Physical and biochemical factors in bone metabolism.
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Animals↗
Biomedical subjects
J D Feinblatt
Publications and source records attributed to J D Feinblatt.
Future horizons for calcitonin: a U.S. perspective.
Injectable salmon calcitonin has been in use in the United States for more than a decade for the treatment of patients with postmenopausal osteoporosis, Paget's disease, and hypercalcemia. Sandoz Pharmaceuticals Corp. is currently in the process of developing a nasal formulation of salmon calcitonin. Studies are in progress to compare the efficacy of this nasal formulation with that of the injectable hormone in preventing bone loss and restoring bone, as well as in reducing pain associated with bone diseases. The rationale for development of a nasal formulation is to attempt to reduce the incidence of systemic side effects, inconvenience, and resulting noncompliance associated with the injectable product. In studies to date, the nasal form of calcitonin has been well tolerated by most subjects and was not notably associated with nasal irritation. The tolerability seen within the context of clinical trials suggests that a nasal formulation might be well accepted, even among asymptomatic osteoporotic patients. Asymptomatic patients with secondary osteoporosis due to steroid administration or solid organ transplantation may also be studied as possible candidates for the prophylactic use of this drug. Additional future research includes the development of an oral calcitonin agent.
Administration, Intranasal↗
Secretion of a bone resorbing factor by chick thyroid glands in organ culture.
The ability of the thyroid gland to secrete a bone resorbing factor in vitro was studied using glands obtained from 20-day-old chick embryos. The glands were incubated in a modified BGJ medium containing 1 mg/ml bovine serum albumin under 5% CO2-40% O2 at 37 C. The culture media were assayed in vitro by measuring the stimulation of the release of previously incorporated 45Ca from cultured 19-day fetal rat bone shafts over a 48 h period. The glands secreted a stimulator of bone resorption which did not appear to be parathyroid hormone (PTH). The dose-response curve for the thyroid gland factor was not parallel to that obtained using PTH and secretion was not under calcium control. Neither thyroxine (T4) nor triiodothyronine (T3) produced a marked stimulation of bone resorption over a wide range of doses. Bone resorption stimulated by the thyroid gland factor was inhibited by calcitonin (CT). Concentrations of TH and thyroid gland factor which were minimally effective when tested separately, produced a marked synergistic response when added together. This synergism was not seen when T4, T3, PGE1, or PGE2 were tested with PTH. Media obtained by culturing explants of embryonic chick liver, heart and muscle did not have bone resorbing activity. Secretion of the bone resorbing factor by thyroid glands was blocked by Indomethacin (10(-5)M) but the effects of the factor on bone were not blocked by this agent. These results suggest that the thyroid gland is capable of secreting a stimulator of bone resorption, possibly a prostaglandin, which is capable of synergizing with PTH, and which may represent a tissue factor which under certain circumstances may exert an influence on bone.
Animals↗
Avian parathyroid glands in organ culture: secretion of parathyroid hormone and calcitonin.
Parathyroid (PT) glands from 20-day-old embryonic chicks cultured in a chemically defined medium secreted a stimulator of in vitro bone resorption. This stimulator was presumed to be parathyroid hormone (PTH) because: 1) the in vitro dose response curve was parallel to that obtained with bovine PTH; 2) the activity was eluted on Sephadex G-1-- chromatography at a position similar to that for PTH; and 3) the material produced hypercalcemia in vivo in chicks. The amount of PTH-activity secreted was inversely proportional to the calcium concentration of the medium over the range of 0.75-2.25 mM. The chick PT glands also secreted an inhibitor of PTH-stimulated bone resorption in vitro. This inhibitor was presumed to be calcitonin (CT) because: 1) the in vitro dose-response curve was parallel to that obtained with synthetic salmon CT; 2) the activity was eluted on Sephadex G-50 chromatography at a position similar to that for salmon CT; and 3) the material produced hypocalcemia in vivo in rats. In contrast to what would be expected for CT secretion, the CT-activity was secreted by the PT glands in response to a low, not high calcium concentration. The data suggest that the secretion of avian PTH is similar to that of the mammalian hormone, and that the ultimobranchialectomized chick with an intact parathyroid gland may not be deficient in CT.
Animals↗