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Biomedical subjects

N H Bell

Publications and source records attributed to N H Bell.

At least 73 records · Page 4Linked to original sources
PubMed1988

Diminished rates of bone formation in normal black adults.

Blacks have a greater bone mass and a lower incidence of osteoporosis and hip fractures than whites. We performed biopsies of the iliac crest in 12 blacks (6 men and 6 women) and 13 whites (8 men and 5 women) who were matched for age (range, 19 to 46 years) and weight, to determine whether histomorphometric differences between blacks and whites could be identified. The static measurements of cortical and cancellous bone architecture were not significantly different in the two groups. In contrast, the dynamic measurements, determined with tetracycline markers, showed that the mean rate of bone formation in the blacks was only 35 percent of that in the whites (P less than 0.001). We conclude that the rate of bone turnover is lower in blacks than in whites, since bone resorption and bone formation are closely coupled in the steady state. If reconstitution of previously resorbed cavities at remodeling sites is incomplete in osteoporosis, a reduction in the rate of skeletal remodeling could provide a means for maintaining and preserving bone mass in blacks.

Adult↗
PubMed1988

The effects of muscle-building exercise on vitamin D and mineral metabolism.

Exercise and muscle strength are important determinants of bone mass. Studies were carried out in normal young adult white males to determine the effects of exercise on vitamin D and mineral metabolism. Fourteen men who had engaged in regular muscle-building exercises for at least 1 year and 14 age-matched controls (age range, 19-36 year) were hospitalized on a metabolic ward and were given a constant daily diet estimated to contain 400 mg of calcium, 900 mg of phosphorus, 110 mEq of sodium, 65 mEq of potassium, and 18 mEq of magnesium. Body weight averaged 78 +/- 3 kg in the exercisers and 72 +/- 2 kg in the controls (NS). Serum calcium, ionized calcium, phosphate, magnesium, somatomedin-C, and immunoreactive parathyroid hormone (PTH) were not different in the two groups, whereas serum Gla-protein (39 +/- 5 vs. 24 +/- 2 ng/ml, p less than 0.01), 25-hydroxyvitamin D (23 +/- 2 vs. 16 +/- 2, p less than 0.05) and 1,25-dihydroxyvitamin D [1,25(OH)2D] (40 +/- 2 vs. 29 +/- 2 pg/ml, p less than 0.01) were higher in the exercisers than in the controls. Urinary calcium, phosphorus, sodium, potassium, creatinine clearance, and norepinephrine were not different in the two groups, whereas urinary magnesium (12.6 +/- 1.0 vs. 9.4 +/- 0.5 mEq/d, p less than 0.01) and urinary cyclic adenosine 3',5'-monophosphate (cyclic AMP) (2.52 +/- 0.19 vs. 1.72 +/- 0.20 nM/dl glomerular filtrate, p less than 0.01) were higher in the exercisers than in the controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Evidence of a probable role for 25-hydroxyvitamin D in the regulation of human calcium metabolism.

1,25-Dihydroxyvitamin D [1,25-(OH)2D] is the principal mediator of the biologic effects of vitamin D. We showed previously that obese white subjects have low serum vitamin D and 25-hydroxyvitamin D (25-OHD) with increased serum-immunoreactive parathyroid hormone (PTH) and 1,25-(OH)2D, low urinary calcium, and increased urinary cyclic adenosine 3',5'-monophosphate (cyclic AMP) compared with nonobese white individuals. To determine whether 25-OHD modulates calcium metabolism, the effects of 25-OHD3, 40-100 micrograms/day for 9 days, were compared in seven obese and seven nonobese white subjects who were between the ages of 20 and 34 years. Each of them was hospitalized on a metabolic ward and given a constant daily diet that contained 400 mg calcium, 900 mg phosphate, and 18 mEq magnesium. Whereas 25-OHD3 increased mean serum 25-OHD from 7 +/- 1 to 37 +/- 5 ng/ml (P less than 0.01) and urinary calcium from 102 +/- 18 to 146 +/- 17 mg/day (P less than 0.001) and decreased mean serum 1,25-(OH)2D from 40 +/- 2 to 28 +/- 2 pg/ml (P less than 0.01) and urinary cyclic AMP from 3.23 +/- 0.57 to 2.00 +/- 0.17 nM/dl GF (P less than 0.05), it did not change mean serum calcium, ionized calcium, phosphate, magnesium, immunoreactive PTH or urinary phosphate, or creatinine clearance in the obese subjects. In contrast, 25-OHD3 increased mean serum 25-OHD from 16 +/- 1 to 46 +/- 4 pg/ml (P less than 0.001) but did not alter mean serum 1,25-(OH)2D or urinary calcium or cyclic AMP in the nonobese subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Low circulating vitamin D in obesity.

