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Biomedical subjects

M Staun

Publications and source records attributed to M Staun.

At least 37 records · Page 2Linked to original sources
PubMed1998

The effect of 1,25-vitamin D3 on calbindin-D and calcium-metabolic variables in the rat.

Intraperitoneal injection of 1,25-(OH)2D3 4 micrograms/kg was given to 84 calcium- and vitamin D-repleted Wistar rats and samples of plasma, duodenal mucosa and renal tissue were taken after 0, 3, 6, 12, 24, 48 and 96 hr (n = 12 at each time interval). Plasma-ionized Ca increased after 6 hr, reached a maximum after 24 hr and returned to the initial values after 96 hr. The concentrations of renal calbindin-D28k and intestinal calbindin-D9k did not increase until 48 hr after injection and remained elevated until 96 hr after. Therefore, significantly elevated concentrations of the cytosolic calbindin-D were found at a time with normal values of plasma Ca. The present data suggest that calbindin-D does not alone increase the transcellular Ca transport and, therefore, supports the view that calbindin-Ds may serve as Ca buffer proteins.

Animals↗
PubMed1998

Effect of intravenous ranitidine and omeprazole on intestinal absorption of water, sodium, and macronutrients in patients with intestinal resection.

BACKGROUND: H2 receptor blockers and proton pump inhibitors reduce intestinal output in patients with short bowel syndrome. AIMS: To evaluate the effect of intravenous omeprazole and ranitidine on water, electrolyte, macronutrient, and energy absorption in patients with intestinal resection. METHODS: Thirteen patients with a faecal weight above 1.5 kg/day (range 1.7-5.7 kg/day and a median small bowel length of 100 cm were studied. Omeprazole 40 mg twice daily or ranitidine 150 mg twice daily were administered for five days in a randomised, double blind, crossover design followed by a three day control period with no treatment. Two patients with a segment of colon in continuation were excluded from analysis which, however, had no influence on the results. RESULTS: Omeprazole increased median intestinal wet weight absorption compared with no treatment and ranitidine (p<0.03). The effect of ranitidine was not significant. Four patients with faecal volumes below 2.6 kg/day did not respond to omeprazole; in two absorption increased by 0.5-1 kg/day; and in five absorption increased by 1-2 kg/day. Absorption of sodium, calcium, magnesium, nitrogen, carbohydrate, fat, and total energy was unchanged. Four high responders continued on omeprazole for 12-15 months, but none could be weaned from parenteral nutrition. CONCLUSION: Omeprazole increased water absorption in patients with faecal output above 2.50 kg/day. The effect varied significantly and was greater in patients with a high output, but did not allow parenteral nutrition to be discontinued. Absorption of energy, macronutrients, electrolytes, and divalent cations was not improved. The effect of ranitidine was not significant, possibly because the dose was too low.

Adult↗
PubMed1997

Urinary calcium excretion and renal calbindin-D28k.

The present investigation examined the possible influence of urinary calcium excretion on the concentration of renal calbindin-D28k. Thiazide diuretics stimulate calcium transport across the epithelial cells of the distal tubule, which express calbindin-D28k in high concentrations. Calbindin-D28k is assumed to facilitate transcellular Ca diffusion. Reduced urine calcium excretion and increased urine output were induced in Wistar rats by infusion of bendroflume-thiazide 1 mg/kg/day. The two control groups had infusions of either furosemide 20 mg/kg/day or vehicle, n = 8 in each group. Urinary Ca excretion was reduced to 10% in the thiazide group and increased by 50% in the furosemide group. Renal concentrations of calbindin-D28 showed no difference between vehicle, thiazide- and furosemide-treated rats. No differences in plasma concentrations of calcium, magnesium, phosphorus, urea, PTH, calcitonin and 1,25-(OH)2D were found between the groups. The present study describes that urine calcium excretion selectively can be manipulated without accompanying changes in renal calbindin-D28k concentrations. The data, therefore, suggest that urinary calcium excretion is not a significant determinator of cytosolic concentrations of renal calbindin-D28k.

Animals↗
PubMed1997

Body composition changes measured by dual-energy X-ray absorptiometry in patients receiving home parenteral nutrition.

