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L V Avioli

Publications and source records attributed to L V Avioli.

At least 163 records · Page 9Linked to original sources

Preventing osteoporosis: the new significance of hyperparathyroidism.

Although a cautious approach is essential, there is still no safe and effective chronic medical therapeutic regimen that can substitute for surgical management of primary hyperparathyroidism in the elderly. The primary care physician should recognize that: the natural history of this disease is variable and unpredictable; symptomatic disease in the elderly patient may be easily overlooked; and therefore, older patients who have vague and varied nonspecific neuromuscular, GI, and constitutional complaints or acquired behavior disturbances should be carefully scrutinized. This approach to hyperparathyroidism should lead to earlier diagnosis and symptomatic relief in many patients who would otherwise be viewed as merely "old" or as chronic complainers.

Aged↗

(Ca2+ + Mg2+)-ATPase activity in plasma membrane of circulating mononuclear cells. Lack of a direct effect of vitamin D.

The in vivo effect of vitamin D on (Ca2+ + Mg2+)-ATPase activity was examined in a plasma membrane fraction of rat circulating mononuclear cells (MPM). Although there was no significant difference in the ATPase activities in red blood cell ghosts, (Ca2+ + Mg2+)-ATPase activity in MPM was significantly higher (p less than 0.05) in long-term vitamin D3-replete rats (100 IU/day for 6 months) than that in vitamin D-deplete rats (for 6 months). In rats maintained on vitamin D-deficient diets for 5-7 weeks, in vivo administration of either vitamin D3, 2,000 IU orally, 5 days prior to killing or 1,25-dihydroxyvitamin D3, 2.4 nmol, intraperitoneally, 24 h prior to killing failed to show any significant effect on (Ca2+ + Mg2+)-ATPase activity in MPM. (Ca2+ + Mg2+)-ATPase activity in MPM from rats maintained on vitamin D-deficient diet with high calcium content (1.8%) was significantly higher (p less than 0.05) than that from rats maintained on vitamin D-deficient diet with low calcium content (0.3%). Moreover, in vitro addition of vitamin D3 metabolites did not show any effect on (Ca2+ + Mg2+)-ATPase activity in MPM. These data suggest that decreased (Ca2+ + Mg2+)-ATPase activity in MPM from long-term vitamin D-deplete rats resulted from an adaptation to low extracellular calcium rather than vitamin D depletion.

Animals↗

Effect of heavy exercise on mineral metabolism and calcium regulating hormones in humans.

The relationship between acid base status and mineral metabolism after heavy exercise has been examined in 12 healthy subjects. Following burst exercise (duration 60-130 sec) to the point of exhaustion, blood pH had decreased (7.42 +/- 0.01 vs. 7.18 +/- 0.02, P less than 0.001) and plasma ionized calcium had increased (1.09 +/- 0.01 vs. 1.22 +/- 0.02 mmol/liter, P less than 0.001). Log ionized calcium concentration showed a significant negative correlation with pH (r = -0.90). Although plasma total calcium increased after exercise (2.47 +/- 0.05 vs. 2.67 +/- 0.04 mmol/liter, P less than 0.001), this change was not seen if the observed values were corrected for the accompanying increase in plasma protein concentration, suggesting that hemoconcentration accounted for these increments. Significant increases were also seen in plasma inorganic phosphate concentration, though not in plasma magnesium. Radioimmunoassay of parathyroid hormone using two different region-specific assays, one directed at the mid-region/carboxy-terminal and the other at the amino-terminal portion of the molecule, and of calcitonin, showed no change during exercise-induced hypercalcemia. The results do not suggest significant skeletal buffering of this type of acidosis and indicate that the changes in ionized calcium associated with short bursts of intense exercise are directly related to acidosis and that those in total calcium are a consequence of hemoconcentration.

Acidosis↗

Effects of prostaglandin E2 and indomethacin on 25-hydroxyvitamin D3-1 alpha-hydroxylase activity in isolated kidney cells of normal and streptozotocin-induced diabetic rats.

The effects of prostaglandin E2 (PGE2) (1 microM) and indomethacin (IN) (20 microM) on 1,25 dihydroxyvitamin D3 production were studied in renal cell suspensions isolated from control, streptozotocin-induced diabetic, and insulin-treated diabetic rats. Renal cortex cells were isolated by enzymatic digestion, and preincubated for 30 min at 37 degrees C with the appropriate additive(s) followed by a 1 h incubation with 8 nM 25-hydroxyvitamin D3 in serum-free medium. Radioactivity incorporated into that fraction of the cell suspension extract co-eluting with synthetic 1,25-dihydroxyvitamin D3 on high pressure liquid chromatography was determined. All animals were raised for 5 weeks on a vitamin D-deficient diet. Isolated kidney cells from vitamin D-deficient rats showed dose-dependent response of 1,25 dihydroxyvitamin D3 production to PGE2. Cells from control animals demonstrated a stimulatory effect of PGE2 (P less than 0.05) and a suppressive effect of IN (P less than 0.01) on 1,25 dihydroxyvitamin D3 production. In contrast, cells from diabetic rat kidneys failed to respond to these agents, alterations which were reversed by insulin treatment. The accumulated data suggest that depressed synthesis of 1,25 dihydroxyvitamin D3 previously observed in the experimental diabetic rat is due, at least in part, to an impaired production and response to PGE2-like prostaglandins.