Previous studies demonstrated decreases in serum 25-hydroxyvitamin D in obese subjects. Studies were carried out to determine whiter serum vitamin D is low in obesity. The results indicate that serum vitamin D is significantly lower in obese than in nonobese individuals and may contribute to lower serum 25-hydroxyvitamin D in obesity.

Adult↗
PubMed1988

Osteoinduction by implants of demineralized allogeneic bone matrix is diminished in vitamin D-deficient rats.

Experimental heterotopic bone formation was produced by subcutaneous implants of demineralized allogeneic bone matrix (DABM) in vitamin D-deficient (-D) animals that were either not treated or given vitamin D3 (+D) or 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) to determine the role of vitamin D and its most active metabolite in osteoinduction and implant remodeling. Histologically, implants in both +D and -D groups caused a similar acute inflammatory response, formation of a fibrous capsule, and chondrogenesis by 1 to 2 weeks after implantation. However, by 3 weeks after implantation implants in the -D animals had formed less bone matrix, had developed a defect in matrix mineralization, had reduced bone forming and bone resorbing surfaces, and had altered bone architecture resulting from defective bone remodeling. The altered histology in -D animals was not corrected by 10 weeks after implantation. Treatment of vitamin D-deficient rats with 1,25(OH)2D3, 65 pmol/day for 3 weeks, corrected both the defect in mineralization and the abnormal histology. The results indicate that (1) vitamin D deficiency does not alter either the timing or the sequence of histologic events associated with osteoinduction but dramatically reduces the magnitude of the response, (2) vitamin D deficiency not only impairs mineralization but also reduces bone formation and resorption, and (3) 1,25(OH)2D3 mimics all of the actions of vitamin D with regard to correcting the abnormal osteoinductive response and bone histomorphometry.

Animals↗
PubMed1988

Normal vitamin D and mineral metabolism in essential hypertension.

The effects of dietary sodium upon serum and urinary calcium and selected vitamin D metabolites were studied in two groups (n = 10 each) of age and gender matched, white normotensive subjects and patients with normal-renin hypertension. Isocaloric diets were consumed on a metabolic ward with sequential daily sodium intake of 109 meq for 5 days and 9 meq and 259 meq for 6 days each. Values for serum and urinary calcium, phosphorus, magnesium and electrolytes, creatinine clearance, plasma immunoreactive parathyroid hormone, and serum 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D were similar in both study groups on each diet. Measurements of plasma renin activity and serum aldosterone levels were higher in the hypertensive than in the normotensive group on each diet (p less than .05-.01). Serum 1,25-dihydroxyvitamin D and urinary calcium increased on the high sodium diet in the normotensive (p less than .05) and the hypertensive groups (p less than .01). When the data for normotensive subjects and hypertensive patients were pooled by gender, males had a 1 1/2 to 3 times the urinary calcium excretion than females, regardless of diet. The present study indicates that there are no differences in the selected components of calcium and vitamin D metabolism in response to sodium intake in patients with essential hypertension and normal plasma renin activity as compared to normal controls.

