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Biomedical subjects

R Bouillon

Publications and source records attributed to R Bouillon.

At least 307 records · Page 17Linked to original sources
PubMed1987

Evidence for an interaction of insulin and sex steroids in the regulation of vitamin D metabolism in the rat.

Vitamin D metabolites and vitamin D-binding protein (DBP) were measured in non-diabetic rats and in rats made diabetic with streptozotocin. The animals were studied in the intact state, after gonadectomy and during pregnancy. In male non-diabetic rats the serum concentrations of 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) and DBP decreased after orchidectomy and were restored by treatment with testosterone. In female non-diabetic rats, these parameters increased after ovariectomy. Increased 1,25-(OH)2D3 and decreased DBP concentrations were found during pregnancy in non-diabetic rats. After the induction of diabetes in intact rats of both sexes, the concentration of DBP decreased, but a significant decrease in the concentration of 1,25-(OH)2D3 was found in male animals only. After ovariectomy, however, 1,25-(OH)2D3 decreased also in female diabetic rats. Both orchidectomy and insulin deficiency depressed serum concentrations of 1,25-(OH)2D3 (-22 and -45% respectively) and DBP (-14 and -29% respectively), but the effects of insulin deficiency were greater than those of androgen withdrawal. Moreover, the testosterone concentration was twofold lower in intact male diabetic rats than in non-diabetic animals. Insulin, but not testosterone treatment, however, restored DBP and 1,25-(OH)2D3 concentrations in diabetic rats, and insulin was effective in intact as well as in gonadectomized animals. This study shows that insulin deficiency decreases the concentrations of DBP and 1,25-(OH)2D3 in the rat, and that these decreases are facilitated by androgens, but counteracted by oestrogens.

Animals↗
PubMed1987

Ultrastructural immunocytochemical localization of endogenous 1,25-dihydroxyvitamin D3 and its receptors in osteoblasts and osteocytes from neonatal mouse and rat calvaria.

Immunoreactivity to 1,25-dihydroxyvitamin D3 receptors and endogenous 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) were studied in osteoblasts and osteocytes from calvaria of neonatal mice and rats by immunocytochemistry with the use of ultrathin sections obtained by cryo-ultramicrotomy. Tissue samples were fixed in glutaraldehyde, postfixed in osmium tetroxide and frozen under liquid nitrogen. 1,25(OH)2D3 and 1,25(OH)2D3 receptor-like immunoreactivities were observed in osteoblasts and osteocytes. In both types of cell, 1,25(OH)2D3 and its receptors were similarly located in the cytoplasmic matrix but not in organelles, and mainly in the nucleus (primarily in the chromatin and sometimes near the nuclear membrane or in the nucleolus). Reaction products, however, were never seen at the plasma membrane level. These results provide immunocytological evidence for the presence of 1,25(OH)2D3 and its receptors in osteoblasts and osteocytes. The similar localization of the hormone and its receptors in osteoblasts and osteocytes supports the hypothesis of a direct action of 1,25(OH)2D3 in these bone cells. The fact that the main localization of 1,25(OH)2D3 receptors was nuclear, implies, as postulated for other steroid receptors, that 1,25(OH)2D3 receptors occur primarily in the nucleus.

Animals↗
PubMed1986

Pancreatic secretion in man with subclinical vitamin D deficiency.

The effects of subclinical vitamin D deficiency and vitamin D supplementation on oral glucose tolerance and secretion of pancreatic hormones were studied in 10 diphenylhydantoin-treated epileptic patients and 15 geriatric patients. Their mean serum concentrations of 25-hydroxyvitamin D3 and 1,25-dihydroxyvitamin D3 decreased markedly, but returned to normal within 2 weeks of oral supplementation with 25-hydroxyvitamin D3. The serum concentration of ionized calcium was within the normal range before treatment, and remained unchanged. Serum parathyroid hormone was increased during vitamin D deficiency, but decreased significantly (p less than 0.05) afterwards. In vitamin D-deficient epileptic and geriatric patients, the 2- and 3-h insulin levels after glucose ingestion were increased when compared with control values, and glucagon secretion was not suppressed by glucose. Oral glucose tolerance of both groups of patients did not change after 25-hydroxyvitamin D3 supplementation. Insulin secretion remained unchanged in geriatric patients, but was reduced to normal values in epileptic patients. Glucagon suppressibility by glucose was partly restored after vitamin D supplementation in epileptic patients but not in geriatric patients. In contrast to that observed in severely vitamin D-deficient rats or rabbits, correction of subclinical vitamin D deficiency failed to enhance insulin secretion or to improve glucose tolerance in man.

