ..

Testosterone is the most important androgenic-anabolic steroid. It is biosynthesized in the testes and per day about 4-10 mg of testosterone is produced by a grown up man. About 0.5 mg per day is produced in the adrenaline cortex of men and women.

Androgen Insensitivity Syndrome

The first committed step in steroid biosynthesis is the conversion of the 27-carbon skeleton of cholesterol to a C21-compound, pregnenolone (). This critical step, which is subject to hormonal control by the adrenocorticotropic hormone (ACTH) in the adrenals and by the luteinizing hormone (LH) in the gonads, is catalysed by a P-450 enzyme, the cholesterol side-chain cleavage enzyme P-450scc (also called 20,22-desmolase, or 20,22-lyase). Pregnenolone can be converted either to progesterone, which branches to the glucocorticoid and androgen/estrogen pathways, or to 17α-hydroxypregnenolone, which is another route for the formation of androgens and estrogens (, top-left part). Androgen formation in the adrenals is limited to dehydroepiandrosterone and androstenedione, whereas in the testes the presence of 17ß-hydroxysteroid dehydrogenase (17HSD) in Leydig cells (under the control of LH) ensures the formation of testosterone, the principal " male " hormone. Estrogen formation requires another P-450 enzyme, the aromatase complex (P-450Arom). The substrate is either androstenedione (for estrone) or testosterone (for estradiol). Estrone and estradiol are interconvertible through a reversible reaction involving another 17ß-hydroxysteroid dehydrogenase, as in the androstenedione-testosterone conversion. Aromatase activity is present in the ovary and the placenta (see below). In the ovary, aromatase activity and estrogen formation occur in cells and are controlled by the follicle-stimulating hormone (FSH), whereas production of the androgenic substrates (testosterone, 4-androstenedione) requires LH stimulation of the cells (5).

Použitá vědecká literatura | Adaptogeny

In the case of testosterone solutions for this problem have been found in the use of esters. These derivatives are converted slowly into free testosterone by esterases. Other solutions are the application of plasters or crèmes which slowly release testosterone directly in the bloodstream. As soon as the synthetic testosterone reaches the blood, it is metabolised quickly again, which necessitates a constant supply.