scholarly journals Details of True Calcium Absorption and Calcium Excretion into Feces in Female Rats during Growth.

2001 ◽  
Vol 47 (1) ◽  
pp. 52-56 ◽  
Author(s):  
Kazuo HARAI ◽  
Tomio MOROHASHI ◽  
Tsuneyoshi SANO ◽  
Shoji YAMADA
Keyword(s):  
Calcium Absorption ◽  
Female Rats ◽  
Calcium Excretion

Prolactin is an important regulator of intestinal calcium transport

2007 ◽  
Vol 85 (6) ◽  
pp. 569-581 ◽  
Author(s):  
Narattaphol Charoenphandhu ◽  
Nateetip Krishnamra
Keyword(s):  
Vitamin D ◽  
Small Intestine ◽  
Calcium Transport ◽  
Calcium Absorption ◽  
Intestinal Calcium Absorption ◽  
The Body ◽  
Female Rats ◽  
Calcium Excretion ◽  
Target Tissue ◽  
Intestinal Calcium Transport

Prolactin has been shown to stimulate intestinal calcium absorption, increase bone turnover, and reduce renal calcium excretion. The small intestine, which is the sole organ supplying new calcium to the body, intensely expresses mRNAs and proteins of prolactin receptors, especially in the duodenum and jejunum, indicating the intestine as a target tissue of prolactin. A number of investigations show that prolactin is able to stimulate the intestinal calcium transport both in vitro and in vivo, whereas bromocriptine, which inhibits pituitary prolactin secretion, antagonizes its actions. In female rats, acute and long-term exposure to high prolactin levels significantly enhances the (i) transcellular active, (ii) solvent drag-induced, and (iii) passive calcium transport occurring in the small intestine. These effects are seen not only in pregnant and lactating animals, but are also observed in non-pregnant and non-lactating animals. Interestingly, young animals are more responsive to prolactin than adults. Prolactin-enhanced calcium absorption gradually diminishes with age, thus suggesting it has an age-dependent mode of action. Although prolactin's effects on calcium absorption are not directly vitamin D-dependent; a certain level of circulating vitamin D may be required for the basal expression of genes related to calcium transport. The aforementioned body of evidence supports the hypothesis that prolactin acts as a regulator of calcium homeostasis by controlling the intestinal calcium absorption. Cellular and molecular signal transductions of prolactin in the enterocytes are largely unknown, however, and still require investigation.

Adolescents with anorexia nervosa have decreased calcium absorption and increased urinary calcium excretion

1991 ◽  
Vol 12 (2) ◽  
pp. 171
Author(s):  
Steven A. Abrams ◽  
Tomas J. Silber ◽  
Nora V. Esteban ◽  
Nancy E. Vieira ◽  
Mansoud Majd ◽  
...  
Keyword(s):  
Anorexia Nervosa ◽  
Calcium Absorption ◽  
Urinary Calcium ◽  
Urinary Calcium Excretion ◽  
Calcium Excretion

scholarly journals Enhancement of urinary calcium excretion in aged female rats of Wistar/Tw strain.

1991 ◽  
Vol 55 ◽  
pp. 241
Author(s):  
Yuta Kobayashi ◽  
Keiko Shimoura ◽  
Youko Tanabe ◽  
Keisuke Hattori
Keyword(s):  
Urinary Calcium ◽  
Urinary Calcium Excretion ◽  
Female Rats ◽  
Calcium Excretion

Mechanism of chronic hypocalciuria with chlorthalidone: reduced calcium absorption

1984 ◽  
Vol 247 (5) ◽  
pp. F746-F752 ◽  
Author(s):  
D. A. Bushinsky ◽  
M. J. Favus ◽  
F. L. Coe
Keyword(s):  
Serum Calcium ◽  
Calcium Absorption ◽  
Chronic Administration ◽  
Intestinal Calcium Absorption ◽  
Male Rats ◽  
Calcium Excretion ◽  
Urine Calcium ◽  
X 24 ◽  
Filtered Load ◽  
Urine Calcium Excretion

Chlorthalidone, like other benzothiadiazides, lowers urine calcium excretion chronically. If intestinal calcium absorption did not fall or bone accretion did not increase, serum calcium and the filtered load of calcium would increase and urine calcium would return to pretreatment levels. To determine whether overall intestinal calcium absorption fell, we fed chlorthalidone (5 mg X kg body wt-1 X 24 h-1) to 10 adult male rats eating 15 g/day of a 0.6% calcium diet. Compared with 10 control rats, chlorthalidone reduced urine calcium [2.1 +/- 0.1 (SE) vs. 5.8 +/- 0.5 mg/6 days; P less than 0.001]. Fecal calcium rose (307 +/- 9 vs. 257 +/- 12; P less than 0.005) because percent intestinal calcium absorption fell (41 +/- 2 vs. 52 +/- 2; P less than 0.002). Twenty other rats given the same diet were injected subcutaneously with 1,25(OH)2D3 (50 ng/day). In these rats, chlorthalidone reduced urine calcium (23 +/- 3 vs. 59 +/- 3; P less than 0.001) and percent intestinal calcium absorption (60 +/- 1 vs. 66 +/- 1; P less than 0.01). With or without 1,25(OH)2D3, chronic administration of chlorthalidone reduces intestinal calcium absorption, and this reduction seems to be the mechanism that permits urine calcium excretion to remain low.

