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A Fausto

Publications and source records attributed to A Fausto.

27 records · Page 2Linked to original sources

Effect of short- and long-term stress on plasma calcium and calcitonin in the rat.

Although hypocalcemia has been observed during stress, the cause(s) is still unknown. The effect of short- and long-term restraint stress on calcitonin (CT) secretion and on plasma calcium (Ca), inorganic phosphate (P), total protein (TP), and corticosterone (CORT) were investigated in the male and female Sprague-Dawley rat. The rats were restrained in the supine position for two hours/day for either one day (STS) or for 14 days (LTS), and compared to normal controls (CON). Plasma Ca levels in both STS and LTS rats were significantly lower and mean plasma CORT levels in female stressed rats were significantly higher than those in sex-matched CON rats. However, mean basal levels of plasma CT did not differ among these three groups for either sex. Similarly, mean increment of plasma CT after Ca infusion (Ca 10 mg/100 g, i.v.) did not differ between STS or LTS rats and CON rats. These data reveal no causal relationship between CT and the hypocalcemia during either short-or long-term stressful stimuli.

Animals↗

Bone deficit in ovariectomized rats. Functional contribution of the marrow stromal cell population and the effect of oral dihydrotachysterol treatment.

This study investigates the proliferative and osteogenic role of marrow stromal/osteoprogenitor cells in the development of the cortical bone deficit in ovariectomized (OVX) female rats. In vitro, clonal growth of marrow stromal cells from OVX rats was significantly impaired (vs. sham-operated controls). Yet in vivo, cells from sham-operated and OVX rats had equal osteogenic potential in several in vivo experimental situations, such as in intraperitoneally implanted millipore diffusion chambers and in intramuscular implants of marrow plus osteoinductive bone matrix (composite grafts). Long-term (6 mo) dihydrotachysterol (DHT) treatment of OVX rats enhanced their in vitro proliferative potential and clonal growth, as well as their osteogenic expression in composite grafts. The observation that the in vivo osteogenic performance of OVX rat marrow stromal cells was normal at extraosseous sites suggests that the mechanisms leading to osteopenia may involve an abnormality in cell-matrix interactions.

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↗

Inhibition of calcitonin secretion by exogenous calcitonin in the rat.

The effect of synthetic salmon calcitonin (CT) on calcium- and pentagastrin-stimulated plasma CT was investigated in male Sprague-Dawley rats. Plasma samples were obtained before and 3 and 6 min after calcium (1 mg/100 g BW, iv) or pentagastrin (5 micrograms/100 g BW, iv) infusion. Although salmon CT at the dose of 0.4 MRC U/100 g BW administered 15 min before either the calcium or pentagastrin infusion did not influence circulating endogenous CT levels, salmon CT in doses of 4 and 20 U/100 g BW administered 15 min before the injection of secretogogues significantly reduced the response of CT to either calcium or pentagastrin without significantly changing plasma calcium levels from those of control animals. Salmon CT (20 U/100 g BW) given 5 min before pentagastrin infusion again significantly suppressed the response of plasma CT to this stimulus. Similarly, salmon CT administered chronically in a dose of 2 U/100 g BW for 28 days significantly reduced the response of CT to the calcium infusion. These data suggest that in the rat, at least pharmacological dosage of CT modulates the production and/or secretion of glandular CT itself.

Animals↗

Impaired insulin action in rats with non-insulin-dependent diabetes.

Studies were performed to test the hypothesis that impaired insulin action occurs as an acquired phenomenon in the streptozocin (STZ)-treated, non-insulin-dependent (NIDDM) diabetic rat model. A number of methods were used to evaluate impaired carbohydrate tolerance in these animals. Plasma glucose and insulin levels were measured at 6 and 14 wk of age, and insulin glucose tolerance tests were performed at 4 and 5 wk of age (before overt hyperglycemia ensues), and at 8 and 14 wk of age (after the animals manifest overt diabetes). The STZ-treated rats had higher plasma glucose levels than those of control animals (P less than 0.001) at 6 and 14 wk of age, while their plasma insulin values were decreased to levels 73% of the controls (1.7 ng/ml versus 2.3 ng/ml, P less than 0.04). Glucose disappearance rates after high (0.35 U/kg) and low (0.175 U/kg) insulin challenge were reduced in the experimental diabetic animals at all ages with both insulin doses. The data suggest that these animals have an early and progressive acquired impairment in insulin action, most compatible with a defect in cellular biologic response to insulin. The possibility that this abnormality is secondary to insulin deficiency is raised.

Animals↗

Vitamin D metabolism in the chronic streptozotocin-induced diabetic rat.

Alterations in circulating vitamin D3 metabolites have been documented in both experimental and human diabetes mellitus. Using a recirculating hepatic perfusion system and in vitro kidney mitochondrial assays, we studied vitamin D3 hydroxylation in control and insulin-deficient rats 6 weeks after the induction of streptozotocin-diabetes. Vitamin D3-25-hydroxylase activity, assessed by hepatic conversion of [3H]vitamin D3 to [3H]25-hydroxyvitamin D3 during a 4-h perfusion, was similar in diabetic and control animals. The hepatic degradation of 25-hydroxyvitamin D3 to more polar metabolites was also normal, as was glucuronide conjugation and biliary excretion of vitamin D3 metabolites. The chronic insulin-deficient state resulted in a significantly (P less than 0.01) decreased 1 alpha-hydroxylase activity and enhanced (P less than 0.001) renal 24-hydroxylase activity. These alterations in vitamin D metabolism may relate to the deranged mineral homeostasis and skeletal morphology observed in rats and humans with chronic insulin deficiency.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