scholarly journals The protective effect of supplemental calcium on colonic permeability depends on a calcium phosphate-induced increase in luminal buffering capacity

2011 ◽  
Vol 107 (7) ◽  
pp. 950-956 ◽  
Author(s):  
Marloes A. A. Schepens ◽  
Sandra J. M. ten Bruggencate ◽  
Arjan J. Schonewille ◽  
Robert-Jan M. Brummer ◽  
Roelof van der Meer ◽  
...  
Keyword(s):  
Calcium Phosphate ◽  
Protective Effect ◽  
Intestinal Permeability ◽  
Buffering Capacity ◽  
Phosphate Concentration ◽  
Dietary Adaptation ◽  
Supplemental Calcium ◽  
Dietary Phosphate ◽  
Lactate Levels ◽  
High Phosphate

An increased intestinal permeability is associated with several diseases. Previously, we have shown that dietary Ca decreases colonic permeability in rats. This might be explained by a calcium-phosphate-induced increase in luminal buffering capacity, which protects against an acidic pH due to microbial fermentation. Therefore, we investigated whether dietary phosphate is a co-player in the effect of Ca on permeability. Rats were fed a humanised low-Ca diet, or a similar diet supplemented with Ca and containing either high, medium or low phosphate concentrations. Chromium-EDTA was added as an inert dietary intestinal permeability marker. After dietary adaptation, short-chain fructo-oligosaccharides (scFOS) were added to all diets to stimulate fermentation, acidify the colonic contents and induce an increase in permeability. Dietary Ca prevented the scFOS-induced increase in intestinal permeability in rats fed medium- and high-phosphate diets but not in those fed the low-phosphate diet. This was associated with higher faecal water cytotoxicity and higher caecal lactate levels in the latter group. Moreover, food intake and body weight during scFOS supplementation were adversely affected by the low-phosphate diet. Importantly, luminal buffering capacity was higher in rats fed the medium- and high-phosphate diets compared with those fed the low-phosphate diet. The protective effect of dietary Ca on intestinal permeability is impaired if dietary phosphate is low. This is associated with a calcium phosphate-induced increase in luminal buffering capacity. Dragging phosphate into the colon and thereby increasing the colonic phosphate concentration is at least part of the mechanism behind the protective effect of Ca on intestinal permeability.

Evidence of calcium phosphate supersaturation in the loop of Henle

1996 ◽  
Vol 270 (4) ◽  
pp. F604-F613 ◽  
Author(s):  
J. R. Asplin ◽  
N. S. Mandel ◽  
F. L. Coe
Keyword(s):  
Calcium Phosphate ◽  
Calcium Concentration ◽  
Loop Of Henle ◽  
X Ray ◽  
Ion Interactions ◽  
Collecting Ducts ◽  
Phosphate Phase ◽  
Dietary Phosphate ◽  
Calcium Phosphate Phase

We have used published rat micropuncture data to construct a matrix of ion concentrations along the rat nephron. With an iterative computer model of known ion interactions, we calculated relative supersaturation ratios in all nephron segments. The collecting ducts and urine showed expected supersaturation with stone-forming salts. Fluid in the thin segment of the loop of Henle may be supersaturated with calcium carbonate and calcium phosphate under certain conditions. Because calculations cannot predict the actual course of crystallization, we made solutions to mimic, in vitro, presumed conditions in the loop of Henle. The solid phases that formed were analyzed by X-ray powder diffraction, electron microprobe, and infrared spectroscopy. All samples were identified as poorly crystallized or immature apatite. The descending limb of Henle's loop creates a unique condition as it extracts water but not sodium, bicarbonate, calcium, or phosphate, giving a calcium concentration at the bend of 3 mM, pH 7.4, and a phosphate concentration that varies from 0.8 to 48 mM, depending on parathyroid hormone and dietary phosphate. We conclude that conditions in the thin segment potentially could create a solid calcium phosphate phase, which may initiate nucleation of calcium oxalate salts in the collecting ducts, potentiating nephrolithiasis and nephrocalcinosis.

scholarly journals Dopamine enhances the phosphaturic response to parathyroid hormone in phosphate-deprived rats.