Adult↗
PubMed1988

Chronic alcohol treatment results in disturbed vitamin D metabolism and skeletal abnormalities in rats.

The effect of chronic alcohol consumption on the skeleton was investigated in rats. The treated group received ethanol administered as 38% of caloric intake in a liquid diet (Sustacal) for 10 months. The control rats were pair weighted to the ethanol-treated animals throughout the study; the growth curves of the two groups were the same. The controls were given the same liquid diet except that dextrin:maltose (3:1) was substituted isocalorically for ethanol. Ethanol-treated rats did not differ from the pair-weighted controls in mean serum calcium, phosphorous, or creatinine. In contrast, serum magnesium was reduced (p less than 0.02) in alcohol-treated rats. Ethanol treatment also resulted in changes in the serum concentrations of vitamin D metabolites; serum 25-hydroxyvitamin D3 was increased (p less than 0.001), while serum 1,25-dihydroxyvitamin D3 was decreased (p less than 0.01). Tibial length was reduced in ethanol-treated rats (p less than 0.05) but there was no change in femoral length. Medullary area was increased in tibial diaphyses from alcohol-treated rats compared to weight matched control animals (p less than 0.01), indicating a net increase in resorption. The cross-sectional area of the tibial diaphysis of ethanol-treated rats was the same as the matched controls. Trabecular bone was decreased in the tibial metaphysis of ethanol-treated rats compared to the matched controls (p less than 0.05) indicating a net loss of trabecular bone. Ethanol treatment did not have an effect on the organic weight of the femur but the ash weight was reduced (p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Alcoholism↗
PubMed1988

Demonstration of reduced mitogenic and osteoinductive activities in demineralized allogeneic bone matrix from vitamin D-deficient rats.

Osteoinduction is the formation of ectopic bone that follows implantation of demineralized allogeneic bone matrix (DABM) and is believed to be secondary to the release of associated inductive factors from bone matrix. To clarify the role of vitamin D in osteoinduction, we implanted DABM from vitamin D-deficient rats (-D rats) into normal rats (+D rats). Because mitogens and osteocalcin might be involved in osteoinduction, these were measured. Mitogenic activity in extracts from mineralized allogeneic bone matrix (ABM) and DABM from both +D and -D rats was determined with an assay that utilizes monolayer cultures of embryonic chick calvarial cells. Osteocalcin in serum and DABM was measured by radioimmunoassay. DABM from -D rats did not promote osteoinduction as effectively as DABM from +D rats. Resorption of implant matrix from -D rats was diminished compared with resorption of matrix from +D rats (P less than 0.01), and the decrease was attributed to a corresponding decrease in the number of osteoclasts in the implants (P less than 0.02). Bone formation (P less than 0.01) and total implant mineralization (P less than 0.001) were significantly reduced in implants from -D rats, and the reductions corresponded with a decline in the number of osteoblasts (P less than 0.05). Mitogenic activity in DABM from +D rats was only slightly decreased as compared with activity in ABM, but DABM from -D rats contained significantly less activity (P less than 0.001). No mitogenic activity was identified in implants of DABM from either +D or -D rats 3 wk after implantation. Serum osteocalcin was significantly higher in -D as compared with +D animals. In contrast, the concentrations of osteocalcin in DABM from the two groups of animals were not significantly different from each other. These findings indicate that the diminished osteoinductive activity of DABM from -D rats results from deficiency of one or more mitogenic factors that are essential for inducing the proliferation and differentiation of bone cells at the implant site and that osteocalcin does not play a role in this regard.

Animals↗
PubMed1988

Tamoxifen inhibits osteoclast-mediated resorption of trabecular bone in ovarian hormone-deficient rats.