Animals↗

Intestinal lactase activity and calcium absorption in the aging female with osteoporosis.

In 11 postmenopausal women with histologically proven osteoporosis and normal lactose tolerance, a direct correlation between calcium absorption and intestinal lactase activity was observed. The results suggest that varying degrees of relative deficiencies in intestinal lactase might contribute to the graded decrease in calcium absorption which characterizes the aging female population.

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Classification of idiopathic hypercalciuric patients by isotopic calcium absorption: a comparison with oral calcium tolerance test.

To test the accuracy of calcium tolerance test in estimating calcium absorption, we have measured the radioactive calcium absorption (expressed as Fx) in 27 patients with IH and renal calcium stones. The results of this test were compared with those of a standard oral calcium tolerance test. Although only seven of nine AH patients displayed normal fasting calcium excretion, they all displayed Fx values above normal and a normal parathyroid activity. Conversely, only 5 of our 18 RH patients demonstrated a hyperabsorption of radioactive calcium and an elevation in iPTH and cAMP above normal limits, yet all of them showed an increased calciuric response to an oral calcium challenge. Calcium absorption was inversely related to iPTH (r = -082; P less than 0.001) and cAMP (r = -064 P less than 0.05) in AH, but directly proportional to these parameters (r = 0.62 P less than 0.001 and r = 0.46 P less than 0.05, respectively) in RH patients. In view of these results, two ratios, iPTH/Fx and cAMP/Fx were used to discriminate between the two groups of patients. Both ratios were over normal limits in all RH patients and within normal range in all but one AH patient. Furthermore, no overlap was found between the two groups. Conversely, we were unable to completely separate AH from RH subjects on the basis of the oral calcium tolerance test, since in both groups the fasting and the absolute (or percentage) changes in urinary calcium, cAMP and blood iPTH levels following oral calcium loading, overlapped in each instance.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗

Gender differences in antacid-induced phosphate deprivation in rats.

To determine whether an animal model could be used to study the susceptibility of women to antacid-induced phosphate deficiency, 6-wk-old male and female rats were given basic aluminum carbonate gel (Basaljel) (1 ml/100 g body wt) or distilled water by gastric intubation daily for 3 wk. Rats were fed either ad libitum (group 1) or by pair-feeding (group 2) with pelleted rat food containing 0.74% phosphorus. In group 1, baseline, 1-wk, and 3-wk values for serum phosphorus in Basaljel-treated females were 7.7 +/- 0.2, 6.3 +/- 0.2, and 6.2 +/- 0.2 mg/dl, respectively. Corresponding values for control females were 7.8 +/- 0.3, 7.0 +/- 0.2, and 7.3 +/- 0.2 mg/dl. Values for treated females were significantly lower (p less than 0.02) than values for control females by 1 wk of treatment. Basaljel-treated males did not differ from controls. The pattern for group 2 was similar. Intestinal absorption and intramuscular stores of phosphate were assessed in group 1. After 3 wk of treatment, [32P]phosphate assimilation from the duodenum into the body was lower in Basaljel-treated females than in controls (33.8% +/- 1.9% vs. 49.8% +/- 6.2% of the luminally administered dose, p less than 0.05). This was due to increased retention of [32P]phosphate in the intestine of treated females (19.9% +/- 2.0% vs. 11.9% +/- 2.4% for control females, p less than 0.02). Results in jejunum were similar. Total intramuscular phosphate in females was significantly lower (p less than 0.005) than in males both before and after antacid treatment. Thus hypophosphatemia in the female rat during antacid administration is probably secondary to the additive effects of decreased assimilation and decreased soft tissue stores of phosphate.

Aluminum Hydroxide↗

Effects of deflazacort and the L-6485 metabolite on epiphyseal cartilage carbohydrate metabolism: comparison with prednisone.

