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Biomedical subjects

R Brommage

Publications and source records attributed to R Brommage.

At least 37 records · Page 2Linked to original sources
PubMed1993

Intestinal calcium absorption in rats is stimulated by dietary lactulose and other resistant sugars.

Lactulose is a disaccharide analogue of lactose that is resistant to metabolism in the small intestine but not in the large intestine. The effects of lactulose and other sugars on intestinal Ca absorption were determined from the decrease in the 47Ca:47 Sc ratio between diet and feces after feeding male rats diets containing these sugars during a single night. Dietary lactulose was more potent than lactose in stimulating Ca absorption and was effective between 5 and 38 wk of age. The component sugars of lactulose, galactose and fructose, did not influence Ca absorption when provided together at concentrations equimolar to that of lactulose. The stimulation of Ca absorption by dietary lactulose increased as dietary Ca concentration was raised and was not influenced by prior injections of calcitriol. Lactulose must be present in the same meal as Ca to stimulate Ca absorption, but this stimulation was lost if the rats were fed lactulose continuously for 2 or 7 d prior to the test diet. Other sugars thought to be poorly absorbed in the small intestine (xylitol, lactobionate, arabinose, raffinose, pyroglutamate, sorbitol, gluconate and raftilose) stimulated Ca absorption to an identical extent as lactulose. Cecectomy did not influence the enhancement of Ca absorption by lactulose. These results indicate that sugars resistant to metabolism and absorption in the small intestine but not the large intestine stimulate Ca absorption in the small intestine.

Age Factors↗
PubMed1993

Ovulation-associated increase in intestinal calcium absorption during the rat estrous cycle is blunted by ovariectomy.

Intestinal calcium (Ca) absorption was measured under noninvasive conditions in both normally cycling and ovariectomized rats by determining the decrease in 47Ca/47Sc ratio between diet and feces. In 32-wk-old rats fed a 1.4% Ca diet, both fractional and total intestinal Ca absorption varied during the estrous cycle (p < 0.03), being highest during estrus and lowest during the second day of diestrus. Similarly, in 36-wk-old rats fed a 0.11% Ca diet, both fractional and total intestinal Ca absorption varied during the estrous cycle (p < 0.001), being highest during estrus and lowest during the first day of diestrus. In both studies, Ca absorption in ovariectomized rats was identical to the mean values for all of the cycling rats. Serum zinc (Zn) levels, but not those of Ca, phosphorus (P), and magnesium (Mg), varied during the estrous cycle when measured in 37-wk-old rats fed the 0.11% Ca diet.

Animals↗
PubMed1990

Inhibition of bone mineral loss during lactation by Cl2MBP.

Pregnant rats were injected subcutaneously with either saline or the bisphosphonate Cl2MBP (dichloromethylenebisphosphonic acid) at a daily dose of 15 mg P/kg body weight on days 1 through 16 of gestation. Cl2MBP treatment did not influence maternal body weight nor the number of pups born. When analyzed 1 day after birth, pups from Cl2MBP-treated rats had a normal body weight but a 10% reduction in carcass calcium (Ca) content. The Cl2MBP injections were resumed on day 1 postpartum and led to a 10% reduction in pup body weight gain and carcass Ca content at 16 days of age. In saline-injected rats, lactation resulted in slight hypocalcemia, greatly elevated serum levels of 1,25(OH)2D3, and loss of bone mineral, as indicated by a reduction in femur ash weight. In non-lactating rats, Cl2MBP treatment produced slight hypercalcemia but had no effect on serum 1,25(OH)2D3 levels or bone mineral content. Compared to lactating rats receiving saline, Cl2MBP-treated lactating rats were more hypocalcemic and had higher serum 1,25(OH)2D3 levels. However, the lactation-induced loss of bone mineral was completely inhibited by Cl2MBP treatment.

Animals↗
PubMed1990

Vitamin D-independent intestinal calcium and phosphorus absorption during reproduction.

