androstenedione/necrosis

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Altered function of the hypothalamic stress axes in patients with moderately active systemic lupus erythematosus. II. Dissociation between androstenedione, cortisol, or dehydroepiandrosterone and interleukin 6 or tumor necrosis factor.

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OBJECTIVE To investigate adrenocorticotropin, androstenedione (ASD), cortisol, or dehydroepiandrosterone sulfate (DHEAS) before and during a corticotropin releasing hormone (hCRH) test in patients with moderately active systemic lupus erythematosus (SLE) undergoing low dose longterm glucocorticoid

Tumor necrosis factor-alpha attenuation of luteinizing hormone-stimulated androstenedione production by ovarian theca-interstitial cells: inhibition at loci within the adenosine 3',5'-monophosphate-dependent signaling pathway.

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Tumor necrosis factor-alpha (TNF) blocks LH-stimulated androstenedione production by immature rat theca-interstitial cells (TIC) in vitro. The mechanism for TNF inhibition of LH-induced androstenedione is unknown and was investigated. LH stimulation of androstenedione synthesis in TIC is mediated

Anti-tumour necrosis factor antibody treatment does not change serum levels of cortisol binding globulin in patients with rheumatoid arthritis but it increases androstenedione relative to cortisol.

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BACKGROUND Cortisol binding globulin (CBG) is produced by liver cells and is inhibited by proinflammatory cytokines such as interleukin (IL) 6. CBG serum levels are typically low during prolonged inflammatory processes. Thus, observed changes of cortisol during anti-tumour necrosis factor (TNF)

Effects of tumor necrosis factor-alpha in vitro on steroidogenesis of healthy and atretic follicles of the rat: theca as a target.

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Tumor necrosis factor-alpha (TNF), a pleiotropic cytokine localized within the ovary, alters follicular steroidogenesis. Preovulatory follicles dissected from ovaries of normal cyclic adult rats on the morning of proestrus exhibit steroidogenic and histological signs of atresia after 24 h of culture

The effect of tumor necrosis factor/cachectin on follicle-stimulating hormone-induced aromatase activity in cultured rat granulosa cells.

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We investigated the effects of tumor necrosis factor (TNF)/cachectin on follicle-stimulating hormone (FSH)-induced aromatase activity in cultured rat granulosa cells using the stereospecific transfer of 3H from [1 beta-3H] androstenedione into 3H2O. TNF (10 pg/ml-10 ng/ml) inhibited FSH (250

Tumor necrosis factor alpha versus LH and androstendione as a reliable predictor of spontaneous ovulation after laparoscopic ovarian drilling for women with clomiphene citrate resistance polycystic ovarian disease.

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OBJECTIVE Laparoscopic ovarian drilling (LOD) is still a controversial decision; due to the long term hazards; so short and long term predictors after the procedure should be taken in consideration. The aim of this work was to investigate the role of the serum level of tumor necrosis factor alpha

Role of osteocalcin, tumor necrosis factor-alpha and adiponectin in polycystic ovary syndrome patients with insulin resistance.

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OBJECTIVE Insulin resistance (IR) seems to be the main pathogenic factor in polycystic ovary syndrome (PCOS). Adiponectin and tumor necrosis factor-alpha (TNF-α) are important in IR. The aim of this study was to evaluate the correlations of osteocalcin, adiponectin, and TNF-α with IR in

Receptors for insulin-like growth factor-I and tumor necrosis factor-alpha are hormonally regulated in bovine granulosa and thecal cells.

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Mastitis induces release of tumor necrosis factor-alpha (TNFalpha) and has been linked with reduced reproductive performance. To further elucidate the role and mechanism of action of TNFalpha on ovarian cells, the effect of TNFalpha on insulin-like growth factor-I (IGF-I)-induced steroidogenesis and

Tumor necrosis factor-alpha induces clustering in ovarian theca-interstitial cells in vitro.

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Tumor necrosis factor-alpha (TNF) has been implicated in the regulation of steroidogenesis in theca-interstitial cells (TIC). The purpose of this study was to evaluate any change in TIC morphology during the time course of TNF-induced inhibition of LH-stimulated androstenedione production. Ovaries

Tumor necrosis factor-alpha (TNF-alpha) inhibits steroidogenesis of bovine ovarian granulosa and thecal cells in vitro. Involvement of TNF-alpha receptors.

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The effect of recombinant bovine tumor necrosis factor-alpha (TNF-alpha) on steroidogenesis and numbers of bovine ovarian granulosa and thecal cells has been studied, and specific binding sites for 125I-TNF-alpha on ovarian cells have been determined. Granulosa cells have been examined from small

Seasonal adiposity and delayed ovulation in a vespertilionid bat, Scotophilus heathi: role of tumor necrosis factor-alpha.

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The aim of this article was to evaluate the physiological significance of tumor necrosis factor-alpha (TNF-alpha) in seasonal accumulation of adipose tissue, hyperinsulinemia, and anovulation in Scotophilus heathi. The result showed seasonal variations in the circulating TNF-alpha level. A higher

Tumor necrosis factor as a potent inhibitor of adrenocorticotropin-induced cortisol production and steroidogenic P450 enzyme gene expression in cultured human fetal adrenal cells.

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We have previously demonstrated that tumor necrosis factor alpha (TNF-alpha), a multifunctional cytokine mainly produced by activated monocytes, inhibits the ACTH-induced production of cortisol in cultures of human fetal adrenals. To clarify the molecular basis of this suppression, we investigated

Involvement of protein kinase C and protein tyrosine kinase pathways in tumor necrosis factor-alpha-induced clustering of ovarian theca-interstitial cells.

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Tumor necrosis factor-alpha (TNF) induces clustering of theca-interstitial cells (TIC) isolated from immature, hypophysectomized rats, while inhibiting luteinizing hormone (LH)-stimulated androstenedione in vitro. Stimulators of PKC, 1-oleoyl-2-acetyl-sn-glycerol (OAG, 50 and 100 microM) and

Modulation of human granulosa cell steroid production in vitro by tumor necrosis factor alpha: implications of white blood cells in culture.

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OBJECTIVE To test the hypothesis that the macrophage cytokine, tumor necrosis factor-alpha (TNF-alpha), directly inhibits progesterone, estrone (E1), and estradiol (E2) synthesis by human granulosa cells in vitro in the presence and absence of white blood cells. METHODS Granulosa cells from follicle

Tumor necrosis factor alpha alters follicular steroidogenesis in vitro.

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Preovulatory follicles from cyclic proestrous rats were incubated in vitro in M199 for up to 24 hours with various doses of human tumor necrosis factor alpha (TNF). Stepwise increases in progesterone (P) production (20-80 ng/ml/2 follicle/24 hours) were observed with 30-300 pM TNF; 3000 pM TNF

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