The effects of the nonsteroidal antiestrogen tamoxifen were determined on trabecular bone mass in the proximal tibial metaphysis of intact and ovariectomized rats. Rats were ovariectomized at the beginning of the study. On day 7 of the study, 5-mg slow release pellets of tamoxifen or placebo were implanted sc. All of the rats were killed on day 28 of the experiment. Sections of the proximal tibial metaphysis were stained for acid phosphatase and evaluated histomorphometrically. Ovariectomy resulted in marked loss of bone. Compared to the values in sham-operated animals, the trabecular bone at a sampling site in the secondary spongiosa of ovariectomized rats was reduced by more than 60%, the length of trabecular bone surface covered by osteoclasts was increased by 563%, the percentage of trabecular bone surface covered by osteoclasts was increased by 567%, the mean osteoclast size was increased by 84%, and the number of nuclei per osteoclast was increased by 38%. In contrast, treatment of ovariectomized rats for 3 weeks with tamoxifen restored the histomorphometric measurements to values comparable to those in sham-operated animals. 17 beta-Estradiol increased trabecular bone fractional area in ovariectomized and sham-operated rats, and administration of tamoxifen to estrogen-treated, ovariectomized, and sham-operated animals produced a further increase in trabecular bone. In summary, 1) ovariectomy resulted in large increases in both the number and activity of osteoclasts, 2) the increased bone resorption associated with ovariectomy produced a net loss of trabecular bone, and 3) treatment of ovariectomized rats with tamoxifen prevented these skeletal changes. The results indicate that in the rat, tamoxifen mimics the effects of estrogen on trabecular bone at concentrations that are not uterotropic.

Animals↗
PubMed1988

The effects of race and body habitus on bone mineral density of the radius, hip, and spine in premenopausal women.

The incidence of osteoporosis and fractures of the hip are diminished in blacks and in obese subjects. To determine whether bone mass is increased in them, bone mineral density (BMD) of the lumbar spine, trochanter, and femoral neck was measured by dual photon absorptiometry in 89 nonobese white and 51 nonobese black women, all of whom were within 30% of their ideal body weight and between the ages of 20 and 50 yr, and in 21 obese white women and 21 obese black women, all of whom weighed 30% on more than their ideal body weight and were in the same age range. The BMD of the mid radius was also measured by single photon absorptiometry. The mean BMD of the mid radius was higher in black than in white nonobese women [0.73 +/- 0.01 (+/- SE) vs. 0.70 +/- 0.01 g/cm2; P less than 0.01] and was not altered by obesity in either group. The mean BMD was higher in the black than in the white nonobese women at the lumbar spine (1.23 +/- 0.02 vs. 1.16 +/- 0.01 g/cm2; P less than 0.01), trochanter (0.78 +/- 0.02 vs. 0.72 +/- 0.01 g/cm2; P less than 0.01) and femoral neck (0.96 +/- 0.02 vs 0.90 +/- 0.02 g/cm2; P less than 0.02). The mean body weight was higher in the obese than in the nonobese white women (92 +/- 2 vs. 61 +/- 1 kg; P less than 0.001) and black women (94 +/- 3 vs. 63 +/- 1 kg; P less than 0.001). The mean BMD was higher in the obese than in the nonobese white women at the lumbar spine (1.24 +/- 0.03 g/cm2; P less than 0.05), trochanter (0.89 +/- 0.04; P less than 0.001), and femoral neck (0.99 +/- 0.03; P less than 0.01) and was higher in the obese than in the nonobese black women at the lumbar spine (1.33 +/- 0.03 g/cm2; P less tham 0.01), trochanter (0.88 +/- 0.04 g/cm2; P less than 0.05), and femoral neck (1.04 +/- 0.03 g/cm2; P less than 0.05). Multivariate regression analysis revealed positive correlations between body weight and BMD at each of the 3 weight-bearing sites, but not at the mid radius, in both the black women and white women.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1987

Demonstration that ethanol inhibits bone matrix synthesis and mineralization in the rat.