Age Factors↗
PubMed1986

Decreased free 1,25-dihydroxycholecalciferol index in patients with the nephrotic syndrome.

The serum concentrations of calcium, phosphorus, parathyroid hormone, vitamin D3 metabolites and their transport protein (DBP) were measured in 18 patients with the nephrotic syndrome (mean daily proteinuria 8.8 g). The glomerular filtration rate was normal in 13 patients while the remaining 5 had a mild degree of renal failure. The serum concentrations of total protein, albumin and DBP were significantly decreased in patients with the nephrotic syndrome. The serum calcium concentration was decreased but the calculated ionized calcium concentration remained normal. The serum concentrations of 25-hydroxycholecalciferol (5.3 +/- 3.1 micrograms/l) and 1,25-dihydroxycholecalciferol [1,25-(OH)2D3 (20 +/- 12 ng/l)] were significantly lower in patients with the nephrotic syndrome and normal glomerular filtration rates than in normal controls (14.4 +/- 4 micrograms/l and 42 +/- 13 ng/l, respectively). The free 1,25-(OH)2D3 index was also significantly below normal (0.9 +/- 0.4 vs. 1.8 +/- 0.4). Total and free 1,25-(OH)2D3 were still further reduced in patients with mild renal failure. The nephrotic syndrome thus results in mild vitamin D depletion with decreased free 1,25-(OH)2D3 concentrations but generally without secondary hyperparathyroidism.

Adolescent↗
PubMed1986

Vitamin D and bone mineral homeostasis during pregnancy in the diabetic BB rat.

Vitamin D and bone mineral metabolism during pregnancy were studied in 17 diabetic and 13 control BB rats. On day 21 of pregnancy, reduced mean levels of 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3; 56.9 vs. 97.9 pg/ml; P less than 0.0001] and vitamin D-binding protein (304 vs. 482 micrograms/ml; P less than 0.0001) were found in the diabetic rats, while the free 1,25-(OH)2D3 concentration was not different from the control level. Total plasma calcium and total plasma protein concentrations were also significantly decreased in the diabetic group, but the calculated diffusible calcium was not significantly lower. Calcium and phosphorus urinary excretion were increased in the diabetic rats. There was no difference in bone mineral content. The fetuses of the diabetic BB rat had a lower body weight and were hypoinsulinemic. Both 1,25-(OH)2D3 (41.3 vs. 54.7 pg/ml; P less than 0.01) and vitamin D-binding protein (80 vs. 123 micrograms/ml; P less than 0.001) were decreased in the fetuses of diabetic rats, but the free 1,25-(OH)2D3 concentration was slightly but significantly (6.96 vs. 5.54; P less than 0.05) increased. We observed that the fetuses of diabetic rats had fewer ossification centers, counted with the Alizarin Red S staining method. The fetal ash weight was lower in the diabetic group (16.7 vs. 26.9 mg; P less than 0.0001). In addition, the relative calcium and phosphorus, but not magnesium, content of ash was lower in the fetuses of diabetic rats. This reduced mineral content in fetuses of diabetic mothers could be implicated in the pathogenesis of early neonatal hypocalcemia in infants of diabetic mothers.

Animals↗
PubMed1986

Ontogeny and oestradiol dependence of vitamin D-binding protein blood levels in chickens.

The concentration of 25-hydroxyvitamin D3-binding protein (DBP) was measured, by immunodiffusion, in the blood of chickens from embryonic stages to sexual maturity. Low levels of DBP and 1,25-(OH)2D3 were detectable in the blood of chick embryos from the 12th and 17th day of incubation respectively and stayed at the same low levels until hatching. The blood concentration of DBP doubled between the 1st and 5th days of life, then increased slowly and reached the mean level of the adult male at 7-8 weeks of age. The concentration of DBP was independent of vitamin D status in growing chickens. A large increase was observed in DBP blood levels in hens just before sexual maturity. This change, and those observed in moulting hens, followed the variations in plasma concentrations of oestradiol more closely than those of progesterone or testosterone. Moreover, a large increase in plasma DBP levels was induced in immature chickens by oestradiol (0.5 mg/day), but not by testosterone or progesterone. Finally, the experimental suppression of egg shell formation and the associated decrease in 1,25-(OH)2D3 plasma levels had no effect on plasma DBP concentrations. However, 1,25-(OH)2D3 and DBP levels were higher in hens laying shell-less eggs than in immature pullets. The increases in DBP levels at hatching, in immature pullets treated with oestrogens, in hens laying uncalcified eggs and at the onset of egg production were associated with increases in 1,25-(OH)2D3, suggesting a relationship between the levels of DBP and 1,25-(OH)2D3 in the blood.

