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Biomedical subjects

M L McNatt

Publications and source records attributed to M L McNatt.

6 recordsLinked to original sources
PubMed1979

Alteration of cartilage glycosaminoglycan protein acceptor by somatomedin and cortisol.

The effect of somatomedin and cortisol on embryonic chick cartilage in vitro indicates that somatomedin stimulates 35SO4 uptake while cortisol decreases it with no effect on glycosaminoglycan turnover. Xylosyltransferase activity is increased in crude fractions of somatomedin-treated cartilage but decreased in cortisol-treated cartilage. By using a Smith-degraded proteoglycan as an exogenous acceptor, xylosyltransferase activities from both treatments were equivalent, suggesting that the enzyme was not rate limiting. The results of xylosyltransferase assays conducted by mixing enzyme and endogenous acceptor from control, cortisol-treated and somatomedin-treated cartilage, suggest both effects to be at the level of the acceptor protein.

Animals↗
PubMed1976

Uridine diphosphate xylosyltransferase activity in cartilage from manganese-deficient chicks.

The glycosaminoglycan content of cartilage is decreased in manganese deficiency in the chick (perosis). The activity of xylosyltransferase, the first enzyme in the biosynthetic pathway of sulphated glycosaminoglycans, was studied in the epiphysial cartilage of 4-week-old chicks which had been maintained since hatching on a manganese-deficient diet. Enzymic activity was measured by the incorporation of [14C]xylose from UDP-[14C]xylose into trichloroacetic acid precipitates. Optimal conditions for the xylosyltransferase assay were established and shown to be the same for both control and manganese-deficient cartilage. Assay of the enzyme by using an exogenous xylose acceptor showed no difference in xylosyltransferase activity between control and manganese-deficient tissue. Further, the extent of xylose incorporation was greater in manganese-deficient than in control cartilage preparations, suggesting an increase in xylose-acceptor sites on the endogenous acceptor protein in the deficient cartilage. 35S turnover in the manganese-deficient cartilage was also increased. The data suggest that the decreased glycosaminoglycan content in manganese-deficient cartilage is due to decreased xylosylation of the acceptor protein plus increased degradation of glycosaminoglycan.

Animals↗
PubMed1975

Glucocorticoid therapy in children. Effect on somatomedin secretion.

Glucocorticoids cause growth retardation in children. We have studied the effect of these hormones on serum somatomedin (Sm) levels in seven children with nephrosis. Intravenous administration of methylprednisolone sodium succinate, 2.2 mg/kg, causes a rapid fall in serum Sm activity. The activity remains suppressed during continuous therapy, but returns toward normal when medication is omitted during the course of alternate-day therapy. We conclude that one reason for growth retardation secondary to continuous glucocorticoid therapy is suppression of Sm generation. A direct effect of these hormones on the cartilage cell or induction of an Sm inhibitor cannot be excluded by the reported experiments.

Adolescent↗
PubMedDate not supplied

Somatomedin and the regulation of skeletal growth.

Somatomedin is a polypeptide(s) which "mediates" the actions of growth hormone. This pituitary dependent hormone was previously called "sulfation factor," a term derived from the bioassay technique which measures the incorporation of radioactive sulfate into cartilage glycosaminoglycans. Somatomedin has a more general effect upon cartilage; it is necessary for the cell multiplication and cartilage maturation which results in the growth of long bones. Somatomedin is not found in the plasma in growth hormone deficiency and appears following growth hormone administration. A genetic defect in somatomedin synthesis has been identified in the Laron's dwarf. Growth hormone is present in excess in the plasma and growth hormone administration does not stimulate somatomedin synthesis in this syndrome. Insufficient data are available to delineate the role for somatomedin in other growth disturbances. It has been demonstrated that glucocorticoid hormones interfere with both somatomedin synthesis and its biological activity. Purification of somatomedins in plasma has been achieved and radioreceptor or radioimmunoassays will be available in the future for study of growth problems in children.

Acromegaly↗