Male Sprague-Dawley rats were injected with 1 mg/100 g bw/day of prednisone, 1.25 mg/1--g bw/day of deflazacort, or its metabolite, for a period of 20 days. Epiphyseal cartilage slices were incubated in a modified Krebs Ringer bicarbonate buffer, at 37 degrees C for 60 min, with either 14C-1- or 14C-6-glucose to quantitate both the absolute and relative rates of pentose shunt versus aerobic and anaerobic glycolytic activity, respectively. Measurements of both total and radioactive glucose uptake, lactate production and 14CO2 generation were expressed as either mumoles or DPM/mg cellular DNA/hr, respectively. This study demonstrated: (1) chronic prednisone administration decreased anaerobic glycolysis (glucose uptake and lactate production) 3-fold (P less than 0.01); (2) prednisone on a chronic basis produced no measured alteration in either the pentose shunt or Kreb's cycle activity; (3) both deflazacort and the deflazacort metabolite significantly stimulated (P less than 0.02) anaerobic glycolytic activity in epiphyseal cartilage tissue. In contrast to prednisone, the administration of either deflazacort or its L-6485 metabolite did not inhibit the glycolytic pathway of metabolism so necessary for epiphyseal cartilage growth and mineralization.

Aerobiosis↗

Effect of 1,25-dihydroxyvitamin D3 on phospholipid composition of rat renal brush border membrane.

To analyze the effects of vitamin D on renal tubular cell membrane phospholipid metabolism, the effects of vitamin D depletion and repletion on renal brush border membrane (BBM) phosphatidylethanolamine (PE), phosphatidylcholine (PC), and phosphatidylinositol (PI) were studied. The PC content of BBM from kidneys of rats deprived of vitamin D for 5-6 wk was 33.5 +/- 2.2 nmol Pi/mg protein. This was significantly lower than the PC content of BBM from kidneys of rats supplemented with vitamin D2 for 2 wk, 41.0 +/- 0.4 nmol Pi/mg protein. Vitamin D depletion also decreased the content of BBM PE. The fatty acid composition of BBM PC was altered by vitamin D depletion. Vitamin D depletion increased palmitic acid and decreased stearic, linoleic, and arachidonic acid. Vitamin D repletion with a single physiological dose of 1,25(OH)2D3 (30 pmol), 16 h prior to study tended to increase membrane content of PC and significantly increased the linoleic acid content of the PC fraction. Single-dose vitamin D repletion with a pharmacological dose of 1,25(OH)2D3 (2.4 nmol) produced a significant increase in BBM content of PC and also significantly increased the linoleic acid content of PC. These results demonstrate that vitamin D deficiency affects PC and PE content of rat renal BBM and their fatty acid composition, and that vitamin D repletion with 1,25(OH)2D3 for 16 h partially normalizes the changes in PC.

Animals↗

Bone calcification and calcium homeostasis in rats with non-insulin-dependent diabetes induced by streptozocin.

The effect of mild, non-insulin-dependent diabetes (NIDDM) on bone calcification and calcium (Ca) homeostasis was studied in growing rats (males and females). The diabetic state was characterized by mild insulin deficiency, plasma levels being 73% of controls, and mild hyperglycemia, with nonfasting plasma glucose levels of 1.5 times normal. There was no difference in plasma levels of Ca, phosphate (Pi), magnesium (Mg), alkaline phosphatase, immunoreactive parathyroid hormone (iPTH), calcitonin, 25-(OH)vitamin D (25[OH]D), 1,25-dihydroxyvitamin D (1,25[OH]2D), and 24,25-dihydroxyvitamin D (24,25[OH]2D) between the NIDDM rats and their controls of either sex. Metabolic Ca and Pi balance studies revealed that the experimental animals of both sexes were in positive Ca and Pi balance similar to that of their controls. Histologic studies of the kidney and intestinal slices from the experimental group were normal. Ca and Pi bone content calculated per gram bone ash of the femur, mandible, and second and fourth caudal vertebrae, and the organic content in the bones of the NIDDM animals showed no difference from their controls. Femur bone density and tibial epiphyseal growth plate width and morphology were similar histologically in the experimental and control rats. No decreased osteoid content in the tibial bone was found in the diabetic rats compared with controls. Physiologic sex differences, consisting of lower plasma Pi, higher plasma calcitonin levels, increased ratio of femur dry bone weight to total body weight, and increased percentage of mineralized and total bone volume at the tibial metaphysis seen in female compared with male control rats were also seen in the diabetic animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Effects of prednisone and deflazacort on mineral metabolism and parathyroid hormone activity in humans.

The effects of two different glucocorticoids, prednisone and deflazacort, (an oxazoline derivative of prednisolone) on bone metabolism were analyzed in 10 patients with disorders that required glucocorticoid therapy. Significant elevations in blood immunoreactive parathyroid hormone, alkaline phosphatase and urinary calcium, phosphate, hydroxyproline and nephrogenous cyclic AMP were observed during prednisone therapy in addition to an increase in the exchangeable calcium pool as estimated by 47Ca-kinetic analyses. In contrast to these changes, deflazacort therapy induced minimal, and in some instances, no changes in these indices. In fact, in studies wherein prednisone therapy was followed by deflazacort alterations in bone metabolism, iPTH, and nephrogenous cAMP observed during prednisone were reversed. The data are consistent with the fact that the skeletal effects of prednisone therapy are mediated, at least in part, by increased parathyroid hormone activity, and that deflazacort is less potent in this regard.

Aged↗