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Dietary phosphorus acutely impairs endothelial function.
Emi Shuto1, Yutaka Taketani, Rieko Tanaka
1Department of Clinical Nutrition, Institute of Health Biosciences, University of Tokushima Graduate School, 3-18-15, Kuramoto-cho, Tokushima 770-8503, Japan.
High dietary phosphorus intake acutely impairs blood vessel function in healthy individuals. This post-meal phosphorus surge causes endothelial dysfunction, potentially increasing cardiovascular risk.
Area of Science:
- Cardiovascular Science
- Renal Nutrition
- Endothelial Biology
Background:
- Excess dietary phosphorus is linked to cardiovascular risk in general and CKD populations.
- Mechanisms connecting phosphorus intake to cardiovascular risk remain unclear.
- Investigating acute effects of phosphorus on endothelial function is crucial.
Purpose of the Study:
- To determine if postprandial hyperphosphatemia promotes endothelial dysfunction.
- To investigate the acute effects of dietary phosphorus loading on endothelial function in vitro and in vivo.
Main Methods:
- In vitro: Bovine aortic endothelial cells exposed to phosphorus load.
- In vivo: Rat aortic rings subjected to phosphorus loading.
- Human study: 11 healthy men consumed low (400mg) or high (1200mg) phosphorus meals in a crossover design.
- Measurements included reactive oxygen species, nitric oxide, and flow-mediated dilation (FMD).
Main Results:
- In vitro phosphorus load increased reactive oxygen species and decreased nitric oxide production.
- Phosphorus loading impaired endothelium-dependent vasodilation in rat aortic rings.
- High phosphorus meals in humans increased serum phosphorus and significantly reduced brachial artery FMD.
- Reduced FMD correlated inversely with postprandial serum phosphorus levels.
Conclusions:
- Acute postprandial hyperphosphatemia induces endothelial dysfunction.
- This dysfunction may contribute to the association between serum phosphorus and cardiovascular risk.
- Dietary phosphorus management could be important for cardiovascular health.
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