A special metabolic cage system was employed to measure the intestinal, renal, and mammary gland fluxes of Ca, P, and Mg in vitamin D-deficient rats during late pregnancy and lactation. Dietary Ca, P, and Mg levels were 0.78, 0.34, and 0.083%, respectively; this diet minimizes the reduction in milk production observed during vitamin D deficiency. Compared with identically treated virgin rats, lactating rats were slightly hypocalcemic and severely hypophosphatemic. Hypertrophy of the small intestine, as indicated by increased intestinal length and villus height, occurred during lactation. Net fractional intestinal absorption of Ca and P, but not Mg, was elevated twofold during late pregnancy and throughout lactation. Despite this elevated intestinal absorption, lactating rats were in negative Ca and P balance and lost bone mass. The transfer rates of Ca, P, and Mg into milk were approximately 77% of values previously observed in vitamin D-replete rats. Lactating rats conserved P by dramatically reducing renal P excretion. Pup retention of ingested Ca was virtually complete. These results, together with previous observations using everted duodenal gut sacs, indicate that there is a vitamin D-independent stimulation of intestinal Ca and P absorption during pregnancy and lactation. Because fractional Mg absorption was not similarly enhanced, this stimulation shows some specificity.

Animals↗
PubMed1989

Measurement of calcium and phosphorus fluxes during lactation in the rat.

Novel, two-compartment metabolic cages for rats were constructed to examine Ca and P fluxes during lactation. Four consecutive balance studies of 4 d each were performed in lactating rats and nonlactating controls. Lactating rats had dramatically higher intestinal absorptions of Ca and P resulting from both increased food consumption and elevated fractional absorptions of these elements. Urinary Ca excretion was reduced during lactation whereas urinary P excretion was unchanged. Endogenous fecal Ca excretion (determined by infusing 45Ca and dividing fecal 45Ca content by urinary 45Ca specific activity) was similar in lactating and nonlactating rats. In a separate study, pup retention of ingested Ca averaged 96%. Therefore, the difference in pup carcass Ca content between d 1 and 17 of age is assumed to equal 96% of the Ca transfer rate into milk. Similar calculations were applied to P. Milk transfer rates were determined to be 126 and 99 mg/d for Ca and P, respectively. These calculations indicate that 19% of the Ca transferred to milk was derived from the maternal skeleton with the maternal diet supplying the remaining Ca. This study provides the first comprehensive analysis of the alterations in Ca and P fluxes that occur during lactation in the rat.

Animals↗
PubMed1989

Magnesium fluxes during lactation in the rat.

Lactating rats fed a 0.055% Mg diet transferred 5.5 +/- SEM 0.3 mg per day of Mg into milk but remained in a slightly positive Mg balance by increasing both food consumption and fractional intestinal Mg absorption. Urinary Mg excretion increased continually during the course of lactation to values double those of non-lactating rats.

Animals↗
PubMed1988

Elevated calcium, phosphorus, and magnesium retention in pregnant rats prior to the onset of fetal skeletal mineralization.

Intestinal absorption and renal excretion rates of Ca, P, and Mg were compared in pregnant and control virgin rats fed a purified diet containing 0.55% Ca, 0.54% P, and 0.067% Mg. Four consecutive balance intervals of 5 days each were examined, beginning on day 1 of gestation. During days 6-10 of gestation, pregnant rats had elevated fractional intestinal absorptions of Ca (29.6 +/- 1.7 versus 20.6 +/- 1.5%), P (65.4 +/- 2.0 versus 59.9 +/- 0.9%), and Mg (54.3 +/- 1.5 versus 42.4 +/- 2.6%). Since urinary excretions of these elements did not change, the pregnant rats retained more Ca, P, and Mg than virgin rats. Fractional intestinal absorptions of these elements during pregnancy were similar to control values during days 1-5 and 11-15 of gestation and then rose for each element during days 16-20 of gestation. Presumably because of an increase in glomerular filtration rate, urinary excretions of Ca and Mg were elevated by 40 and 26% during days 16-20 of gestation. In contrast, urinary P excretion was decreased by 30% during days 11-20 of gestation. Analyses of uterine mineral contents indicated the increased maternal Ca and Mg retentions during pregnancy were balanced by the transfers of these elements to the fetuses. In contrast, pregnancy was associated with a net maternal retention of P. These data are consistent with previous observations of increased maternal skeletal mineralization during early pregnancy before the onset of fetal osteogenesis and subsequent enhanced maternal Ca intestinal absorption concurrent with fetal skeletal mineralization.

Animals↗
PubMed1988

The effects of chronic vitamin D deficiency on the skeleton in the adult rabbit.