1992 ◽  
Vol 2 (9) ◽  
pp. 1423-1429
Author(s):  
J Isaac ◽  
T J Berndt ◽  
S L Chinnow ◽  
G M Tyce ◽  
T P Dousa ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Fractional Excretion ◽  
Phosphate Transport ◽  
Dopamine Synthesis ◽  
Dopamine Infusion ◽  
Phosphate Deprivation ◽  
Dietary Phosphate ◽  
Urinary Dopamine ◽  
Fractional Excretion Of Phosphate ◽  
High Phosphate

Phosphate deprivation results in a resistance to the phosphaturic effect of parathyroid hormone. Dopamine is phosphaturic and is synthesized by kidney proximal tubule, the nephron subsegment where parathyroid hormone inhibits phosphate transport. Thus, to test the hypothesis that phosphate deprivation is associated with low intrarenal dopamine synthesis and that dopamine infusion will overcome the resistance to the phosphaturic response to parathyroid hormone, the following study was performed. The effect of dietary phosphate intake on intrarenal dopamine synthesis, as reflected by urinary dopamine excretion, was determined. Rats were placed in metabolic cages (N = 5) and were fed a low-phosphate diet (0.07% Pi) for 4 days and then a high-phosphate diet (1.8% Pi) for 4 days. Twenty-four-hour urinary dopamine excretion was significantly lower in rats fed a low-phosphate diet (2.53 +/- 0.06 versus 4.10 +/- 0.30 micrograms/day). Further, the effect of dopamine infusion on the blunted phosphaturic response to parathyroid hormone was studied in rats fed a low-phosphate diet for 1, 2, and 3 days. Control clearances were taken 2 h after thyroparathyroidectomy; then, parathyroid hormone (33 U/kg plus 1 U/kg/min), dopamine (25 micrograms/kg/min), or parathyroid hormone plus dopamine were infused for 60 min. Changes in the fractional excretion of phosphate were significantly greater in rats fed a low-phosphate diet infused with parathyroid hormone plus dopamine than in rats fed a low-phosphate diet infused with parathyroid hormone alone (delta 27.9 +/- 5.8 versus 11.2 +/- 2.6% for day 1; 28.4 +/- 1.4 versus 7.1 +/- 3.6% for day 2; and 10.7 +/- 2.8 versus -0.2 +/- 0.2% for day 3; N = 5 for all groups).(ABSTRACT TRUNCATED AT 250 WORDS)

Decrease of phosphate concentration in a high rate pond by precipitation of calcium phosphate: Theoretical and experimental results

1992 ◽  
Vol 26 (11) ◽  
pp. 1445-1450 ◽  
Author(s):  
T. Moutin ◽  
J.Y. Gal ◽  
H. El Halouani ◽  
B. Picot ◽  
J. Bontoux
Keyword(s):  
Calcium Phosphate ◽  
Phosphate Concentration ◽  
Experimental Results ◽  
High Rate

Fetuin-A decrease induced by a low-protein diet enhances vascular calcification in uremic rats with hyperphosphatemia

2015 ◽  
Vol 309 (8) ◽  
pp. F744-F754 ◽  
Author(s):  
Shunsuke Yamada ◽  
Masanori Tokumoto ◽  
Kazuhiko Tsuruya ◽  
Narihito Tatsumoto ◽  
Hideko Noguchi ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Calcium Phosphate ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Calcification ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Fetuin A ◽  
Low Protein ◽  
High Phosphate

