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Biomedical subjects

M W Neuman

Publications and source records attributed to M W Neuman.

25 records · Page 2Linked to original sources

The metabolism of labeled parathyroid hormone. V. Collected biological studies.

Biologically active 125I-labeled parathyroid hormone (125I-PTH) was used in a series of studies in dogs and chickens designed to confirm and augment earlier studies in rats. As in rats, a three exponential equation was required to describe disappearance of 125I-PTH from the blood in the dog. The first two "half-lives" (1.8 and 7 min) accounted for the bulk of the dose. Also as in rats, deposition of apparently intact hormone took place rapidly in kidney, liver and bone in both the dog and the chicken. Degradation occurred very rapidly in all three target organs. Three labeled hormones of different biological activities were compared in the rat. Inactive, oxidized hormone was rejected by the liver but showed markedly increased deposition in kidney and the higher the purity of the hormone the higher was its uptake by liver. Exploration of a wide range of dosages revealed few effects on distribution (smaller deposition in liver and kidney at highest dosages, 65 mug/rat). Fresh sera did not degrade hormone rapidly or extensively. There was no deposition of hormone in intestinal mucosa, marrow, and red cells. Nephrectomy increased deposition in liver and bone. Finally, the perfused liver was capable of extensive degradation of the hormone.

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The metabolism of labeled parathyroid hormone. VI. Effects of vitamin D status.

Labeled 125I-PTH with full biological activity was utilized to investigate the interrelationship between vitamin D and parathyroid hormone (PTH) function. The distribution of labeled PTH was studied in rats and chickens on diets containing various amounts of vitamin D and calcium. The effects of vitamin D deficiency were found to be minor. There was a slightly delayed (10--30%) blood clearance of the hormone and a smaller deposition in the liver (20--30%) in the D-deficient animals. Deposition in bone and kidney appeared to be essentially normal. It is concluded that any failure of PTH to evoke a bone response in the deficient animal is not due to the failure of binding of hormone at the target organ.

Animals↗