Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.16.3.1 (ceruloplasmin)
 5,074 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The residual androgenic activity of two new combined oral contraceptives (OCs)--30 mcg of ethinyl estradiol in combination with either 150 mg of desogestrel or 75 mcg of gestodene--was investigated in 40 healthy volunteers. Measured in these volunteers were modifications in transport protein levels. These levels are known to be increased by estrogen, but this increase can be counterbalanced, to varying degrees, by gestagens. For both OCs, there was a marked percentage increase in sex hormone binding globulin (SHBG), corticosteroid binding globulin (CBG), thyroxine binding globulin (TBG), and ceruloplasmin (CP) and a similar reduction in total testosterone and the free androgen index. The modifications in SHBG, CBG, TBG, and CP are interpreted as an expression of the correlated value of the estrogenicity/gestagenicity ratio of the OCs studied and suggest that these particular formulations have greater estrogenicity. The relatively negligible biological androgenic activity of desogestrel and gestodene and their elevated affinity progesterone receptor/androgen receptor ratio reflect the high selectivity of these agents. Moreover, the lack of androgenic effects makes desogestrel and gestodene appropriate treatment agents for hyperandrogenism.
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PMID:Sex hormone binding globulin, cortisol binding globulin, thyroxine binding globulin, ceruloplasmin: changes in treatment with two oral contraceptives low in oestrogen. 182 29

Men who chronically abuse alcohol may display a spectrum of endocrine abnormalities including hypogonadism and feminization, with elevated serum estradiol and low serum testosterone. We examined factors that may result in disruption of hepatic sex hormone homeostasis in alcohol-fed male rats and possible consequences of such changes. Rats were fed alcohol-containing or isocaloric diets for 30, 60, and 90 days. In alcohol-fed rats, serum testosterone levels and hepatic activity of 2 androgen-dependent estrogen metabolizing enzymes were reduced (P <.05) at all times, as was activity of androgen receptor. There was also a significant early and progressive decrease in testes/body ratio in alcohol-fed rats. Compared with this early decrease in testosterone-related parameters, there was a significant increase in serum estrogen levels (at 30 and 90 days, 132% and 168% of control values, respectively). An increase in serum ceruloplasmin, an estrogen-responsive liver protein, was apparent at 60 and 90 days, but not at 30 days of alcohol exposure, suggesting that hypogonadism precedes liver feminization. Hepatic estrogen receptor activity was decreased in alcohol-fed rats at 60 and 90 days, the latter despite elevated serum estrogen levels. Hepatic aromatase was slightly increased in alcohol-fed rats, an elevation probably not sufficient to account for observed increases in serum estrogen. Taken together, these data suggest that (1) alcohol induces profound reduction of serum testosterone, resulting in loss of androgen-regulated hepatic functions such as estrogen-metabolizing enzyme activity and activity of androgen receptors; and (2) such alcohol-induced hypogonadism precedes changes in hepatic sex hormone homeostasis and subsequent feminization.
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PMID:Hypogonadism precedes liver feminization in chronic alcohol-fed male rats. 1079 90