The effects of ethanol on bone and mineral metabolism were investigated in 3 groups of male rats. The first group received ethanol administered as 36% of caloric content in a liquid diet for 3 weeks. A second group of pair-fed animals was given the same liquid diet, except that sucrose was substituted isocalorically for ethanol. A third group of rats was fed standard laboratory chow. The ethanol-treated rats gained significantly less weight than laboratory chow-fed controls but gained the same weight as the pair-fed animals. Ethanol-treated rats had a modest but significant decrease in mean serum calcium compared to pair-fed controls (10.3 +/- 0.1 vs. 10.6 +/- 0.1 mg/dl, p less than .001). Mean serum phosphate, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D and immunoreactive parathyroid hormone were the same in the 3 groups. The ethanol-treated animals showed significant decreases in mean tibial length (1.88 +/- 0.01 vs. 1.98 +/- 0.02 cm, p less than .01), mean endosteal bone formation rate (0.0006 +/- 0.0001 vs. 0.0026 +/- 0.0003 mm3/day, p less than .001) and mean periosteal bone formation rate (0.022 +/- 0.001 vs. 0.026 +/- 0.001 mm3/day, p less than .01) compared to the pair-fed controls. The ethanol-treated rats demonstrated significant decreases in mean periosteal mineralization rate (7.5 +/- 0.3 vs. 10.3 +/- 0.6 micron/day, p less than .01) and mean periosteal apposition rate (8.5 +/- 0.5 vs. 11.0 +/- 0.8 micron/day, p less than .05) and a significant increase in mean periosteal osteoid thickness (15.5 +/- 1.4 vs. 10.4 +/- 0.8 micron, p less than .01) compared to pair-fed controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

The effects of ovariectomy and 17 beta-estradiol on cortical bone histomorphometry in growing rats.

The effects of ovariectomy for four weeks and of 17 beta-estradiol for three weeks on histomorphometry of the tibial diaphysis were determined in young rats. The effects of ovariectomy on histomorphometry of subcutaneous implants of demineralized bone matrix were also examined. Groups of young female rats were either ovariectomized or sham operated. After surgery, the animals were weight matched and pair fed. Despite the same caloric intake, ovariectomized rats grew more rapidly than pair-fed, sham-operated controls but were significantly heavier at sacrifice in only one of three experiments. Ovariectomy did not change mean serum calcium, phosphate, 25-hydroxyvitamin D (25-OHD), or 1,25-dihydroxyvitamin D [1,25(OH)2D] but significantly lowered mean serum magnesium. Serum estradiol was not detectable in ovariectomized animals. 17 beta-Estradiol in ovariectomized animals significantly increased mean serum estradiol and lowered mean serum phosphate but did not change mean serum calcium, magnesium, 25-OHD, or 1,25(OH)2D, as compared to values in sham-operated controls. Bone formation rate was significantly enhanced in ovariectomized animals at both the endosteal and periosteal surfaces of the tibial diaphysis as compared to values in sham-operated controls. The increase in bone formation rate was reversed by 17 beta-estradiol at the periosteal but not endosteal surface. Ovariectomy increased the bone apposition rate, mineralization rate, and osteoid thickness of the tibial diaphysis. These increases were reversed by 17 beta-estradiol. In implants, ovariectomy increased the resorption of implant matrix and enhanced the formation of new matrix. Ovariectomy resulted in increases in forming surface and resorbing surface in the implants.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Evidence that calcium modulates circulating 25-hydroxyvitamin D in man.

