scholarly journals Bone Mineralization and Calcium Phosphorus Metabolism

Nutrients ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 3692
Author(s):  
María Luz Couce ◽  
Miguel Saenz de Pipaon
Keyword(s):  
Mineral Content ◽  
Bone Mineralization ◽  
Phosphorus Metabolism ◽  
Normal Bone ◽  
Calcium Phosphorus

The accretion of adequate mineral content is essential for normal bone mineralization [...]

Abstract #1017 Parathyroid Function in Hyperthyroidism in Relation to Calcium-Phosphorus Metabolism

2018 ◽  
Vol 24 ◽  
pp. 226-227
Author(s):  
Ayotunde Ale ◽  
Olatunbosum Olawale ◽  
Onyido Okwuchi ◽  
Sunday Ogundele ◽  
Anthonia Ogbera
Keyword(s):  
Phosphorus Metabolism ◽  
Parathyroid Function ◽  
Calcium Phosphorus

P1237TISSUE-NONSPECIFIC ALKALINE PHOSPHATASE, A CULPRIT DURING ARTERIAL MEDIA CALCIFICATION BUT INDISPENSABLE DURING PHYSIOLOGICAL BONE FORMATION/-MINERALIZATION IN RATS

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Britt Opdebeeck ◽  
José Millan Luis ◽  
Anthony Pinkerton ◽  
Anja Verhulst ◽  
Patrick D'Haese ◽  
...  
Keyword(s):  
Alkaline Phosphatase ◽  
Bone Formation ◽  
Vascular Calcification ◽  
Rat Model ◽  
Bone Mineralization ◽  
Calcium Content ◽  
Marker Genes ◽  
Peripheral Arteries ◽  
Calcium Phosphorus ◽  
Chondrogenic Marker

Abstract Background and Aims Vascular media calcification is frequently seen in elderly and patients with chronic kidney disease (CKD), diabetes and osteoporosis. Pyrophosphate is a well-known calcification inhibitor that binds to nascent hydroxyapatite crystals and prevents further incorporation of inorganic phosphate into these crystals. However, the enzyme tissue-nonspecific alkaline phosphatase (TNAP), which is highly expressed in calcified arteries, degrades extracellular pyrophosphate into phosphate ions, by which pyrophosphate loses its ability to block vascular calcification. Here, we aimed to evaluate whether a TNAP inhibitor is able to prevent the development of arterial calcification in a rat model of warfarin-induced vascular calcification. Method To induce vascular calcification, rats received a diet containing 0.30% warfarin and 0.15% vitamin K1 throughout the entire study and were subjected to the following daily treatments: (i) vehicle (n=10) or (ii) 10 mg/kg/day TNAP-inhibitor (n=10) administered via an intraperitoneal catheter from start of the study until sacrifice at week 7. Calcium, phosphorus and parathyroid hormone (PTH) levels were determined in serum samples as these are important determinants of vascular calcification. As TNAP is also expressed in the liver, serum alanine aminotransferase (ALT) and aspartate (AST) levels were analyzed. At sacrifice, vascular calcification was evaluated by measurement of the total calcium content in the arteries and quantification of the area % calcification on Von Kossa stained sections of the aorta. The mRNA expression of osteo/chondrogenic marker genes (runx2, TNAP, SOX9, collagen 1 and collagen 2) was analyzed in the aorta by qPCR to verify whether vascular smooth muscle cells underwent reprogramming towards bone-like cells. Bone histomorphometry was performed on the left tibia to measure static and dynamic bone parameters as TNAP also regulates physiological bone mineralization. Results No differences in serum calcium, phosphorus and PTH levels was observed between both study groups. Warfarin exposure resulted in distinct calcification in the aorta and peripheral arteries. Daily dosing with the TNAP inhibitor (10 mg/kg/day) for 7 weeks significantly reduced vascular calcification as indicated by a significant decrease in calcium content in the aorta (vehicle 3.84±0.64 mg calcium/g wet tissue vs TNAP inhibitor 0.70±0.23 mg calcium/g wet tissue) and peripheral arteries and a distinct reduction in area % calcification on Von Kossa stained aortic sections as compared to vehicle condition. The inhibitory effects of SBI-425 on vascular calcification were without altering serum liver markers ALT and AST levels. Furthermore, TNAP-inhibitor SBI-425 did not modulate the mRNA expression of osteo/chondrogenic marker genes runx2, TNAP, SOX9, collagen 1 and 2. Dosing with SBI-425 resulted in decreased bone formation rate and mineral apposition rate, and increased osteoid maturation time and this without significant changes in osteoclast- and eroded perimeter. Conclusion Dosing with TNAP inhibitor SBI-425 significantly reduced the calcification in the aorta and peripheral arteries of a rat model of warfarin-induced vascular calcification and this without affecting liver function. However, suppression of TNAP activity should be limited in order to maintain adequate physiological bone mineralization.

