Dietary intake of inorganic phosphorus has a stronger influence on vascular-endothelium function than organic phosphorus

Kawamura, H.; Tanaka, Saburo; Ota, Yuichi; Endo, Shogo; Tani, Makoto; Ishitani, Midori; Sakaue, Motoyoshi; Ito, Mikiko

doi:10.3164/jcbn.17-97

Cited by 17 publications

(11 citation statements)

References 31 publications

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“…Kawamura et al. 14 compared 2 meals of equal phosphorus content but with different phosphorus sources (phosphorus supplement or natural phosphorus sources). They found a higher plasma phosphate after ingestion of phosphorus supplements compared to that after consumption of a meal with a high natural phosphorus content.…”

Section: Discussionmentioning

confidence: 99%

“…However, the acute effects of meals with varying degrees of phosphorus-containing meals on the postprandial levels of plasma phosphate is sparsely described. A few studies have been conducted in healthy subjects 10 , 11 , 12 , 13 , 14 and in subjects with CKD stage 3 to 4, 15 but none have been conducted in subjects with ESKD. 16 This study aimed to investigate how a single meal with high phosphorus content acutely affects plasma phosphate compared to a single meal with low phosphorus content in patients with ESKD treated with peritoneal dialysis (PD).…”

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confidence: 99%

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Randomized Trial of Acute Changes in Plasma Phosphate After Phosphorus-Standardized Meals in Peritoneal Dialysis

Lundin

Bressendorff

Kristensen

et al. 2021

Kidney International Reports

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Introduction Hyperphosphatemia is associated with increased morbidity and mortality in patients with chronic kidney disease. The aim of this study was to assess whether a meal with high phosphorus content would affect plasma phosphate in the hours that follow among subjects with end-stage kidney disease on peritoneal dialysis. Methods This was a single-blinded randomized cross-over trial of 12 subjects on maintenance peritoneal dialysis, in which subjects were randomized to consume a meal with either high or low phosphorus content on 2 separate trial days. On each trial day, plasma phosphate was measured immediately before consumption of the standardized meal and after 1, 2, 3, and 5 hours. Results The mean fasting plasma phosphate at baseline was 1.69 ± 0.22 mmol/l. Plasma phosphate was similar between the 2 meals at baseline, as well as at 1, 2, 3, and 5 hours after consumption. The largest observed difference in plasma phosphate between the 2 meals was 0.15 mmol/l, which occurred 5 hours after consumption (high-phosphorus meal 1.75 ± 0.32 mmol/l vs. low-phosphorus meal 1.60 ± 0.14 mmol/l ( P = 0.06)). Using summary analyses for repeated measures, we observed a significant difference in the plasma phosphate between the 2 meals ( P = 0.03). Conclusion Our results show that in subjects with end-stage kidney disease, a meal with high phosphorus content has only a negligible effect on plasma phosphate compared to a meal with low phosphorus content. Thus, large increases in plasma phosphate cannot be accounted for by a high intake of phosphorus in the hours before blood sampling.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Randomized Trial of Acute Changes in Plasma Phosphate After Phosphorus-Standardized Meals in Peritoneal Dialysis

Lundin

Bressendorff

Kristensen

et al. 2021

Kidney International Reports

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“…International Publisher of additives in processed foods has strong impacts on vascular endothelial functions [7][8][9].…”

Section: Ivyspringmentioning

confidence: 99%

Pathobiological Mechanisms of Endothelial Dysfunction Induced by tert-Butyl Hydroperoxide via Apoptosis, Necrosis and Senescence in a Rat Model

Yeh

Liu²,

Lai³

2020

Int. J. Med. Sci.