BACKGROUND: To monitor changes in body composition in patients receiving home parenteral nutrition (HPN) and to ascertain whether changes were related to the amount of energy supplied by HPN, we studied prospectively patients with gut failure maintained on HPN. METHODS: Patients were subjected to repeated measurement of body composition by dual-energy X-ray absorptiometry (DXA), the second investigation being performed after a mean period of 20 (range, 11-26) months. Thirty-two patients were included, one patient was excluded, and five patients died during the study period. At inclusion, the patients had received HPN for a mean period of 30 (range, 6-216) months. The indication for HPN was inflammatory bowel disease (n = 16), abdominal cancers (n = 5), and scleroderma and others (n = 11). The fat-free mass (FFM), fat mass (FM), and total body mineral content (TBMC) were measured by DXA. RESULTS: Mean body mass index decreased from 21.18 to 20.96 kg/m2 (P = 0.36). The mean FFM showed a small, insignificant increase to 37.68 kg (P = 0.71). Mean TBMC was unchanged at 2.28 kg, and mean FM decreased from 19.25 to 18.17 kg (P = 0.055). During the study period the mean daily energy supply by HPN was reduced from kcal 1195 to kcal 959 (P = 0.004). There was a direct positive correlation between the individual changes in HPN energy supply and body weight and FFM (r = 0.437, r = 0.410, P < 0.05). CONCLUSION: The body composition of HPN patients was stable, with no change in mean FFM, FM, or TBMC. Individual changes in body weight and FFM correlated with change in HPN energy supply.

Absorptiometry, Photon↗
PubMed1997

Bone mineral content in patients with Crohn's disease. A longitudinal study in patients with bowel resections.

BACKGROUND: Low bone mineral content (BMC) has been reported in patients with inflammatory bowel disease. The aim of the present study was to measure BMC in patients with Crohn's disease. METHODS: BMC was monitored for a mean period of 5.5 years in 108 patients. The patients were divided into two groups: group A, patients with the colon preserved; group B, patients with a resected colon. The mean length of the resected small intestine was 90 cm. RESULTS: The BMC of the lumbar spine expressed as Z-score ((actual value-mean)/s) was significantly reduced: mean Z-score for group A, -0.51, P < 0.05; group B, -0.80, P < 0.001. The BMC of the femoral neck was significantly reduced: mean Z-score for group A, -1.24, P < 0.001; group B, -1.23, P < 0.001. A Z-score below -2.0 of spine or femoral neck BMC was found in 10% and 23% of the patients, respectively. The BMC of the femoral neck decreased significantly in both groups during the study period (group A, -2.2%, P < 0.001; group B, -1.21%, P < 0.05). The BMC of the lumbar spine did not change. There was an inverse correlation between the initial Z-score and the rate of change in BMC (P < 0.05). We found no correlation between Z-score or change in BMC and period of prednisolone treatment. Moreover, there was no correlation between the length of the resected small intestine and BMC or annual percentage change in BMC. CONCLUSION: At inclusion the BMC of the spine and femoral neck was low in patients with Crohn's disease. During the study significant bone loss was only demonstrated in the femoral neck. BMC or rate of change in BMC was not related to treatment with steroids or length of the resected small intestine.

Absorptiometry, Photon↗
PubMed1996

Effect of parathyroid hormone on renal calbindin-D28k.

The present investigation was conducted to examine the effects of parathyroid hormone (PTH) and parathyroid hormone related peptide (PTHrP) on renal calbindin-D28k in rats. Four groups of studies were performed: (1) parathyroidectomy (PTX) or a sham operation followed by infusion of 1,25-dihydroxyvitamin D (1,25[OH]2D) or vehicle; (2) infusions of PTH(1-34), PTH(1-84), 1,25(OH)2D, or vehicle; (3) infusion of PTHrP(1-34), PTHrP (1-86), PTH(1-34), or vehicle; and (4) injections of calcium or vehicle. PTX reduced renal calbindin-D28k levels even when plasma concentrations of 1,25(OH)2D were kept constant by infusion of 1,25(OH)2D. Infusions of PTH(1-34), PTH(1-84), and 1,25(OH)2D all increased renal calbindin-D28k and plasma calcium, whereas PTHrP(1-34) and PTHrP(1-86) increased renal calbindin-D28k before an increase of plasma calcium took place. Hypercalcemia induced by the injection of calcium did not affect the levels of renal calbindin-D28k. The present data suggest that PTH and PTHrP exert a direct effect on renal calbindin-D28k, which is not mediated by changes of 1,25(OH)2D or calcium.

