scholarly journals A high-calcium diet failed to rescue an osteopenia phenotype in claudin-18 knockout mice

2014 ◽  
Vol 2 (1) ◽  
pp. e00200 ◽  
Author(s):  
Fatima Z. Alshbool ◽  
Catrina Alarcon ◽  
Jon Wergedal ◽  
Subburaman Mohan
Keyword(s):  
Knockout Mice ◽  
Calcium Diet ◽  
High Calcium ◽  
High Calcium Diet

Parathyroid Hormone- and Deoxycorticosterone Acetate-Induced Hypertension in the Rat

1980 ◽  
Vol 58 (5) ◽  
pp. 365-371 ◽  
Author(s):  
A. Berthelot ◽  
A. Gairard
Keyword(s):  
Parathyroid Hormone ◽  
Hormone Secretion ◽  
Sprague Dawley ◽  
Physiological Concentration ◽  
Deoxycorticosterone Acetate ◽  
Calcium Diet ◽  
Arterial Blood ◽  
Sprague Dawley Rats ◽  
High Calcium ◽  
High Calcium Diet

1. Hypertension induced by treatment with deoxycorticosterone acetate and sodium chloride was studied in male Sprague-Dawley rats and related to parathyroid hormone secretion. 2. Lack of parathyroid hormone (due to parathyroidectomy) or decreased parathormone secretion (due to a high-calcium diet) partially inhibited the development of arterial hypertension. 3. In contrast, in thyroparathyroidectomized rats supplemented with thyroxine, the administration of parathyroid hormone rapidly elevated arterial blood pressure. 4. Maintaining a physiological concentration of serum calcium in the absence of parathyroid hormone (by feeding a high-calcium diet to parathyroidectomized rats) was not sufficient to establish mineralocorticoid hypertension. 5. These results show that parathyroid hormone is necessary for the complete development of mineralocorticoid hypertension.

scholarly journals Effect of High‐Calcium Diet on Coronary Artery Disease in Ossabaw Miniature Swine With Metabolic Syndrome

2015 ◽  
Vol 4 (8) ◽  
Author(s):  
Alyssa K. Phillips‐Eakley ◽  
Mikaela L. McKenney‐Drake ◽  
Martin Bahls ◽  
Sean C. Newcomer ◽  
John S. Radcliffe ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Metabolic Syndrome ◽  
Coronary Artery ◽  
Miniature Swine ◽  
Calcium Diet ◽  
High Calcium ◽  
High Calcium Diet ◽  
Artery Disease

Effect of High-Calcium Diet on Urinary Oxalate Excretion in Urinary Stone Formers

1988 ◽  
Vol 15 (3-4) ◽  
pp. 264-270 ◽  
Author(s):  
Teruhiro Nakada ◽  
Isoji Sasagawa ◽  
Hidekatsu Furuta ◽  
Takashi Katayama ◽  
Jun Shimazaki
Keyword(s):  
Urinary Stone ◽  
Urinary Oxalate ◽  
Oxalate Excretion ◽  
Calcium Diet ◽  
Stone Formers ◽  
High Calcium ◽  
High Calcium Diet ◽  
Urinary Oxalate Excretion

scholarly journals High calcium diet augments vascular potassium relaxation in hypertensive rats.

Hypertension ◽  
1992 ◽  
Vol 19 (1) ◽  
pp. 85-92 ◽  
Author(s):  
I Pörsti ◽  
P Arvola ◽  
H Wuorela ◽  
H Vapaatalo
Keyword(s):  
Hypertensive Rats ◽  
Calcium Diet ◽  
High Calcium ◽  
High Calcium Diet

scholarly journals Calcium Regulates FGF-23 Expression in Bone

Endocrinology ◽  
2013 ◽  
Vol 154 (12) ◽  
pp. 4469-4482 ◽  
Author(s):  
Valentin David ◽  
Bing Dai ◽  
Aline Martin ◽  
Jinsong Huang ◽  
Xiaobin Han ◽  
...  
Keyword(s):  
Culture Media ◽  
Fibroblast Growth Factor 23 ◽  
Dihydroxyvitamin D3 ◽  
Pooled Data ◽  
Calcium Diet ◽  
High Calcium ◽  
High Calcium Diet ◽  
Calcium Phosphorus ◽  
Serum Pth ◽  
Fgf 23

Calcium has recently been shown to regulate fibroblast growth factor 23 (FGF-23), a bone-derived phosphate and vitamin D-regulating hormone. To better understand the regulation of FGF-23 by calcium, phosphorus, 1,25 dihydroxyvitamin D3 [1,25(OH)2D], and PTH, we examined FGF-23 expression under basal conditions and in response to PTH, doxercalciferol, or high-calcium diet treatment in Gcm2−/− and Cyp27b1−/− mutant mice. Gcm2−/− mice exhibited low serum PTH and 1,25(OH)2D concentrations, hypocalcemia, and hyperphosphatemia, whereas Cyp27b1−/− mice had high PTH, undetectable 1,25(OH)2D, hypocalcemia, and hypophosphatemia. Serum FGF-23 levels were decreased in both mutant models. Doxercalciferol administration increased serum FGF-23 levels in both mutant models. PTH administration to Gcm2−/− mice also increased serum FGF-23 levels, in association with an increase in both 1,25(OH)2D and calcium concentrations. Multiple regression analysis of pooled data indicated that changes in FGF-23 were positively correlated with serum calcium and 1,25(OH)2D but not related to changes in serum phosphate concentrations. A high-calcium diet also increased serum FGF-23 concentrations in Cyp27b1−/− mice in the absence of 1,25(OH)2D and in Gcm2−/− mice with low PTH. The addition of calcium to the culture media also stimulated FGF-23 message expression in MC3T3-E1 osteoblasts. In addition, FGF-23 promoter activity in cultured osteoblasts was inhibited by the L-calcium-channel inhibitor nifedipine and stimulated by calcium ionophores. The effects of chronic low calcium to prevent 1,25(OH)2D and PTH stimulation of FGF-23 in these mutant mouse models suggest that suppression of FGF-23 plays an important physiological adaptive response to hypocalcemia.

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