Although dietary phosphate restriction is important for treating hyperphosphatemia in patients with chronic kidney disease, it remains unclear whether a low-protein diet (LPD), which contains low phosphate, has beneficial effects on malnutrition, inflammation, and vascular calcification. The effects of LPD on inflammation, malnutrition, and vascular calcification were therefore assessed in rats. Rats were fed a normal diet or diets containing 0.3% adenine and low/normal protein and low/high phosphate. After 6 wk, serum and urinary biochemical parameters, systemic inflammation, and vascular calcification were examined. The protective effect of fetuin-A and albumin were assessed in cultured vascular smooth muscle cells. Rats fed the diet containing 0.3% adenine developed severe azotemia. LPD in rats fed high phosphate induced malnutrition (decreases in body weight, food intake, serum albumin and fetuin-A levels, and urinary creatinine excretion) and systemic inflammation (increases in serum tumor necrosis factor-α and urinary oxidative stress marker). LPD decreased the serum fetuin-A level and fetuin-A synthesis in the liver and increased serum calcium-phosphate precipitates. A high-phosphate diet increased aortic calcium content, which was enhanced by LPD. Reduced fetal calf serum in the medium of cultured vascular smooth muscle cells enhanced phosphate-induced formation of calcium-phosphate precipitates in the media and calcification of vascular smooth muscle cells, both of which were prevented by fetuin-A administration. Our results suggest that phosphate restriction by restricting dietary protein promotes vascular calcification by lowering the systemic fetuin-A level and increasing serum calcium-phosphate precipitates and induces inflammation and malnutrition in uremic rats fed a high-phosphate diet.

Ultrafiltration and Reverse Osmosis in Dairy Technology: A Review

1991 ◽  
Vol 54 (10) ◽  
pp. 801-809 ◽  
Author(s):  
FATHY E. EL-GAZZAR ◽  
ELMER H. MARTH
Keyword(s):  
Calcium Phosphate ◽  
Reverse Osmosis ◽  
Milk Fat ◽  
Buffering Capacity ◽  
Pathogenic Microorganisms ◽  
Dairy Foods ◽  
Cheese Flavor ◽  
Energy Equipment ◽  
Principal Advantage ◽  
Dairy Technology

Ultrafiltration and reverse osmosis processes can be useful in the dairy foods industry. When milk is processed, milk fat and casein are rejected fully (e.g., are in retentate) and thus are concentrated by ultrafiltration and reverse osmosis membranes. Lactic cultures are slow to reduce the pH of retentate because of its increased buffering capacity since concentrated calcium phosphate and proteins are present. Conditions for growth of pathogenic microorganisms and inhibition of such bacteria in ultrafiltered milk differ from those of unfiltered milk. The principal advantage of using ultrafiltered milk for conversion into such cheeses as Cheddar, cottage, Havarti, Feta, brick, Colby, and Domiati is an increase in yield of product. Additional benefits claimed for use of ultrafiltered milk in cheese making include reduction in costs of energy, equipment, and labor; improved consistency of cheese flavor; and possible production of new byproducts.

scholarly journals Supplemental Calcium Attenuates the Colitis-Related Increase in Diarrhea, Intestinal Permeability, and Extracellular Matrix Breakdown in HLA-B27 Transgenic Rats

2006 ◽  
Vol 139 (8) ◽  
pp. 1525-1533 ◽  
Author(s):  
Marloes A. A. Schepens ◽  
Arjan J. Schonewille ◽  
Carolien Vink ◽  
Evert M. van Schothorst ◽  
Evelien Kramer ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Intestinal Permeability ◽  
Hla B27 ◽  
Transgenic Rats ◽  
Supplemental Calcium ◽  
Related Increase

Capacity Control of Phosphate in Caofeidian Sea Area

2011 ◽  
Vol 255-260 ◽  
pp. 2841-2844
Author(s):  
Dong Du ◽  
Cui Ping Kuang ◽  
Rui Huo ◽  
Xiao Ming Sun
Keyword(s):  
Numerical Model ◽  
Tidal Flow ◽  
Phosphate Concentration ◽  
Water Quality Standards ◽  
Capacity Control ◽  
3D Flow ◽  
Flood Season ◽  
Standard Values ◽  
Sea Area ◽  
High Phosphate