CALCIUM INFUSION IN THE DETECTION OF BONE DISEASE IN PARATHYROID DISORDERS

1963 ◽  
Vol 43 (2) ◽  
pp. 170-183 ◽  
Author(s):  
Heinrich G. Haas ◽  
John J. Canary ◽  
Laurence H. Kyle ◽  
Daniel H. Mintz
Keyword(s):  
Alkaline Phosphatase ◽  
Calcium Absorption ◽  
Osteitis Fibrosa ◽  
Idiopathic Hypercalciuria ◽  
Calcium Excretion ◽  
List Type ◽  
Elevated Alkaline Phosphatase ◽  
Calcium Retention ◽  
High Calcium ◽  
Wide Range

ABSTRACT The retention of an infused load of calcium was determined under standard conditions in 25 patients with various parathyroid disorders, in 12 normal control subjects, and in 3 patients with idiopathic hypercalciuria. A normal range of 40–60 per cent calcium-retention was found, and there was some support to the thesis that hypercalciuria per se may lower the retention of calcium. Patients with primary hyperparathyroidism showed a wide range of calcium retention reflecting on one side probably hypercalciuria (low calcium retention) and on the other osteitis fibrosa generalisata (high calcium retention). In detecting early bone involvement in parathyroid hyperfunction, the calcium retention test was of equal or greater value than alkaline phosphatase determination in the serum. In secondary hyperparathyroidism due to severe renal insufficiency, a high calcium retention was seen pointing either to delayed calcium excretion (low GFR) or increased avidity of the skeleton for calcium as a consequence of an admixture of osteomalacia and osteitis fibrosa. All hypoparathyroid patients retained large quantities of calcium. In three of these cases, an elevated alkaline phosphatase level indicated osteomalacia, possibly following inadequate calcium absorption from the gut, while in two patients a low filtered load of calcium accounted for the apparent high calcium retention.

Idiopathic infantile hypercalcemia: case report and review of the literature

2016 ◽  
Vol 29 (2) ◽  
Author(s):  
Brynn E. Marks ◽  
Daniel A. Doyle
Keyword(s):  
Vitamin D ◽  
Enzyme Activity ◽  
Calcium Absorption ◽  
Calcium Excretion ◽  
Review Of The Literature ◽  
Active Vitamin ◽  
Supplemental Vitamin ◽  
Idiopathic Infantile Hypercalcemia ◽  
Therapeutic Doses ◽  
Renal Calcium Excretion

AbstractThe widespread use of supplemental vitamin D has dramatically reduced the incidence of rickets. While generally considered a safe practice, there is potential for toxicity in patients with idiopathic infantile hypercalcemia (IIH). Inadequate 24-hydroxylase-enzyme activity renders these individuals unable to degrade active vitamin D, resulting in hypercalcemia due to increased intestinal calcium absorption, decreased renal calcium excretion, and increased osteoclastic bone activity. Clinicians should be aware that even therapeutic doses of vitamin D can prove harmful for patients with

Increased sensitivity to 1,25(OH)2D3 in bone from genetic hypercalciuric rats

1996 ◽  
Vol 271 (1) ◽  
pp. C130-C135 ◽  
Author(s):  
N. S. Krieger ◽  
V. M. Stathopoulos ◽  
D. A. Bushinsky
Keyword(s):  
Bone Resorption ◽  
Calcium Absorption ◽  
Immunoblot Analysis ◽  
Calcium Excretion ◽  
Sprague Dawley ◽  
Urine Calcium ◽  
Fourfold Increase ◽  
Low Calcium Diet ◽  
Slot Blot Analysis ◽  
Urine Calcium Excretion

As a model of human hypercalciuria, we have selectively inbred genetic hypercalciuric stone-forming (GHS) Sprague-Dawley rats whose mean urine calcium excretion is eight to nine times greater than that of controls. A large component of this excess urine calcium excretion is secondary to increased intestinal calcium absorption, which is not due to an elevation in serum 1,25(OH)2D3, but appears to result from an increased number of intestinal 1,25(OH)2D3 receptors (VDR). When GHS rats are fed a low-calcium diet, the hypercalciuria is only partially decreased and urine calcium excretion exceeds intake, suggesting that an additional mechanism contributing to the hypercalciuria is enhanced bone demineralization. To determine if GHS rat bones are more sensitive to exogenous 1,25(OH)2D3, we cultured calvariae from neonatal (2- to 3-day-old) GHS and control rats with or without 1,25(OH)2D3 or parathyroid hormone (PTH) for 48 h at 37 degrees C. There was significant stimulation of calcium efflux from GHS calvariae at 1 and 10 nM 1,25(OH)2D3, whereas control calvariae showed no significant response to 1,25(OH)2D3 at any concentration tested. In contrast, PTH induced similar bone resorption in control and GHS calvariae. Immunoblot analysis demonstrated a fourfold increase in the level of VDR in GHS calvariae compared with control calvariae, similar to the increased intestinal receptors described previously. There was no comparable change in VDR RNA levels as measured by slot blot analysis, suggesting the altered regulation of the VDR occurs posttranscriptionally. That both bone and intestine display an increased amount of VDR suggests that this may be a systemic disorder in the GHS rat and that enhanced bone resorption may be responsible, in part, for the hypercalciuria in the GHS rat.