Animals↗
PubMed1996

Effect of vitamin D metabolites and analogs on renal and intestinal calbindin-D in the rat.

The effects on renal and intestinal calbindin-D of vitamin D3 metabolites and synthetic 20-epi-vitamin D3 analogs with different calcemic actions were examined in Wistar rats. The compounds were administered intraperitoneally once daily for 5 days. The dosages of the metabolites were 1,25-(OH)2D3 0.01, 0.05, 0.1, and 0.4 microg/kg x d, 24,25-(OH)2D3 0.1, 1 and 10 microg/kg x d, and 25-(OH)D3 10 and 400 microg/kg x d. The dosage of the synthetic analogs were MC903 0. 1, 10, and 100 microg/kg x d, EB1213 0.1 and 10 microg/kg x d, KH1060 0.1 and 0.4 microg/kg x d, and GS1725 0.01 and 0.1 microg/kg x d. Two control groups had either vehicle alone or no treatment. N = 8 in each group. 1,25-(OH)2D3 increased renal and intestinal calbindin-D levels, induced hypercalcemia, and suppressed plasma PTH and magnesium concentrations. 24,25-(OH)2D3 increased intestinal calbindin-D9k and plasma calcium, but had no effect on renal calbindin-D28k, plasma PTH, and magnesium. The dosage of 24, 25-(OH)2D3 that was required to increase plasma calcium was larger than the dosage required to increase intestinal calbindin-D9k. 25-(OH)D3 did not change the calcium metabolic parameters. MC903, a low calcemic analog with a relative high affinity for the vitamin D receptor and a short half-life, increased renal calbindin-D28k without increasing ionized calcium or intestinal calbindin-D9k. EB1213, an analog with a reduced calcemic action and short half-life, increased renal calbindin-D28k and ionized calcium without increasing intestinal calbindin-D9k. The effect of the high calcemic vitamin D analogs KH1060 and GS1725 on calbindin-D was directly related to their calcemic activity. In conclusion, these results demonstrate that 24,25-(OH)2D3 increases intestinal calbindin-D9k, but has no effect on renal calbindin-D28k, that low calcemic analogs may increase renal calbindin-D28k without increasing intestinal calbindin-D9k, and that the effect of high calcemic analogs on calbindin-D is directly related to their calcemic activity.

Administration, Cutaneous↗
PubMed1996

Body composition in patients on home parenteral nutrition.

Dual energy X-ray absorptiometry (DXA) measures and separates three of the principal compartments of the body, fat mass (FM), fat-free mass (FFM), comprising muscle, inner organs and body water, and the total bone mineral content (TBMC). The aim of the present study was to determine body composition by DXA scan in 37 patients who had been on home parenteral nutrition (HPN) for 6-216 months. The height and weight of patients were significantly lower when compared to a group of healthy subjects. The weight, however, was relatively more reduced than the height. This is reflected by a significantly reduced body mass index in young female and male patients (p < 0.05). Fat-free mass and total body mineral content were significantly reduced (p < 0.05) in patients on home parenteral nutrition compared to a group of healthy subjects. However, the percentage of fat-free mass was unchanged. No significant change in fat mass was observed. We conclude that patients, with intestinal failure due to short bowel syndrome, who are on HPN have a smaller body size with a normal relative body composition.

Absorptiometry, Photon↗
PubMed1995

Regulation of renal calbindin-D28K: the role of calcitonin.