Caofeidian is a large harbor being constructed in north of China. It is greatly meaningful to investigate the pollution situation of this area. In this paper, firstly, a tidal flow and pollutant transport numerical model based on Delft 3D-FLOW was established and verified by measured data to simulate and analyze phosphate distribution in Caofeidian sea area. Then, phosphate concentration under six hydrological conditions (spring, middle and neap tides of flood season; and spring, middle and neap tides of dry season) was computed by this numerical model, and the comparisons were made between the computed phosphate concentration at the boundary of the mixing zones and corresponding water quality standards. At last, the allowances discharge amount and cut rate of phosphate of each outfall was calculated. The results show that the high phosphate concentration appears the sea area around the river outlets of Douhe and Shahe, and the phosphate concentration of Douhe and Shuanglonghe rivers’ mixing zones exceed their allowed standard values, the total phosphate discharge from these rivers must be cut down.

IGF-I mediates the stimulatory effect of high phosphate concentration on osteoblastic cell proliferation

2002 ◽  
Vol 190 (3) ◽  
pp. 306-312 ◽  
Author(s):  
Masanori Kanatani ◽  
Toshitsugu Sugimoto ◽  
Junichi Kano ◽  
Kazuo Chihara
Keyword(s):  
Cell Proliferation ◽  
Phosphate Concentration ◽  
Osteoblastic Cell ◽  
Igf I ◽  
High Phosphate

scholarly journals Beneficial Effects of Celastrol on Immune Balance by Modulating Gut Microbiota in Dextran Sodium Sulfate-Induced Ulcerative Colitis

2021 ◽  
Author(s):  
Desheng Hu ◽  
Mingyue Li ◽  
Weina Guo ◽  
Yalan Dong ◽  
Wenzhu Wang ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Gut Microbiota ◽  
Protective Effect ◽  
Intestinal Permeability ◽  
Chronic Inflammatory Bowel Disease ◽  
Protective Mechanism ◽  
Therapeutic Effects ◽  
Dependent Manner ◽  
Colonic Inflammation ◽  
Anti Inflammatory

Ulcerative colitis (UC) is a chronic inflammatory bowel disease caused by multi-factors including colonic inflammation and microbiota dysbiosis. Previous studies have indicated that Celastrol (CSR) has strong anti-inflammatory and immune-inhibitory effects. Here, we investigated the effects of CSR on colonic inflammation and the mucosal immunity in an experimental colitis model, and addressed the mechanism by which CSR preforms the protective effect. We characterized the therapeutic effects and the potential mechanism of CSR in treating UC using histological staining, intestinal permeability assay, cytokine assay, flow cytometry, fecal microbiota transplantation (FMT), 16S rRNA sequencing, untargeted metabolomics, and cell differentiation approaches. CSR administration significantly ameliorated DSS-induced colitis, as evidenced by the recovery of body weight and colon length, decreased disease activity index (DAI) score, as well as decreased intestinal permeability. CSR down-regulated the secretion of proinflammatory cytokines, upregulated the anti-inflammatory mediators, and improved the balances of Treg/Th1 and Treg/Th17 to maintain colonic immune homeostasis. However, the protective effects of CSR disappeared when the antibiotic cocktail was applied to deplete the gut microbiota, and the gut microbiota-mediated effect was confirmed by FMT. Furthermore, CSR treatment increased the gut microbiota diversity and composition, and raised the metabolic productions of pyruvate and adenosine, which probably involve in gut microbiota mediated protective effect. In conclusion, CSR ameliorates colonic inflammation in a gut microbiota-dependent manner. The underlying protective mechanism is associated with the rectified Treg/Th1 and Treg/Th17 balance, and increased pyruvate and adenosine production. The study provided the solid evidence that CSR might be a promising therapeutic drug for UC.

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