Observations on the mineral metabolism of pullets. II

1936 ◽  
Vol 26 (1) ◽  
pp. 85-100 ◽  
Author(s):  
R. H. Common
Keyword(s):  
Calcium Carbonate ◽  
Egg Production ◽  
Mineral Metabolism ◽  
Ammonium Phosphate ◽  
Ammonia Nitrogen ◽  
Egg Laying ◽  
Phosphorus Metabolism ◽  
Phosphorus Excretion ◽  
Calcium Phosphorus ◽  
Digestible Protein

1. Where heavy phosphorus excretion accompanies egg laying in the pullet the excretion of ammonia nitrogen is simultaneously increased. It is probable that this indicates an excretion of excess phosphate in the urine as ammonium phosphate.2. It is shown that heavy phosphorus excretion does not accompany egg laying provided the calcium carbonate intake is sufficiently high.3. The origin of the excess of phosphorus excretion is discussed in relation to calcium-phosphorus metabolism.4. Pullets on a ration containing 5 per cent, calcium carbonate laid eggs containing a higher percentage of P2O5 than pullets receiving a similar ration but from which the calcium carbonate supplement was omitted.5. Some evidence is put forward in support of the view that current standards pitch the requirements of digestible protein for egg production at too high a level.

62 Growth Performance and Mineral Status of 6 Kg Piglets Fed Reduced Levels of Dietary Calcium

2021 ◽  
Vol 99 (Supplement_1) ◽  
pp. 42-42
Author(s):  
Laura A Merriman ◽  
Craig Wyatt ◽  
Marie-Pierre Létourneau-Montminy ◽  
Xaviere Rousseau ◽  
Dan Bussières
Keyword(s):  
Bone Mineral Content ◽  
Growth Performance ◽  
Bone Mineral ◽  
Mineral Content ◽  
Bone Mineralization ◽  
Phase 1 ◽  
Short Term ◽  
Plasma Parameters ◽  
Dietary Treatments ◽  
The Impact

Abstract Imbalances between calcium (Ca) and phosphorus (P) impair growth performance and bone mineralization. However, reducing dietary limestone may change the buffering capacity of feed in early nursery piglets, which may help prevent post-weaning diarrhea. An experiment was conducted to evaluate the impact of reducing Ca post weaning compared to recommendations outlined by NRC (2012) or a low P diet. Dietary treatments consisted of 1) Low Ca (LCa; Phase 1, 0.51% Ca and 0.47% STTD P), 2) NRC recommendations (NRC; Phase 1, 0.85% Ca and 0.42% STTD P), and 3) a recommendation lower in phosphorus (LP; Phase 1, 0.65% Ca and 0.36% STTD P). Each diet was fed over 4 phases. Piglets (n = 953; 276/275 Fast X PIC 800 genetics) were blocked by room, sex, and initial BW (6 kg). Feed intake and pig weights were recorded weekly. At 12 d and 41 d, blood was collected and Dual-X ray (DXA) measurements were taken using 8 piglets per treatment. Fecal scores were evaluated during wk 4 and 5. Data were analyzed using MIXED procedure of SAS (SAS Inst. Inc., Cary, NC). There were no differences observed in mortality, overall growth performance, plasma Ca and P, and scour scores at either time point. At 12 d, the bone mineral content was reduced (P = 0.001) in LP pigs compared to LCa and NRC. At 41 d, bone mineral content was reduced in NRC in comparison to LCa while LP was intermediate (P = 0.001). Plasma parameters showed an increased magnesium (Mg) and Ca:Mg in LCa (P < 0.01) that can be related to bone resorption to face Ca hypocalcemia. Pigs were healthy with no enteric challenges, limiting the ability to observe a benefit in fecal scores. In conclusion, piglets can maintain growth and bone mineralization through a short-term limestone removal program.

