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R V Talmage

Publications and source records attributed to R V Talmage.

At least 37 records · Page 2Linked to original sources
PubMed1984

Bone density in women: college athletes and older athletic women.

Bone density was studied in intercollegiate athletes and older athletic women. Single-photon densitometry was used to assess bone density parameters at a new distal radial site, the midradius, and the first metatarsus. Dual-photon densitometry assessed bone density of the lumbar spine. Eleven intercollegiate tennis players, 23 swimmers, and 86 older "athletic" women from 23 to 75 years of age were compared with age-matched nonathletic controls. "Athletic" describes adult women who exercised at least three times per week, 8 or more months of the year, for a minimum of 3 years. The radius and metatarsus bone content of intercollegiate athletes was significantly above control values. Lumbar spine density was significantly higher only in tennis players. Mean bone density values for adult "athletic" women were also significantly greater than in age-matched controls. In the oldest athletic group (55-75 years of age) bone measurement values in radius and lumbar spine were in the same range as for younger "athletic" women. In contrast, after 50 years of age, these values in the control population decreased by 0.7%/year. Therefore the largest variance (increase) from age-matched controls occurred in the oldest "athletic" group. Also, we have established a distal radial density value (using our modified site) below which we consider women "at risk" and recommend further bone health evaluation. Only two adult athletic women greater than 55 years of age fell into this category. It is concluded from this cross-sectional study that a regularly maintained athletic program for adult women may reduce the rate of "normal" bone mass loss accompanying age, particularly postmenopausally.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1983

Rat kidney microsomes convert 25-hydroxyvitamin D3 to an unidentified metabolite.

Kidney microsomes from vitamin D-deficient rats and from thyroparathyroidectomized rats converted 25-hydroxyvitamin D3 to an unidentified metabolite. The addition of the cytosolic fraction enhanced microsomal synthesis of this metabolite two-fold. The kinetics of the conversion in the presence of the cytosolic fraction was allosteric, suggesting that the enzyme responsible for synthesis of this metabolite might serve some role in the regulation of vitamin D metabolism. Microsomes from vitamin D-fed thyroparathyroidectomized rats also produced a second metabolite, tentatively identified as 25,26-dihydroxyvitamin D3 because of its comigration with 25,26-dihydroxyvitamin D3 in three different chromatographic systems.

Animals↗
PubMed1982

Vitamin D deficiency in rats with normal serum calcium concentrations.

Rats were raised after weaning on a vitamin D-deficient diet which used whole wheat and casein as the major protein source. For at least the first year of life, plasma calcium concentrations of these rats were the same as those of vitamin D-replete rats, and the rate of growth was normal for at least 6 months. The following evidence establishes the vitamin D deficiency of the rats (both male and female) on this diet: (i) plasma levels of 1,25-dihydroxycholecalciferol (1,25-dihydroxyvitamin D3) became undetectable after 6 weeks on the diet; (ii) by 4 months of age, the epiphyseal growth plates of the tibia were significantly enlarged and disorganized; (iii) when subjected to fracture in a dynamic torsion machine, the femur showed marked weakening as indicated by stress analysis; (iv) isolated kidney cells from the deficient rats showed a 3-fold increase in 25-hydroxyvitamin D 1-hydroxylase activity. When mother rats were placed on the vitamin D-deficient diet during lactation, plasma calcium values in the pups decreased and remained low throughout life and there was a stunted body growth pattern. It is concluded that hypocalcemia is not a necessary manifestation of vitamin D deficiency, that the onset of vitamin D deficiency during neonatal life influences the calcium homeostatic system, and that the normocalcemic, vitamin D-deficient animal provides an experimental model in which the effects of vitamin D deficiency can be studied independently of hypocalcemia.

Animals↗
PubMed1982

Changes in calcium phosphate on bone surfaces and in lining cells after the administration of parathyroid hormone or calcitonin.

Small doses of parathyroid hormone and calcitonin were injected into thyroparathyroidectomized newborn rats to investigate the histological and chemical changes in bone surfaces and in mitochondrial granules of bone lining cells. Nondecalcified tissue specimens were observed under transmission electron microscope, electron probe X-ray microanalyzer, and microdiffraction after "freeze substitution" preparation of tibia shafts. Amorphous calcium phosphate, which appears as clusters and globules by this "freeze substitution" preparation, appears on the bone surfaces in a short time after the administration of a small dose of calcitonin. The Ca:PO4 ratio in the mitochondria of bone lining cells rises slightly with a small dose of parathyroid hormone and is reduced with a small dose of calcitonin. These data support the postulate that both parathyroid hormone and calcitonin act directly on bone lining cells in the process of influencing calcium concentrations of blood and temporarily storing calcium at bone surfaces.

