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Biomedical subjects

F Bronner

Publications and source records attributed to F Bronner.

At least 73 records · Page 4Linked to original sources
PubMed1981

Calcium uptake in isolated brush-border vesicles from rat small intestine.

Ca2+ uptake in brush-border vesicles isolated from rat duodena was studied by a rapid-filtration technique. Ca2+ uptake showed saturation kinetics, was dependent on the pH and ionic strength of the medium and was independent of metabolic energy. Uptake activity was readily inhibited by Ruthenium Red, La3+, tetracaine, EGTA, choline chloride and Na+ or K+. The effect of variations in medium osmolarity on Ca2+ uptake and the ionophore A23187-induced efflux of the cation from preloaded vesicles indicated that the Ca2+-uptake process involved binding to membrane components, as well as transport into an osmotically active space. Scatchard-plot analyses of the binding data suggested at least two classes of Ca2+-binding sites. The high-affinity sites, Ka = (2.7 +/- 1.1) x 10(4) M-1 (mean +/- S.D.) bound 3.2 +/- 0.8 nmol of Ca2+/mg of protein, whereas the low-affinity sites (Ka = 60 +/- 6 M-1) bound 110 +/- 17 nmol of Ca2+/mg of protein. In the presence of 100 mM-NaCl, 1.7 and 53 nmol of Ca2+/mg of protein were bound to the high- and low-affinity sites respectively. Decreased Ca2+-uptake activity was observed in vesicles isolated from vitamin D-deficient as compared with vitamin D-replete animals and intraperitoneal administration of 1,25-dihydroxycholecalciferol to vitamin D-deficient rats 16 h before membrane isolation stimulated the initial rate of Ca2+ uptake significantly. The data indicated that Ca2+ entry and/or binding was passive and may involve a carrier-mediated Ca2+-uptake component that is associated with the brush-border membrane. Altering the electrochemical potential difference across the membrane by using anions of various permeability and selected ionophores appeared to increase primarily binding to the membrane rather than transport into the intravesicular space. Since there is considerable binding of Ca2+ to the vesicle interior, a comprehensive analysis of the transport properties of the brush-border membrane remains difficult at present.

Animals↗
PubMed1981

Effect of Ca intake on saturable and nonsaturable components of duodenal Ca transport.

Calcium absorption was studied by an in situ ligated-loop procedure in 9-wk-old male Wistar rats that had been placed from weaning on one of three semisynthetic regimens, 0.17% Ca, 0.44% Ca, or 0.44% Ca plus lactose. Lactose was added because it is known to increase intestinal calcium retention. When the amount of calcium absorbed was expressed as a function of calcium instilled in the loop, it became possible to describe absorption as the sum of a hyperbolic and a linear function, equivalent to a saturable and a nonsaturable process, respectively. The slope of the nonsaturable component was independent of prior calcium intake, while the maximum saturable flux (Jmax) decreased as calcium intake increased. Analysis of the duodenal content of the vitamin D-dependent calcium-binding protein (CaBP, Mr congruent to 10(4)) revealed a positive relation between Jmax and CaBP. Thus, vitamin D appears to be implicated in the saturable, but not in the nonsaturable, component of calcium absorption.

Animals↗
PubMed1979

Regulation of intestinal calcium-binding protein in rats: role of parathyroid hormone.

Intestinal calcium-binding protein (CaBP) levels of rats fed a high (1.5%) Ca diet were the same whether the animals were parathyroidectomized (PTX), sham-operated controls pair-fed with the PTX animals, or sham-operated controls fed ad libitum. Consequently, a given base level of CaBP seems to be parathyroid hormone independent and not closely related to feed intake. On the other hand, whereas the ad libitum fed controls more than doubled their intestinal CaBP in response to a 2-day low-calcium (0.02%) regimen, neither the parathyroidectomized animals nor the pair-fed sham-operated controls were able to do so. Since the latter two groups consumed less feed and therefore less vitamin D than the ad libitum fed animals, the inability to increase CaBP in response to a low-calcium diet may have been caused by a restricted vitamin D intake rather than by the absence of parathyroid hormone.

Animals↗
PubMed1979

Effect of lactose on duodenal calcium-binding protein and calcium absorption.

Rats were fed a purified diet containing 30% lactose and calcium absorption was measured in duodenal loops in situ following instillation of 1.25 or 10 mM CaCl2 solutions. Lactose feeding caused absorption to be depressed from 88 to 69% (1.25 mM Ca solution) and from 71 to 43% (10 mM Ca solution). The effect of lactose feeding was more pronounced in 5-month old rats than in 2-month old rats. In the lactose-fed rats, calcium-binding protein (CaBP), measured by a competitive binding assay following partial purification, was depressed on the average from 24 to 10 nmoles Ca bound per mg protein. The effect of the lactose ingestion can be likened to the effect expected from continued high calcium intake, i.e., a decrease in the efficiency of calcium absorption and a decrease in CaBP.

Aging↗
PubMed1978

Vitamin D metabolism and expression in rats fed on low-calcium and low-phosphorus diets.

1. Cholecalciferol, radioactively labelled with both (14)C and (3)H, was administered weekly for 7 weeks to rats that had been depleted of vitamin D for 4 weeks before repletion with the radioactive vitamin. This permitted measurement of the steady-state effect on vitamin D metabolism of low-calcium and low-phosphorus regimens, as compared with a normal mineral intake. These dietary manoeuvres were carried out during the last 3 weeks of repletion. Cholecalciferol, 25-hydroxycholecalciferol and 1,25-dihydroxycholecalciferol were determined in plasma, intestine, kidney and bone. Ca(2+)-binding-protein content was measured in intestine and kidneys of comparable animals. 2. In rats on the low-calcium diets, 1,25-dihydroxycholecalciferol concentration was elevated in plasma, bone, kidney and intestine, and intestinal Ca(2+)-binding protein was increased to over twice the concentration found in the control animals. 3. The low-phosphorus regimens led to a decrease in plasma phosphate and 1,25-dihydroxycholecalciferol in all tissues studied, for the latter to the point where it was undetectable in plasma and bone. Intestinal and renal concentrations of Ca(2+)-binding protein were unchanged in the low-phosphate-intake group and decreased in the very-low-phosphate-intake group. 4. It is concluded that in the rat, unlike in the chick, hypophosphataemia is not associated with a stimulation of the production of 1,25-dihydroxycholecalciferol or its expression in the synthesis of Ca(2+)-binding protein. Therefore the plasma phosphate concentration does not appear to be directly involved in the regulation of the functional metabolism of vitamin D.

Animals↗
PubMed1976

Vitamin D deficiency and rickets.

Classical experimental rickets in the rat is a dual deficiency, resulting from both phosphate and vitamin D deficiency, with many of the features of rickets reproducible by simple phosphorus deficiency. Simple vitamin D deficiency differs markedly from experimental rickets, with only the absence of the vitamin D-dependent calcium-binding proteins common to both situations. The expression at the bone level of vitamin D deficiency differs in the two conditions, with rickets leading to profound structural and metabolic changes, whereas simple vitamin deficiency primarily compromises the regulatory function of bone, without obvious structural alterations. It is proposed that human nutritional rickets is the result of a nutritional vitamin D deficiency that aggravates the expression of a pre-existing metabolic defect in phosphate transport. Simple nutritional vitamin D deficiency, unaccompanied by rickets, may occur, but probably has always been rare.

Animals↗