scholarly journals Dietary Calcium to Digestible Phosphorus Ratio for Optimal Growth Performance and Bone Mineralization in Growing and Finishing Pigs

Animals ◽  
2020 ◽  
Vol 10 (2) ◽  
pp. 178 ◽  
Author(s):  
Patrick Schlegel ◽  
Andreas Gutzwiller
Keyword(s):  
Growth Performance ◽  
Mineral Content ◽  
Bone Mineralization ◽  
Dietary Calcium ◽  
Phosphate Removal ◽  
Volumetric Density ◽  
Dietary Phosphorus ◽  
Maximal Load ◽  
Bone Properties ◽  
Bone Ash

Within the context of maximizing the use of dietary phosphorus, a growing-finishing pig study was conducted to determine the optimal total dietary calcium (Ca) to digestible phosphorus (dP) ratio and to verify the possibility of mineral phosphate removal during the finishing period on growth performance and mineral status. The potential for replacing chemical and mechanical bone properties by dual energy X-ray absorptiometry (DXA) measures on non-dissected feet was also verified. Three Ca to dP ratios (2.2:1, 2.5:1 and 2.8:1) within two dP levels (P+, P–) were fed during 91 days to 84 pigs. The grower and finisher P+ diets contained 3.0 and 2.4 and P– diets contained 2.5 and 1.7 g dP/kg, respectively. Growth performance and blood serum mineral content were independent of treatments, except that 2.2:1 impaired finisher feed conversion ratio compared to 2.5:1 and 2.8:1. Urinary P concentration increased by 37% in 2.2:1 compared to 2.5:1 and 2.8:1. Maximal load on bone and DXA mineral density were reduced in 2.2:1 compared to 2.8:1. Bone ash and volumetric density were reduced in 2.2:1 and 2.5:1 compared to 2.8:1. Diet P– reduced bone ash, maximal load, volumetric density and DXA bone mineral content and density. No interaction was observed between Ca and dP level. Therefore, 2.2:1 was insufficient for an efficient metabolic use of P, 2.5:1 was sufficient to maximize growth performance and 2.8:1 further improved bone mineralization. Increasing dietary Ca did not impair bone zinc content. Diets P– without supplemented mineral phosphates during the finisher period resulted, per pig, in a decrease of its use by 65% and of the calculated P excretion by 41%, without impaired growth performance. Finally, DXA data responded to dietary treatments as did labor intensive chemical and mechanical bone properties.

scholarly journals Preventive Effects of Evodiamine on Dexamethasone-Induced Osteoporosis in Zebrafish

2019 ◽  
Vol 2019 ◽  
pp. 1-6 ◽  
Author(s):  
Heng Yin ◽  
Jianwei Wang ◽  
Mao Wu ◽  
Yong Ma ◽  
Shanfu Wang ◽  
...  
Keyword(s):  
Western Blot ◽  
Mapk Pathway ◽  
Bone Mineralization ◽  
Tartrate Resistant Acid Phosphatase ◽  
Mrna Levels ◽  
Rt Pcr ◽  
Alizarin Red ◽  
Calcium Phosphorus ◽  
Commercial Kits ◽  
Preventive Effects

The aim of this study was to investigate the effect of evodiamine (EV) on dexamethasone-induced osteoporosis in zebrafish. Zebrafish larvae were exposed to different concentrations of dexamethasone to obtain the osteoporosis in zebrafish. Calcium, phosphorus, and alizarin red staining determination were performed to evaluate the effects of EV on bone mineralization. Alkaline phosphatase (ALP), hydroxyproline (HP), and tartrate resistant acid phosphatase (TRAP) were also measured by commercial kits. The expression of MMP3-OPN-MAPK pathway in zebrafish was measured by Western blot. RT-PCR was used to determine mRNA levels of MMP3, OPN, and MAPK. EV could significantly increase the content of calcium and phosphorus. The results of alizarin red staining showed that EV could significantly increase the calcium sink of horse fish, increasing the area of bone formation. EV could increase the content of hydroxyproline in zebrafish. EV also increased ALP and TRAP in zebrafish. Western blot and RT-PCR results showed that EV restored the MMP3-OPN-MAPK pathway in zebrafish. In conclusion, we found that EV can alleviate dexamethasone-induced osteoporosis in zebrafish. The mechanism is related to activating MMP3-OPN-MAPK pathway and then activating bone remodeling.

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