Infusion of calcitonin lowers circulating calcium, but in the distal tubule of the kidney, pharmacological doses of calcitonin increase the active calcium reabsorption. Calbindin-D28k plays a significant role in the calcium reabsorption in the distal convoluted tubule of the kidney. The effect of calcitonin on renal calbindin-D28k in relation to calcium metabolic changes was therefore examined. In study 1, thyroparathyroidectomy followed by autotransplantation of the parathyroid glands (TX) was compared with a sham operation in rats. TX reduced plasma calcitonin from 54 +/- 2 to 9 +/- 1 pg/ml (P < 0.001), whereas ionized calcium and parathyroid hormone were returned to the control value after an initial decrease, indicating a successful implantation of the parathyroid glands. No changes were seen in calbindin-D or plasma 1,25(OH)2D. In study 2, subcutaneous infusion of salmon calcitonin 2.5 U/kg/hour via osmotic pumps was compared with infusion of vehicle in rats. Ionized calcium was reduced from 1.37 +/- 0.01 to 1.33 +/- 0.02 mmol/liter (P < 0.05), whereas no changes were seen in renal or intestinal calbindin-D or in plasma 1,25(OH)2D. After TX, only calcitonin decreased whereas the other calcium metabolic parameters showed no change. This indicates that in rats, selective elimination of calcitonin does not influence other parameters of the calcium metabolism and that the effect of calcitonin on calcium transport in the distal tubule is not mediated via an increase in renal calbindin-D28k.

Animals↗
PubMed1994

Bone mineral content in patients on home parenteral nutrition.

Bone mineral content (BMC) was monitored in 15 patients with short bowel syndrome receiving home parenteral nutrition (HPN). Thirteen patients had Crohn's disease and 2 ulcerative colitis (mean age 36 years, range 23-69 years). During the study the patients received HPN for a mean period of 62 months, range 20-106 months. At the time of inclusion the patients had a significantly reduced BMC of lumbar spine and femoral neck compared to normals (Z-scores = -3.35 +/- 3.49, p < 0.05 and Z-score = -2.23 +/- 2.11, p < 0.05). During HPN the Z-score of lumbar spine BMC decreased in 8 patients and increased slightly or was unchanged in 7 patients. The mean Z-score of BMC of lumbar spine declined by 1.46 +/- 2.48 (p < 0.05) and the Z-score of femoral neck BMC declined by 0.831 +/- 1.14 (p < 0.05). This corresponds to a yearly decrease of lumbar spine BMC of 4%. There was no correlation between the decline in BMC during the study and the period of length the patients were on HPN. We conclude that patients on HPN have a low bone mineral density and that the bone loss continues during prolonged HPN.

Journal Article↗
PubMed1994

Effects of magnesium on renal and intestinal calbindin-D.

The possible effects of magnesium on the vitamin D-dependent renal and intestinal calbindin-D were investigated. In a low magnesium model 70 Wistar rats were allocated to either a normomagnesemic diet (Mg 3.2 g/kg) or a Mg-deficient diet (Mg 0.18 g/kg) for 10 or 24 days. The rats had intraperitoneal injections of 1,25-(OH)2 vitamin D3 0.2 microgram, MgSO4 100 mumol or placebo daily for the last 4 days. In a high magnesium model 60 Wistar rats were allocated to three groups on a normomagnesemic diet supplied with intraperitoneal MgSO4 20 mumol, 100 mumol or placebo daily. Half of the animals in each group were further supplied with intraperitoneal 1,25-(OH)2 vitamin D3 0.2 micrograms daily. The concentrations of intestinal calbindin-D9k increased on the low Mg diet from 1.6 (1.1-2.0) to 2.7 (2.0-2.9) micrograms/mg protein (p < 0.02), but were unchanged in the high Mg groups. Vitamin D treatment raised the levels of calbindin-D9k in the normomagnesemic group (p < 0.01), but not significantly in the low Mg group. Administration of MgSO4 to the low Mg rats normalized the elevated levels of intestinal calbindin-D9k (p < 0.05). The concentrations of renal calbindin-D28k were not changed by the low Mg diet, but were lower in the high Mg group [0.8 (0.6-1.1) micrograms/mg protein] than in the control group [1.5 (1.1-1.8) micrograms/mg protein; p < 0.05]. Animals in the low, high and normal magnesium group showed no differences in plasma concentrations of 1,25-(OH)2 vitamin D.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Calcium metabolic changes and calbindin-D in experimental hypertension.

