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M Thomasset

Publications and source records attributed to M Thomasset.

119 records · Page 7Linked to original sources
PubMed1976

Duodenal calcium-binding protein (CaBP) and phosphorus deprivation in growing rats.

The present study has been undertaken to elicit the effects of a low-phosphorous diet on intestinal calcium absorption. Measurements of duodenal calcium-binding protein (CaBP), mucosal calcium, fractional calcium absorption and duodenal calcium transport capacity has been performed in growing rats fed for three weeks a low-phosphorous diet adequate in vitamin-D3. In animals on low-phosphorous diet, the mucosal concentration of CaBP measured by a quantitative competitive binding assay has increased in parallel with the mucosal calcium concentration, the fractional absorption and the calcium transport capacity. Analytical gel electrophoresis of calcium-binding protein in animals fed low-phosphorous diet has shown the presence of a protein band which would involve more than the effect of the stimulated biosynthesis of 1alpha,25-DHCC.

Animals↗
PubMed1976

[Increase in the renal calcium-binding protein (CaBPr) in the presence of vitamin D in growing, phosphate deficient rats. Possible role in tubular calcium reabsorption].

Vitamin D-dependent CaBP isolated from Rat renal cortex (rCaBP) was measured in phosphorus-depleted (OP) and control (C) Rats, either vitamin D-deficient (OD) or vitamin D-supplemented (1 or 10 i. u.). A low molecular weight fraction was isolated from renal cortex by "Sephadex G-100" chromatography and rCaBP activity quantitated by saturation analysis using a 45 Ca chelex assay. The results indicated that phosphorus deprivation resulted in the increase in the vitamin D-dependent rCaBP as well as in the intestinal CaBP. As a marked hypercalciuria was noted in all OP Rats and as the rCaBP activity was high in vitamin D-supplemented Rats and hardly detectable in vitamin D-deficient Rats, the implication of the rCaBP in the large hypercalciuria can be definitely ruled out. Furthermore when vitamin D-supplementation ranged from 1 to 10 i. u. vitamin D, while the serum calcium level was increasing a decrease could be noticed in the large hypercalciuria. This deserves to be related to the increase in rCaBP activity. The high CaBP activity probably resulting from the renal synthesis of 1,25-dihydroxycholecalciferol stimulated by phosphorus-deprivation could represent the molecular basis of the calcium tubular reabsorption increased by vitamin D. Thus a vitamin D-dependent protein implicated in an ion-selective transport could be involved in the tubular calcium reabsorption as well as in the intestinal calcium absorption.

Animals↗
PubMed1976

Bone resorption measurement with unusual bone markers: critical evaluation of the method in phosphorus-deficient and calcium-deficient growing rats.

An in vivo method to evaluate bone resorption in rats, by using unusual bone seekers not dependent on renal tubular transfer, is described and a critical evaluation of the method is made. In our experimental conditions, 85Sr and 177Lu are virtually exclusively localized in bone whereas 237Np remains unchanged in different soft organs, so that the concomitant use of these markers can be used for measuring bone resorption. If osteolysis occurs 21 days after the injection of these markers, under our experimental conditions, any increase in the urinary excretion of 177Lu and 237Np represents a rise in bone resorption, whereas an increase in Sr excretion reflects both and renal tubular events. According to our bone localization studies, the enhancement of Lu and Np excretion reflects primarily an increase in cortical bone resorption localized at the endosteal (Lu) and at the periosteal (Np) surfaces respectively. In addition, strontium is considered to be the marker of mineral resorption whereas Lu and Np, under our experimental conditions, would reflect the organic bone resorption. This method is tested in phosphorus-deficient rats and in calcium-deficient rats which exhibit disturbances of calcium metabolism at both the bone and kidney levels. In agreement with previous investigations, the use of these bone markers to evaluate osteolysis shows: (a) after a 1-week phosphorus deficiency, a slight increase in cortical bone resorption with a simultaneous fall in calcium and strontium renal tubular reabsorption, and (b) after a 1-week calcium deficiency, a high rise in cortical bone resorption with a simultaneous increase in the renal tubular reabsorption of calcium and strontium.

Animals↗
PubMed1976

Phosphorus deficiency, parathyroid hormone and bone resorption in the growing rat.