Animals↗
PubMed1981

Calcitonin and phosphate.

This report summarizes the relationship of calcitonin to phosphate. The hypocalcemic action of calcitonin is dependent upon phosphate, while the hypophosphatemic action is independent of calcium. Calcitonin moves phosphate into bone cells and bone fluid in contrast to reducing the movement of calcium from bone to blood. Calcitonin acts rapidly and at low doses on the osteocytes and lining cells at bone surfaces. Morphological changes can be identified within 7 min. This action causes the accumulation of an electron-dense material both in bone lining cells and their microenvironment. It is postulated that both the hypocalcemic action of calcitonin and its ability to cause an accumulation of material at bone surfaces may result from the movement of phosphate into these areas. The biochemical action which could produce the phosphate movement is unknown. The possibility is suggested that calcitonin increases phosphate transport into bone cells.

Adult↗
PubMed1981

Influence of parathyroid hormone on bone cell ultrastructure.

A study in rats demonstrated that morphologic changes in the bone osteocytes and osteoblasts are produced following parathyroid hormone (PTH) injection into thyroparathyroidectomized animals. It further showed that similar changes occur in normal rats as the result of of extended fasting. Plasma calcium concentrations were determined at sacrifice to ascertain that these changes in bone occurred at times when plasma calcium is rising as the result of parathyroid hormone stimulation. Tibias from these animals were removed and prepared for morphologic observation using both transmission (TEM) and scanning (SEM) electron microscopy. Specific structural features characterized bone cells stimulated by exogenous or endogenous PTH. The most significant morphologic alterations involved surface microvilli and blebs as determined by SEM. TEM studies showed alterations in the cisternae of the rough endoplasmic reticulum (RER). Additionally, cell shape varied markedly from the control cuboidal morphology. These morphologic changes occurred during peak periods of plasma calcium change and returned to control morphology as plasma calcium levels normalized. Use of an extracellular electron-dense tracer (lanthanum) confirmed the patency of the intercellular channels and the presence of a fluid space between the bone cell plasma membranes and the mineralized surface. PTH stimulation modified cell activity such that the tracer material entered the cell more readily, possibly by inducing increased pinocytosis (endocytosis). This study supports the concept that the osteocytes and lining cells on the surface of bone play a role in maintenance of plasma calcium concentrations.

Animals↗
PubMed1980

Evidence for an important physiological role for calcitonin.

We propose that calcitonin, secreted in response to the intake of food, aids in routing calcium, obtained by intestinal absorption, into bone fluid. Here calcium is temporarily stored in combination with phosphate for return to the extracellular fluid (blood) during intervals between oral intakes of calcium. The net result is a conservation of calcium postprandially and a decrease in parathyroid hormone-induced bone destruction during subsequent fasting periods. Evidence for this postulate is provided in the following six sequential steps from the time a calcium-containing meal is consumed until that portion of calcium stored in bone fluid is utilized during fasting periods to aid in plasma calcium maintenance. (i) Calcitonin secretion is stimulated by feeding and subsequent digestive processes. (ii) Postprandial secretion of calcitonin restricts the efflux of calcium from bone fluid to blood, thereby maintaining parathyroid hormone (PTH) secretion. (iii) In thyroid-intact individuals, both PTH and calcitonin are secreted postprandially and act in concert on calcium homeostasis. (iv) Calcitonin actively moves phosphate into bone and prevents its loss from bone fluid to blood. (v) Postprandial storage of calcium with phosphate occurs in bone fluid of thyroid-intact individuals. (vi) This labile storage form of calcium is the first to be utilized during fasting periods. In the absence of partial disruption of this storage mechanism, rapid development of pathological bone conditions would not be expected because PTH action permits the extended utilization of bone calcium for plasma calcium control. However, augmentation of osteopenic conditions could be expected if long-term low calcium intake were accompanied by a malfunction of this calcitonin-induced system for calcium storage.

Animals↗