We previously demonstrated in normal subjects that 1,25-dihydroxyvitamin D3 (1,25(OH)2D) can prevent the increase in serum 25-hydroxyvitamin D (25-OHD) which occurs in response to vitamin D. An investigation was carried out in eight normal subjects, therefore, to determine whether increases in calcium intake would alter the response of serum 25-OHD to challenge with vitamin D. In control studies, vitamin D, 100,000 U/d for 4 d, significantly increased mean serum 25-OHD from 18 +/- 3 to 42 +/- 5 ng/ml (p less than 0.001), an increment of 24 ng/ml (133%). Mean serum calcium, ionized calcium, phosphorus, creatinine, and 1,25(OH)2D did not change. In contrast, the same dose of vitamin D and calcium, 2,000 mg/d for 4 d, administered to the same eight subjects produced an increase in mean serum 25-OHD from 19 +/- 3 to 31 +/- 4 ng/ml (p less than 0.001), an increment of only 12 ng/ml (63%) and significantly less than the control (p less than 0.02). Mean serum calcium (8.8 +/- 0.1 vs. 9.2 +/- 0.1 mg/dl, p less than 0.01) and ionized calcium (4.79 +/- 0.07 vs. 4.85 +/- 0.08 mg/dl, p less than 0.05) increased significantly in response to vitamin D and calcium, mean serum phosphorus and creatinine did not change, and mean serum 1,25(OH)2D decreased significantly (37 +/- 2 vs. 31 +/- 4 pg/ml, p less than 0.02). In a postcontrol study in six of the normal subjects, vitamin D again significantly increased mean serum 25-OHD from 17 +/- 3 to 39 +/- 9 ng/ml (p less than 0.02), an increment of 22 ng/ml (129%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Tamoxifen prevents the skeletal effects of ovarian hormone deficiency in rats.

To determine whether the nonsteroidal antiestrogen tamoxifen behaves as either an agonist or antagonist of estrogen on bone, the effects of ovariectomy, 17 beta-estradiol, and tamoxifen were compared on radial growth at the tibial diaphysis in young adult female rats. Ovariectomy and 17 beta-estradiol did not alter serum calcium, phosphate, or 25-hydroxyvitamin D. Ovariectomy increased serum 1,25-dihydroxyvitamin D in one experiment but not in the other. Tamoxifen increased the serum calcium and phosphate by itself and did not change serum 1,25-dihydroxyvitamin D in ovariectomized rats. Ovariectomy produced significant increases in medullary area, periosteal bone formation rate, and periosteal bone apposition rate compared to values in sham-operated animals and did not change endosteal bone formation rate. The increase in medullary area resulted from an increase in osteoclast number and resorbing surface length. Although endosteal forming surface length decreased, this was compensated for by an increase in the apposition rate. 17 beta-estradiol and tamoxifen each prevented the increases in bone formation rate and medullary area in ovariectomized rats. Tamoxifen reduced the length of the resorbing surface and osteoclast number to values observed in sham-operated animals. The findings demonstrate that in the rat, tamoxifen acts as an estrogen agonist by preventing the skeletal alterations that result from ovarian hormone deficiency.

Animals↗
PubMed1987

Regulation of 25-hydroxyvitamin D3 metabolism in chick embryo.

We investigated the time course of the development of renal 25-hydroxyvitamin D-1-hydroxylase and 25-hydroxyvitamin D-24-hydroxylase in chick embryos grown in the presence and absence of the eggshell. In embryos with the eggshell, the specific activity (SA) of 25-hydroxyvitamin D-1-hydroxylase in kidney homogenates increased from 0.68 fmol X min-1 X mg protein-1 at 12 days of gestation to a peak of 2.55 +/- 0.50 fmol X min-1 X mg-1 protein-1 at 17 days. In contrast, the SA of 25-hydroxyvitamin D-24-hydroxylase decreased from 2.5 fmol X min-1 X mg protein-1 to 0.90 +/- 0.25 fmol X min-1 X mg protein-1 during the interval. The total plasma calcium was significantly reduced in embryos without shells at 14 to 15 days of gestation (1.1 +/- 0.1 mM, mean +/- SE) compared with normal embryos of the same gestation (2.3 +/- 0.3 mM, P less than 0.002). In embryos without the eggshell, renal 25-hydroxyvitamin D-1-hydroxylase increased from 6.0 to 8.2 +/- 0.6 fmol X min-1 X mg protein-1 at 17 days of gestation and was from four- to sixfold higher than corresponding enzymatic activities for intact embryos. The increased enzyme activity resulting from loss of the eggshell was due to an increase in Vmax. The findings indicate that renal 25-hydroxyvitamin D-1-hydroxylase and 25-hydroxyvitamin D-24-hydroxylase in the chick embryo exhibit activity and show a large capacity for regulation in response to changes in calcium metabolism.

