Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.5 (5'-nucleotidase)
 3,167 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To test the hypothesis of a defect in GH-receptor interaction, which could explain the growth failure of thalassemic children, the binding of [125I]human (h) GH to membrane fractions prepared from liver biopsies was studied. Small amounts of liver were obtained from 6 girls and 11 boys with homozygous beta-thalassemia, aged 3-15 yr, all prepubertal, at the time of splenectomy. Specific binding of [125I]hGH ranged from 0.37-5.11% of the added radioactivity/100 micrograms liver membrane protein, with variations in both receptor number and binding affinity. This 14-fold variation in hGH binding to liver membranes of thalassemic children was comparable to that in membrane fractions of livers obtained from normal donors at the time of liver transplant. The binding of insulin to liver membranes from the thalassemic patients ranged from 9.8-17.9% of the added radioactivity/100 micrograms membrane protein and from 2.8-15.0%/100 micrograms membrane protein in the normal donors. Insulin and GH binding to liver membranes did not vary in a consistent way. A 3-fold difference was found in 5'-nucleotidase activity of the membrane fractions. Histological hepatic modifications were assessed with respect to siderosis and fibrosis. No correlation was found between these parameters and GH binding. These results suggest that possible membrane alterations are not the only reason for the variations in hGH binding. All patients had retarded growth, and all but 2 had low plasma insulin-like growth factor I levels. No relationship was found between the level of GH binding to liver membranes and the growth failure. Thus, a defect in GH binding to liver membranes is probably not the cause of the growth retardation of thalassemic children.
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PMID:No evidence for a defect in growth hormone binding to liver membranes in thalassemia major. 264 90

Non-insulin-dependent diabetes mellitus (NIDDM) may cause vulnerability to moderate zinc deficiency. In this study, short-term zinc supplementation (30 mg/d as amino acid chelate for 3 wk) elevated plasma zinc and activities of 5'-nucleotidase, a zinc-dependant enzyme, in 20 postmenopausal women with NIDDM. Placebo, given to 20 other women with NIDDM, had no effects on these indexes nor on any others taken in this study. Although zinc supplementation doubled the mean value for 5'-nucleotidase activity, values were still significantly lower than those of age-matched control subjects. Plasma insulin-like growth factor I concentrations increased with zinc treatment if starting concentrations were < 165 microg/L but were unchanged if they were > 165 microg/L. Lipoprotein oxidation in vitro, which has abnormal lag times and propagation rates for subjects with NIDDM and for moderately zinc-deficient rats, were unchanged by zinc supplementation. Possibly, this lack of effect occurred because the zinc treatment did not normalize zinc status. In conclusion, this study supports the contention that moderate zinc deficiency occurs frequently in subjects with NIDDM.
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PMID:Short-term zinc supplementation in women with non-insulin-dependent diabetes mellitus: effects on plasma 5'-nucleotidase activities, insulin-like growth factor I concentrations, and lipoprotein oxidation rates in vitro. 949 98