Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P02774 (Gc-globulin)
 196 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sera were sampled from 83 people (pre- and post-menopausal women and men). Climacteric symptoms of 23 women were treated with conjugated estrogen. Sera were sampled serially until the 21st day of estrogen administration. Serum concentrations of 40 protein components were measured by micro single radial immunodiffusion. The serum proteins were classified into 5 types according to changes after menopause and estrogen therapy, respectively. Type 1 (decreased after menopause and increased by estrogen; alpha 1-antitrypsin, alpha 2-HS - glycoprotein, beta 2-glycoprotein III, Gc-globulin, alpha 1-lipoprotein and alpha 2-AP-glycoprotein), type 2 (unchanged and increased; ceruloplasmin), type 3 (increased and decreased; alpha 1-acid glycoprotein, haptoglobin, serum amyloid P-component, Zn-alpha 2-glycoprotein, beta-lipoprotein and C1-components), type 4 (unchanged and decreased; hemopexin, antithrombin III, beta 2-glycoprotein I, prealbumin and retinol-binding-protein), type 5 (unchanged by estrogen; immunoglobulin M (IgM), IgG and others). Estrogen replacement therapy restored pre-menopausal levels of serum proteins, types 1 and 3. However, estrogen therapy was associated with significantly abnormal levels of proteins, types 2 and 4 in post-menopausal women. Serum levels of type 1 proteins and some type 5 proteins (IgM, alpha 1B-glycoprotein, C9-component and alpha 2-macroglobulin) were higher in pre-menopausal women than in men, whereas type 3 proteins were the opposite.
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PMID:Changes in 40 serum proteins of post-menopausal women. 186 40

We evaluated the effect of estrogens on "free" and total calcitriol levels and on the calcitriol response to a hypocalcemic challenge in 12 postmenopausal women, age 55-74 yr. Endogenous calcitriol production was induced by intravenous Na-EDTA before and after conjugated estrogens, 1.25 mg/d for 30 d. Free calcitriol was determined by centrifugal ultrafiltration and by the molar ratio of calcitriol to vitamin D-binding protein (DBP). Estrogen increased fasting total calcitriol from 38.5 +/- 3.8 to 62.3 +/- 7.0 pg/ml (P less than 0.05). This was accompanied by a rise in free calcitriol from 104.5 +/- 11.4 to 158.7 +/- 16.4 fg/ml (P less than 0.05). Vitamin D-binding protein increased from 348 +/- 16 to 428 +/- 12 micrograms/ml (P less than 0.001), and the ratio of calcitriol/DBP increased from 1.50 +/- 0.14 to 1.94 +/- 0.18 (P less than 0.005), confirming the rise in free calcitriol. Increases in free calcitriol and in calcitriol/DBP ratios were significantly correlated, r = 0.72. Hypocalcemia led to a rapid increase in circulating immunoreactive parathyroid hormone, and to a rise in calcitriol at 24 h. The hypocalcemia-induced rise in total and free calcitriol was similar before and after estrogen, whether expressed as increments or as percent changes. We conclude that estrogen increases circulating levels of biologically active free calcitriol in postmenopausal women, but that a 30-d period of estrogen administration does not apparently improve the renal 1 alpha-hydroxylase response to a PTH challenge.
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PMID:Effects of estrogen on circulating "free" and total 1,25-dihydroxyvitamin D and on the parathyroid-vitamin D axis in postmenopausal women. 249 9