Albino rabbits were fed a 1.0% Ca, 0.5% P, vitamin D-deficient diet for 11.7 to 31.3 mo. Control rabbits were fed either this diet with the addition of 2.2 units/gm of vitamin D3 or a standard laboratory rabbit ration. Serum levels of 25-OH-D and 1,25-(OH)2D were both undetectable in all vitamin D-deficient rabbits but were present at levels typically found in other species in the control rabbits. Vitamin D deficiency resulted in elevated serum PTH values but did not produce significant changes in serum Ca levels, femur length, femur ash weight to body weight ratio, or tibial breaking strength. The vitamin D-deficient rabbits could be readily separated into two distinct subgroups. Four of these rabbits were normophosphatemic (P = 3.7 +/- 0.4 mg/dl) whereas the other five were severely hypophosphatemic (P = 0.8 +/- 0.2 mg/dl). During the last 10 days of the study the control and normophosphatemic vitamin D-deficient rabbits were in positive Ca and zero P balance. The hypophosphatemic vitamin D-deficient rabbits were in zero Ca and negative P balance. This negative P balance resulted from a net intestinal secretion, as urinary P excretion was negligible. Femur ash weight as a percentage of dry weight was decreased in hypophosphatemic but not the normophosphatemic vitamin D-deficient rabbits. Histomorphometric analyses indicated the bones from the normophosphatemic vitamin D-deficient rabbits were normal. In contrast, vertebral trabecular bone from the hypophosphatemic rabbits contained large amounts of osteoid that was not mineralizing, as indicated by a failure to take up the fluorescent label calcein.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

The action of various vitamin D3 metabolites on calcium and phosphorus metabolism in chick embryo calvariae.

Chick embryos from vitamin D-deficient hens given physiological doses of 1,25-dihydroxyvitamin D3 or 24,25-dihydroxyvitamin D3 or both become severely hypocalcemic, hyperphosphatemic and fail to hatch as compared to those derived from hens given 25-hydroxyvitamin D3 or 24,25-difluoro-25-hydroxyvitamin D3. Calvariae from the former contain less mineral and on incubation in vitro produce significantly lower calcium and higher phosphate concentration in the medium than do the calvariae derived from the embryos of hens supported on 25-hydroxyvitamin D3 or 24,24-difluoro-25-hydroxyvitamin D3.

24,25-Dihydroxyvitamin D 3↗
PubMed1986

Role of vitamin D in neonatal skeletal development in rats.

The role of vitamin D in rat pup growth and skeletal development without the influence of nutritional factors was investigated. Pups from vitamin D-replete and vitamin D-deficient dams receiving identical amounts of milk for 20 days were compared. Body weight gain, femur ash content and histomorphometric analyses of diaphysial and distal femur were determined. Up to 20 days of age, growth and skeletal development of the pups were completely normal in the absence of vitamin D. Skeletal changes found in vitamin D deficiency were not observed, i.e., there was no increased volume of osteoid or lack of bone mineralization as demonstrated by tetracycline labeling and ash content. Only increased cortical porosity was found in vitamin D-deficient pups. Therefore, abnormalities previously attributed to vitamin D deficiency in neonatal rats can be corrected by sufficient milk consumption and are thus not a direct function of vitamin D.

Animals↗
PubMed1985

Regulation of bone mineral loss during lactation.

The effects of varying dietary calcium and phosphorus content, vitamin D deficiency, oophorectomy, adrenalectomy, and simultaneous pregnancy on bone mineral loss during lactation were examined in rats. Unless otherwise stated, the diet contained 0.47% calcium and 0.3% phosphorus and the rats were given 26 nmol of vitamin D3. Femur ash weights were determined after 21 days of lactation and on age-matched nonlactating rats. Decreasing dietary calcium to 0.02% caused an increased loss of bone mineral, whereas increasing dietary calcium to 1.4% increased plasma calcium levels to 12 mg/100 ml but did not diminish the bone mineral loss observed during lactation. Varying dietary phosphorus did not have a major effect on bone mineral loss during lactation. In vitamin D-deficient rats, bone mineral loss during lactation was independent of dietary calcium levels and slightly greater than the loss observed in vitamin D-replete rats fed the normal calcium diet. Oophorectomy and adrenalectomy did not produce changes in femur ash weights of nonlactating rats or reduce bone mineral loss during lactation. Rats mated during their postpartum estrus and thus simultaneously pregnant and lactating, lost the same amount of bone mineral as caused by lactation alone.