Sham-operated and parathyroidectomized (PTX) rats were divided into two pair-fed groups, one on a normal mineral intake (0.5% Ca, 0.3% P), the other on a regimen low in phosphorus (0.5% Ca, 0.03% P). P depletion led to a drop in plasma P and urine P, a rise in plasma Ca and a marked rise in urine Ca, a drop in serum magnesium and a rise in urine Mg. The changes were more pronounced in the PTX animals, but final values were the same in both groups. Parallel bone-seeking isotope (85Sr, 177Lu, 237Np) studies in nonablated animals revealed an increase in the urinary nuclide output and in the urine/tibia ratio in P-deficient animals. Normal and primary bone osteocytes decreased and enlarged osteocytes increased as a result of P deficiency; osteoclasts and osteoblasts also increased. Bone composition showed a drop in ash content and a rise in water, with a light decrease in both Ca and P, and a corresponding rise in hydroxyproline and nitrogen in the P-deficient animals. The results are interpreted to mean that P-deficiency in the young growing rat leads to an increase in bone resorption which occurs also in the absence of parathyroid hormone (PTH). The fact that final values were similar in the control and PTX P-deficient animals suggests that steady-state regulation can also occur without PTH. Because P-deficiency leads to rapid hypercalcemia and rapid marked hypercalciuria, there may exist a mechanism for phosphate regulation which would then supersede Ca homeostasis. The change in serum and urine Mg levels may reflect a decrease in tubular Ca and Mg reabsorption associated with P-deficiency.

Animals↗
PubMed1975

[Acid-base homeostasis and the thyro-parathyroid glands].

Chronic metabolic acidosis entails hyperparathyroidism and osteopathy. In order to elucidate the role of the thyroparathyroids in this bone lesion production the effects of acidic diet for 7 weeks were studied in parathyroidectomized (PTX), thyroparathyroidectomized (TPTX) and shamoperated (Sh-O) growing rats. In all animals urinary excretion of calcium, phosphate, ammonium and titrable acidity was similarly increased. The rise in hydroxyproline excretion and urinary 85-sr (that was injected previous to acidic feeding) was more marked in PTX and TPTX rats. Moreover, in these animals the serum calcium level was increased, the blood pH was decreased. According to these data, an acidic diet intake that is not sufficient to elicit a fall in blood pH of normal young rats can induce severe acidosis in chronically parathyroidectomized or thyroparathyroidectomized animals; moreover the bone resorption appears more marked. It is concluded that parathyroids are involved in the extra-cellular fluid defense mechanism against acidosis by a no bone resorptive mechanism. We hypothesize that the parathyroids permit the necessary and adequate supply of bicarbonates by the bone to maintain blood pH homeostasis.

Acid-Base Equilibrium↗
PubMedDate not supplied

Vitamin-D dependent 9 kDa calcium-binding protein gene: cDNA cloning, mRNA distribution and regulation.

Cholecalciferol (calcitriol) the active hormonal form of vitamin D induces the synthesis of at least two intracellular calcium-binding proteins (Ka = 10(6) M-1), the cholecalcins (CaBP) in mammals. We used the synthesis of these proteins to study the genomic steroid-like action of vitamin D. The 9 kDa CaBP is mainly concentrated in the duodenum while 28 kDa CaBP is located in the kidney and cerebellum. Complementary DNA copies of rat intestinal 9 kDa CaBP mRNA were cloned in E. coli. The deduced amino acid sequence for 9 kDa CaBP contains two 'EF hand' domains corresponding to calcium-binding sites I and II. The homology observed suggests, after comparison with the structures of other intracellular CaBPs, that rat 9 kDa CaBP mRNA contains the remains of an untranslated calcium-binding site III-like structure seen in 28 kDa CaBP from kidney and cerebellum of rat. Northern blots showed that the cDNA sequence hybridizes to a homogeneous 500-600 nucleotide mRNA species from rat duodenum. Larger mRNA species encoding 28 kDa CaBP were undetectable in rat kidney and cerebellum even under low stringency conditions. These findings demonstrate that there is no cross-hybridization between 9 kDa and 28 kDa CaBP mRNAs, and Southern analysis indicates that there are distinct genes coding for each rat cholecalcin. The cDNA probe was used to analyze the specific 9 kDa CaBP gene expression along the intestine of growing rats and during gestation and fetal development.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