Animals↗
PubMed1986

Transcortin and vitamin D-binding protein levels in mouse serum.

The influence of age, sex and strain on the serum concentration of transcortin (corticosteroid-binding globulin) and vitamin D-binding protein (DBP) in mice was investigated. The effect of age was studied in two strains, C57BL/6JPfd and BALB/cmHeAPfd. The concentration of transcortin and DBP increased with age. In young animals the concentration of each protein showed a significant strain difference, which disappeared in older mice for DBP, but not for transcortin. In 7-day-old animals, no sex difference was observed for either protein, but in older animals a clear sex difference was found for transcortin. Adult males tended to have somewhat higher levels of DBP than adult females, but this difference was significant only on day 70. The variation in transcortin and DBP levels was further investigated in a large number of mouse strains. The DBP concentration did not markedly vary among strains (5.98-9.65 mumol/l in males and 5.08-8.85 mumol/l in females). Transcortin, however, showed marked strain variations, ranging from 0.72 to 2.06 mumol/l in males and from 1.02 to 4.55 mumol/l in females and there was a significant correlation (r = 0.66, n = 26, P less than 0.001) between the mean transcortin levels in males and females of different strains. Interstrain variation was much higher than intrastrain variation or variation among related strains, suggesting that the transcortin concentration is largely controlled by genetically determined factors. There was a significant correlation (r = 0.82, n = 9, P less than 0.01) between the mean corticosterone and transcortin concentrations (measured at 21.00 h).(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1986

Vitamin D metabolites and their binding protein in adult diabetic patients.

Vitamin D metabolites and vitamin D-binding protein were measured in the serum of nonketotic Bantu and Caucasian insulin-requiring diabetic subjects from Zaire and Belgium, respectively. In Caucasian diabetics, whether untreated (N = 18) or insulin treated (N = 26), no abnormalities were found. The Bantu diabetics (N = 20) were more insulin-deficient and had a poorer glucose control than the Caucasians. They presented, compared with Bantu controls, a significant decrease in the serum concentrations of 25-hydroxyvitamin D3 (26 +/- 10 vs. 35 +/- 14 micrograms/L, P less than .01), 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] (38 +/- 15 vs. 58 +/- 17 ng/L, P less than .001), and vitamin D-binding protein (303 +/- 55 vs. 356 +/- 41 mg/L, P less than .001). The decreased concentrations of vitamin D metabolites in the adult Bantu diabetic patients may be partly explained by a concomitant decrease in the concentration of vitamin D-binding protein, possibly due to insulin deficiency. The ratio between the molar concentrations of 1,25-(OH)2D3 and vitamin D-binding protein, used as an index of the free hormonal level, was also decreased, in association with a decreased serum calcium level. In conclusion, no abnormalities in vitamin D metabolism were found in Caucasian insulin-dependent diabetics, whereas low serum 1,25(OH)2D3 concentrations and hypocalcemia were found in poorly controlled Bantu diabetic subjects.

Adult↗
PubMed1986

Mineral and bone metabolism in thyroid disease: a review.

This review discusses the abnormalities in bone and mineral metabolism encountered in thyroid disorders. Thyroid hormones probably stimulate bone resorption directly, thereby increasing serum calcium and phosphorus concentrations and suppressing serum parathyroid hormone and 1,25-dihydroxyvitamin D3 concentrations. The decrease in these bone-resorbing hormones limits further increase in serum calcium concentration but also results in an enhanced intestinal calcium absorption. Such a negative calcium balance will eventually lead to hyperthyroid osteopenia. In adult hypothyroidism the opposite effects are seen.

Alkaline Phosphatase↗