Adrenalectomy↗
PubMed1984

Self-selection of a high calcium diet by vitamin D-deficient lactating rats increases food consumption and milk production.

Lactating and nonlactating rats, both deficient and replete in cholecalciferol, were allowed a free selection among three diets containing 0.47% Ca, 0.3% P (normal Ca, normal P diet); 2.0% Ca, 0.3% P (high Ca diet); and 0.47% Ca, 1.0% P (high P diet). An additional group of vitamin D-deficient lactating rats was fed only the normal Ca, normal P diet. Vitamin D-deficient rats showed a strong selection preference for the high Ca diet but avoided the high P diet, whereas cholecalciferol-replete rats consumed the normal Ca, normal P diet predominantly. Compared to the nonselecting rats, the selection of the high Ca diet by the lactating rats deficient in vitamin D resulted in an increase in plasma calcium levels, hypophosphatemia, a doubling of food consumption, a reduction in maternal body weight loss and a stimulation of milk production as indicated by pup growth. These results demonstrate that vitamin D-deficient rats select a high Ca diet and that the decrease in milk production found in vitamin D deficiency results from a decrease in food consumption and that this anorexia is at least partially dependent on the hypocalcemia normally occurring in vitamin D deficiency.

Animals↗
PubMed1984

A maternal defect is responsible for growth failure in vitamin D-deficient rat pups.

Vitamin D deficiency was induced in lactating rats and their pups by placing female rats on a vitamin D-deficient diet immediately after mating. Evidence of vitamin D deficiency included undetectable plasma levels of 25-hydroxyvitamin D3 in the dams, maternal hypocalcemia, the lack of pup growth, and pup hypocalcemia following starvation. This method of producing vitamin D-deficient pups was then used to determine whether the failure of vitamin D-deficient pups to grow properly results from a maternal or neonatal defect. Vitamin D-deficient dams and pups were injected with either vitamin D3 or the ethanol vehicle, and pup growth was monitored over the subsequent 6 days. Providing vitamin D3 to the pups directly had no effect on their growth, but administering vitamin D3 to the dams resulted in a tripling of the pup growth rate. The failure of vitamin D3 to promote pup growth when given directly to the pups was not the result of their inability to metabolize the vitamin because these pups converted [3H]-vitamin D3 to 25(OH)D3, 24,25(OH)2D3, and 1,25(OH)2D3 as determined by comigration with standards on both straight and reverse phase high-performance liquid chromatography systems. These results demonstrate that a maternal defect is responsible for the growth failure observed in vitamin D-deficient rat pups.

Animals↗
PubMed1984

Vitamin D-deficient rats produce reduced quantities of a nutritionally adequate milk.

Pups raised by lactating rats deficient in vitamin D do not grow normally, and we have shown previously that this growth failure results from a maternal rather than a neonatal defect. This result indicates that vitamin D-deficient rats produce reduced amounts of milk and/or the milk they do produce is nutritionally incomplete. To examine the first of these possibilities, 3H2O and 42K in separate experiments were given to lactating rats at 13 days postpartum, and the amount of isotope transferred to their pups during the next 24 h was determined. The amount of milk produced during this period was calculated from the measured concentrations of 3H2O and 42K in milk. The specific activity of 3H2O in maternal plasma was kept constant by providing 3H2O in the drinking water of the dams. Vitamin D-deficient rats were found to produce only 19.5 +/- 1.8% determined by the 3H2O method and 23.2 +/- 1.1% by the 42K method (means +/- SD) of the amount of milk produced by vitamin D-replete rats. The composition of milk from vitamin D-deficient rats was examined to determine its nutritional value. Vitamin D-deficient milk contains elevated levels of fat, and the skim fraction contains more protein, potassium, calcium, and inorganic phosphorus but less carbohydrate than normal milk. When vitamin D-deficient dams were given two pups to nurse rather than the eight usually provided, pup growth was equivalent to that of vitamin D-replete pups. Furthermore, femur dry weights and degree of mineralization were similar in vitamin D-deficient and -replete pups of equivalent body weight.(ABSTRACT TRUNCATED AT 250 WORDS)

Animal Nutritional Physiological Phenomena↗
PubMed1984

1,25-Dihydroxyvitamin D3 normalizes maternal food consumption and pup growth in rats.