OBJECTIVE: To examine renal and intestinal calbindin-D in relation to calcium metabolic changes in three different models of experimental hypertension. DESIGN: Spontaneously hypertensive rats (SHR), hypertension-prone Dahl salt-sensitive (Dahl-S) rats and the Goldblatt two-kidney, one clip rat model of renovascular hypertension were examined. RESULTS: Both prehypertensive and hypertensive SHR had significantly lower concentrations of both renal calbindin-D28k and intestinal calbindin-D9k than Wistar control rats. This was accompanied by hypocalcaemia, hypomagnesaemia and increased plasma 1,25(OH)2 vitamin D levels. Induction of hypertension in Dahl-S rats reduced intestinal calbindin-D9k and increased plasma levels of 1,25(OH)2 vitamin D, while renal calbindin-D28k levels, plasma calcium levels and plasma magnesium levels were unchanged. Renovascular hypertension was associated with a significant increase in the intestinal calbindin-D9k, plasma 1,25(OH)2 vitamin D, parathyroid hormone and magnesium levels, while renal calbindin-D2k, plasma calcium and phosphorus levels were unaffected. CONCLUSIONS: These three models of experimental hypertension have clearly demonstrated three separate patterns in the regulation of renal and intestinal calbindin-D, which relate to different alterations of factors involved in calcium and magnesium metabolism. In all three models hypertension was accompanied by a significant increase in plasma concentrations of 1,25(OH)2 vitamin D. Only rats with renovascular hypertension showed increased intestinal calbindin-D9k levels, whereas reduced concentrations were found in the SHR and in the hypertensive Dahl-S rats. This indicates the existence of a resistance at the cellular level to 1,25(OH)2 vitamin D affecting the expression of calbindin-D in both SHR and Dahl-S rats.

Animals↗
PubMed1993

Calbindin-D9k gene expression during the perinatal period in the rat: correlation to estrogen receptor expression in uterus.

Calbindin-D9k (CaBP-9k) is a cytosolic calcium binding protein mainly expressed in duodenum, placenta and uterus. The gene encoding the rat CaBP-9k is subject to tissue specific induction by 1,25 dihydroxyvitamin D3 (intestine) and estradiol (E2) (uterus). Control of placental expression remains unknown. The expression of CaBP-9k mRNA during the perinatal period was studied (pregnancy day 21 (P21)-lactation day 4 (L4)). In uterus, maximal expression levels were found at P21 and maintained until L1. With the transition to L2, the CaBP-9k mRNA concentration dropped drastically below the detection limit as quantitated by Northern blot analysis. Measurements of E2 and progesterone (P) levels showed a gradual decrease at late pregnancy (P21; birth). Post partum E2 levels continued to decline and P concentrations increased slightly. Uterine estrogen receptor (ER) mRNA levels determined by cDNA/PCR analysis revealed close correlation between expression of ER and CaBP-9k mRNAs. ER mRNA levels were maximal at P22 and declined at parturition and with onset of lactation. At L2 and L3 ER mRNA levels were minimal and had decreased 5-fold compared to late pregnancy. CaBP-9k protein concentrations fluctuated only slightly dependent on the stage of the estrous cycle: estrus > proestrus > diestrus. During the perinatal period CaBP-9k concentration was overall lower than in non-pregnant uterus and revealed only a moderate increase at birth and decrease in early lactation. Similar to the uterine levels, placental CaBP-9k mRNA was highest at P21 and remained high until birth. Fetal duodenal CaBP-9k rose sharply just prior to birth and plateaued in the early postpartal period.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Effects of methylprednisolone and uremia on renal and intestinal calbindin-D in the rat.