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Background: Endothelial dysfunction is one of the underlying causes for vascular diseases. tert-Butyl hydroperoxide (t-BHP), a short-chain lipid hydroperoxide analog, has been reported to cause adverse effects in different systems. However, the adverse actions of t-BHP on inducing endothelial dysfunction are unclear and remain under investigation. Aim of the present study was to identify the pathobiological mechanisms of t-BHP in rat aortic endothelial cells and thoracic aorta. Methods: Primary cultured cells were treated with vehicle or t-BHP (50, 100, 250, 500, and 1,000 µM). Cells were harvested and specific analyses regarding cellular apoptosis, necrosis, and senescence were conducted. Additionally, t-BHP (0.1, 0.2, and 0.4 mmol/kg body weight) or vehicle were administered to male rats (the young group at 6 weeks of age and the mature adult group at 24 weeks of age) daily through intraperitoneal injections. At 10 days after the first drug treatment apoptotic endothelial toxicity was evaluated by biochemical, histological, and immunofluorescent staining analyses. Results: Dose-dependent effects of t-BHP were observed for the reduction of cell viability, deterioration of cell toxicity, initiation of cell cycle arrest, and triggering of apoptosis and necrosis. Moreover, increase of cells stained positive for senescence-associated beta-galactosidase (SA-β-Gal), amelioration of telomerase activity, and precipitations of necrotic, cell cycle, and apoptotic signaling regulatory proteins were also found in the in vitro model. In the in vivo study, results indicated that t-BHP at higher doses enlarged the intima-medial thickness of descending aorta in the mature adult group, but led to aortic narrowing in the young group. Increased injuries were observed by upregulating endothelial apoptosis-and senescence-positive staining, along with caspase-3 activity and down-regulating telomerase activity. Conclusion: These results confirmed that t-BHP impaired aortic endothelial cell survival at least partially by the activation of p53-mediated signaling pathways, inhibition of cell cycle regulatory proteins, and initiation of cellular senescence-related signaling pathways. In conclusion, t-BHP was found to be a major trigger for impairing aortic endothelial cell survival and deteriorating vascular dysfunction in experimental practice.

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“…However, studies in human have yielded conflicting evidence. Studies in young healthy men showed that brachial artery flow-mediated dilation (FMD), an indirect index of endothelial function, was reduced acutely after consumption meals containing inorganic Pi additives between 800-1200 mg [35][36][37], while FMD was unaffected by meals with 400 mg of inorganic Pi additives [36]. A longer term study showed reduction in brachial artery FMD after 2 weeks of high Pi (1,500 mg/day) administration in healthy middle-aged adults [32].…”

Section: Role Of Phosphotoxicity On Endothelial Cells and Vascular Smmentioning

confidence: 99%

Phosphate, the forgotten mineral in hypertension

Kim¹,

Mizuno²,

Vongpatanasin

2019

Current Opinion in Nephrology and Hypertension

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Purpose of review: To review the current literature related to the role of inorganic phosphate (Pi) in the pathogenesis of hypertension Recent findings: An increasing number of publications has revealed a detrimental role of inorganic Pi, which is commonly used as a flavor enhancer or preservative in the processed food, in promoting hypertension in otherwise healthy individuals. Animal experimental data indicate that dietary Pi excess engages multiple mechanisms that promote hypertension, including overactivation of the sympathetic nervous system, increased vascular stiffness, impaired endothelium-dependent vasodilation, as well as increased renal sodium absorption or renal injury. These effects may be explained by direct effects of high extracellular Pi levels or increase in phosphaturic hormones such as fibroblast growth factor 23 (FGF23), or downregulation of klotho, a transmembrane protein expressed in multiple organs which possess anti-aging property. Summary: Dietary Pi, particularly inorganic Pi, is an emerging risk factor for hypertension which is ubiquitous in the western diet. Large randomized clinical trials are needed to determine if lowering dietary Pi content constitutes an effective nonpharmacologic intervention for prevention and treatment of hypertension.

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Dietary intake of inorganic phosphorus has a stronger influence on vascular-endothelium function than organic phosphorus

Cited by 17 publications

References 31 publications

Randomized Trial of Acute Changes in Plasma Phosphate After Phosphorus-Standardized Meals in Peritoneal Dialysis

Randomized Trial of Acute Changes in Plasma Phosphate After Phosphorus-Standardized Meals in Peritoneal Dialysis

Pathobiological Mechanisms of Endothelial Dysfunction Induced by tert-Butyl Hydroperoxide via Apoptosis, Necrosis and Senescence in a Rat Model

Phosphate, the forgotten mineral in hypertension

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