Maternal food consumption, maternal body weight loss, and pup growth were studied in the following six groups of rats: vitamin D-deficient, vitamin D3-replete, vitamin D3-replete but pair-fed with the vitamin D-deficient rats and rats given either 50, 150, or 450 pmol/day of 1,25-dihydroxyvitamin D3 as their sole source of vitamin D by continuous infusion from an Alzet osmotic minipump. As expected, vitamin D-deficient rats were hypocalcemic and lost body weight, and their pups stopped growing at 1 wk of age. Food consumption by the vitamin D-deficient rats was one-third that of the vitamin D3-replete rats. Although normalization of plasma calcium levels was not perfect, 1,25-dihydroxyvitamin D3 treatment led to normal maternal food consumption, prevented maternal body weight loss, and promoted normal pup growth. Pups from the vitamin D3-replete rats pair-fed with the vitamin D-deficient rats did not grow properly and their dams lost body weight. These data indicate that 1,25-dihydroxyvitamin D3 is fully capable of replacing vitamin D3 in promoting maternal food consumption in lactating rats and that maintaining adequate food consumption is a major factor in the stimulatory effect of vitamin D3 on pup growth and hence milk production. The anorexia and reduced milk production of vitamin D-deficient lactating rats did not result from changes in plasma glucose or triglyceride levels.

Animals↗
PubMed1984

Placental transport of calcium and phosphorus is not regulated by vitamin D.

The role of 1,25-dihydroxyvitamin D3 in regulating the maternal-to-fetal transfer of calcium and phosphorus across the placenta was examined by measuring maternal and fetal plasma levels of these elements in vitamin D-replete and -deficient rats. Pregnant rats in their 20th day of gestation and their fetuses were studied. Two diets with different calcium and phosphorus contents were used to produce either hypocalcemia or hypophosphatemia in the vitamin D-deficient rats. Calcium and phosphorus levels in fetal plasma were always higher than maternal values, and in vitamin D deficiency a twofold gradient of calcium and a fivefold gradient of phosphorus concentrations across the placenta were observed. Since protein levels in fetal plasma were approximately fivefold lower than maternal values, protein binding does not account for the higher fetal than maternal concentrations of plasma calcium. These results, together with previous data showing normal calcium content of vitamin D-deficient fetuses, indicate that 1,25-dihydroxyvitamin D3 and other vitamin D3 metabolites are not involved in the active transport of calcium and phosphorus across the placenta in the rat.

Animals↗
PubMed1984

Calcitriol but no other metabolite of vitamin D is essential for normal bone growth and development in the rat.

To determine the relative importance of different metabolites of vitamin D in bone growth and development, weanling male rat pups suckled by vitamin D-deficient mothers were given either calcitriol (1,25-dihydroxycholecalciferol) by continuous subcutaneous infusion, oral calcidiol (25-hydroxycholecalciferol), or oral 24,24-difluoro-25-hydroxycholecalciferol, a synthetic compound that can undergo 1-hydroxylation but not 24-hydroxylation, as their sole source of vitamin D for 40 d. Pups raised in the same manner, but given no vitamin D, served as controls. The three metabolites compared were given in doses that restored normal plasma calcium levels and normal increments in body weight. After in vivo double tetracycline labeling, bone histomorphometry by standard methods was performed on one femur and one tail vertebra. There were no significant differences between the three metabolite-treated groups in length, periosteal or endosteal diameter, cortical cross-sectional area, cortical porosity, osteoid thickness and volume, appositional rate and bone formation rate in the femur, or in qualitative and quantitative indices of endochondral ossification in the tail vertebra. All three groups differed markedly from the untreated controls with respect to all measurements. Collectively, the data indicate that neither calcidiol nor any 24-hydroxylated metabolite of calcidiol is needed in the rat (other than as a precursor) for longitudinal or transverse bone growth, for normal endochondral ossification, or for normal periosteal and endosteal formation, mineralization, and resorption of bone. Calcitriol was fully active with respect to each of the indices listed when given in a manner resembling its continuous endogenous production by the kidney, suggesting that previous reports of incomplete skeletal response to calcitriol result from its rapid clearance and infrequent oral administration. We demonstrated that calcitriol is the only metabolite that is both necessary and sufficient for normal bone growth and development in the rat, but our data do not indicate the extent to which its beneficial skeletal effects were mediated by direct action on bone, either of calcitriol itself or of some metabolite thereof, or by restoration of normal plasma levels of calcium and phosphate.

Animals↗