Animals↗
PubMed1986

Enhancement of parathyroid hormone-responsive renal cortical adenylate cyclase activity by a cytosol protein activator from rat reticulocytes.

The effects of the cytosol activator protein obtained from rat reticulocytes (RCAP) were investigated in a heterologous membrane system--partially purified cell membranes from dog renal cortex. RCAP enhanced the response of dog renal cortical adenylate cyclase to bovine parathyroid hormone (1-34) [bPTH (1-34)] from two- to three-fold. RCAP also enhanced the response to 5 microM arginine vasopressin, 10 microM glucagon, and 10 microM isoproterenol. Analysis of double-reciprocal plots of substrate concentration and enzyme activity indicated that bPTH (1-34) alone and together with RCAP increased the Vmax of the adenylate cyclase enzyme and did not alter the apparent Km of the enzyme for MgATP. Membranes from dog renal cortex contain 42K and 39K proteins that are ADP-ribosylated by cholera toxin and pertussis toxin, respectively, and appear to be the stimulatory (Ns) and inhibitory (Ni) guanine nucleotide binding proteins described in many other hormone-responsive membrane preparations. Similar to its effects in rat reticulocytes, RCAP inhibited ADP-ribosylation of Ns and enhanced ADP-ribosylation of Ni. The muscarinic agonist, carbachol, inhibited PTH-responsive adenylate cyclase activity in dog renal cortical membranes and this inhibition was reversed by RCAP. These results indicate that RCAP enhances stimulation of adenylate cyclase by a variety of hormones in a heterologous membrane preparation and supports the hypothesis that RCAP's site of action is common to all adenylate cyclase systems. RCAP may facilitate coupling between Ns and the catalytic unit of adenylate cyclase by a pertussis toxin-like effect to inactivate Ni. The dual effects of RCAP upon ADP-ribosylation of Ni and Ns alpha subunits suggest that a binding site for RCAP may exist at a site of homology between Ns alpha and Ni alpha.

Adenosine Diphosphate Ribose↗
PubMed1986

Evidence that obesity does not influence the vitamin D-endocrine system in blacks.

As compared to nonobese white men and women, age-matched nonobese black subjects and obese white individuals show alterations in the vitamin D-endocrine system that are characterized by increases in mean serum immunoreactive parathyroid hormone (PTH), serum 1,25-dihydroxyvitamin D [1,25-(OH)2D], and urinary cyclic adenosine 3,5-monophosphate (cAMP) and by decreases in mean serum 25-hydroxyvitamin D (25 OHD) and in urinary calcium. Thus, both groups show secondary hyperparathyroidism which is associated with increased renal tubular reabsorption of calcium and increased renal synthesis of 1,25-(OH)2D. In view of these findings, studies were conducted in 10 obese black subjects (3 men and 7 women) and in 12 nonobese black individuals (7 men and 5 women), ranging in age from 20 to 35 yr, to determine whether obesity influences the vitamin D-endocrine system in blacks. Body weight averaged 99 +/- 4 kg in the obese and 73 +/- 3 kg in the nonobese subjects (p less than .001). All of them were hospitalized on a metabolic ward and were given a constant daily diet containing 400 mg of calcium, 900 mg of phosphorus, 110 meq of sodium, 65 meq of potassium, and 18 meq of magnesium.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