Effects of Calcium Source on Calcium-Metabolic Parameters in Healthy Women and Men

2021 ◽  
Vol 8 (2) ◽  
Author(s):  
Hitz MF ◽  
◽  
Dahl M ◽  
Jørgensen NR ◽  
◽  
...  
Keyword(s):  
Vitamin D ◽  
Steady State ◽  
Calcium Carbonate ◽  
Calcium Absorption ◽  
Menopausal Status ◽  
Daily Intake ◽  
Dietary Calcium ◽  
Calcium Excretion ◽  
Steady State Condition

Background/Objectives: Calcium and vitamin D are important for bone health. We compared 24-hour urinary calcium-excretion (Uca/24hrs), during dietary calcium steady-state condition, for different calcium-sources and effects of vitamin D, age and sex. Subjects/Methods: Fifty-two healthy pre- and postmenopausal women and men completed the regimens: placebo, calcium carbonate (400mg) +18μg vitamin D, calcium carbonate (400mg) +38μg vitamin D and 400mg calcium phosphate (milk). Uca/24hrs was measured during dietary calcium steady state as a surrogate measure of calcium-absorption. Serum-calcium, parathyroid hormone (PTH), 25-hydroxy-vitamin D, Procollagen Type 1 N-terminal Pro- Peptide (P1NP) and C-terminal Telopeptide of type 1 collagen (CTX) were measured. Results: Mean daily intake of calcium for the study group ± SD was 1105 ±396 mg. Mean-Uca ± SD: placebo 5.19 ± 2.04 mmol/24hrs, milk 5.88 ± 2.39 mmol/24hrs, (CaCO3+D) 6.19 ± 2.34 mmol/24hrs and (CaCO3 + DD) 6.26 ± 2.32 mmol/day. Uca were higher for all regimens compared to placebo (p <0.001), no difference was found between regimens. CTX was lower during all regimens compared to placebo (p <0.001): placebo 450 ± 243 μg/L, Milk 377 ± 248 μg/L, (CaCO3+D) 392 ± 266 μg/L and (CaCO3+DD) 361 ± 232 μg/L. Conclusions: Uca was higher during supplementation with calcium compared to placebo. Supplementation with calcium reduced bone resorption significantly without effecting PTH. Menopausal status, sex and supplement with vitamin d demonstrated no effect on calcium excretion.

Impaired body calcium metabolism with low bone density and compensatory colonic calcium absorption in cecectomized rats

2012 ◽  
Vol 302 (7) ◽  
pp. E852-E863 ◽  
Author(s):  
Prapaporn Jongwattanapisan ◽  
Panan Suntornsaratoon ◽  
Kannikar Wongdee ◽  
Nitita Dorkkam ◽  
Nateetip Krishnamra ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Calcium Transport ◽  
Calcium Metabolism ◽  
Calcium Absorption ◽  
Calcium Excretion ◽  
Compensatory Mechanism ◽  
Calcium Balance ◽  
Balance Study ◽  
Colonic Epithelial Cells ◽  
Calbindin D

An earlier study reported that cecal calcium absorption contributes less than 10% of total calcium absorbed by the intestine, although the cecum has the highest calcium transport rate compared with other intestinal segments. Thus, the physiological significance of the cecum pertaining to body calcium metabolism remains elusive. Herein, a 4-wk calcium balance study in cecectomized rats revealed an increase in fecal calcium loss with marked decreases in fractional calcium absorption and urinary calcium excretion only in the early days post-operation, suggesting the presence of a compensatory mechanism to minimize intestinal calcium wasting. Further investigation in cecectomized rats showed that active calcium transport was enhanced in the proximal colon but not in the small intestine, whereas passive calcium transport along the whole intestine was unaltered. Since apical exposure to calcium-sensing receptor (CaSR) agonists similarly increased proximal colonic calcium transport, activation of apical CaSR in colonic epithelial cells could have been involved in this hyperabsorption. Calcium transporter genes, i.e., TRPV6 and calbindin-D9k, were also upregulated in proximal colonic epithelial cells. Surprisingly, elevated serum parathyroid hormone levels and hyperphosphatemia were evident in cecectomized rats despite normal plasma calcium levels, suggesting that colonic compensation alone might be insufficient to maintain normocalcemia. Thus, massive bone loss occurred in both cortical and trabecular sites, including lumbar vertebrae, femora, and tibiae. The presence of compensatory colonic calcium hyperabsorption with pervasive osteopenia in cecectomized rats therefore corroborates that the cecum is extremely crucial for body calcium homeostasis.

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