The effects of glucocorticoids on renal and intestinal calcium binding protein (calbindin-D28K and calbindin-D9K) were examined in normal and uremic rats. Chronic uremic rats and normal controls were treated with either methylprednisolone (MP) 1.3 mg/kg/d or isotonic saline given as a continuous intraperitoneal infusion for 1 week before sacrifice. Renal calbindin-D28K was measured by rocket immunoelectrophoresis and intestinal calbindin-D9K was measured by an enzyme-linked immunoadsorbent assay. Methylprednisolone treatment of chronic uremic rats increased plasma phosphate levels (P < 0.05), but plasma calcium and 1,25-dihydroxyvitamin D3 were unchanged in all groups. MP treatment did not affect the renal calbindin-D28K in either normal or uremic rats. In normal rats, MP treatment reduced intestinal calbindin-D9K by 28% when compared to placebo (P < 0.05). In contrast, chronic uremia increased renal calbindin-D28K by 51% and 38% (P < 0.001) in placebo and MP treated uremic rats, respectively, while intestinal calbindin-D9K was unchanged. Thus, MP treatment and chronic uremia induced different changes in renal and intestinal calbindin-D of the rat suggesting that different mechanisms are involved in the regulation of these vitamin D dependent proteins.

Animals↗
PubMed1991

Intestinal and renal calcium-binding protein in rats with experimental short bowel syndrome.

Intestinal calcium-binding protein (calbindin-D9K) and renal calcium-binding protein (calbindin-D28K) levels were measured by enzyme-linked immunoadsorbent assays in rats with short bowel syndrome induced by resection of about 85% of the small intestine. Rats with short bowel syndrome had significantly lower mucosal concentrations of calbindin-D9K (P less than 0.001) and a parallel reduction of both intestinal calcium absorption (P less than 0.001) and p-1,25-dihydroxyvitamin D (P less than 0.01) in spite of a general hypertrophy of the duodenal mucosa. Interestingly, the renal concentration of calbindin-D28K was significantly elevated (P less than 0.05) in rats with short bowel syndrome, a change apparently related to factors independent of vitamin D.

Animals↗
PubMed1991

Measurement of calbindin-D9K in small intestinal biopsy specimens of children.

The vitamin D dependent intestinal calcium-binding protein (calbindin-D9K) was measured by an enzyme-linked immunoadsorbent assay in small intestinal biopsy specimens from 10 children (aged 15-126 months). The aim was to study the relationship between calcium-binding protein and age, bone age, and height. The patients were examined due to complaints of chronic diarrhea, but no evidence of malabsorption was found. The amount of calbindin-D9K per mg of soluble protein in the small intestinal biopsy specimens was higher than previously studied in normal adults. Calbindin-D9K correlated inversely with chronological age, bone age, and height of the children (p = -0.87, rho = -0.66, and rho = -0.66; p less than 0.05). A direct correlation was found between calbindin-D9K and intestinal alkaline phosphatase activity (p = 0.60; p less than 0.05). The decline in calbindin-D9K may indicate that the active vitamin D dependent intestinal calcium absorption decreases during childhood.

Age Determination by Skeleton↗
PubMed1991

Renal and intestinal calcium-binding proteins in normal and uraemic rats.

The effect of chronic uraemia on the concentrations of the 28 kDa renal and 9 kDa intestinal calcium-binding proteins (calbindin-D28K and calbindin-D9K) was investigated in rats. Calbindin-D9K was measured by a competitive enzyme-linked immunoadsorbent assay and calbindin-D28K by rocket immunoelectrophoresis. Chronic uraemia was induced by 5/6 nephrectomy and the results were compared to sham-operated animals. Rats were fed on a diet containing 0.9% calcium and 1.2% phosphorous. Plasma creatinine and plasma urea were elevated in the nephrectomized rats (p less than 0.001), while plasma-1,25-dihydroxycalciferol vitamin D and fractional calcium absorption were unchanged. Plasma parathyroid hormone was significantly elevated in the uraemic rats. The concentration of calbindin-D28K in renal tissue was increased (p less than 0.001) in rats with chronic uraemia and a direct correlation was found between renal calbindin-D28K and plasma urea (p less than 0.05). Intestinal calbindin-D9K correlated inversely with plasma creatinine (p less than 0.05), but the mean level of calbindin-D9K was unchanged in this model of moderate chronic uraemia. Thus, different regulatory mechanisms control levels of calbindin-D9K and calbindin-D28K.

Animals↗