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Fluctuating plasma phosphorus level by changes in dietary phosphorus intake induces endothelial dysfunction.

Watari E, Taketani Y, Kitamura T, Tanaka T, Ohminami H, Abuduli M, Harada N, Yamanaka-Okumura H, Yamamoto H, Takeda E - J Clin Biochem Nutr (2014)

Bottom Line: Here we examined whether fluctuating plasma P caused by changes in dietary P intake may be involved in endothelial dysfunction, resulting in increased cardiovascular risk.In the LH and HL groups, endothelial-dependent vasodilation significantly decreased plasma 8-(OH)dG level significantly increased, and the expression of inflammatory factors such as MCP-1 increased in the endothelium as compared with the control group.These data indicate that repetitive fluctuations of plasma P caused by varying dietary P intake can impair endothelial function via increased oxidative stress and inflammatory response.

View Article: PubMed Central - PubMed

Affiliation: Department of Clinical Nutrition, Institute of Health Biosciences, University of Tokushima Graduate School, 3-18-15, Kuramoto-cho, Tokushima 770-8503, Japan.

ABSTRACT
High serum phosphorus (P) impairs endothelial function by increasing oxidative stress and decreasing nitric oxide production. Serum P levels fluctuate due to circadian rhythms or dietary P intake in healthy people and due to dialysis in end-stage chronic kidney disease patients. Here we examined whether fluctuating plasma P caused by changes in dietary P intake may be involved in endothelial dysfunction, resulting in increased cardiovascular risk. Rats were fed a diet containing 0.6% P for 16 days (control group), or a diet alternating between 0.02% P and 1.2% P (LH group) or between 1.2% P and 0.02% P (HL group) every 2 days; the total amount of P intake among the groups during the feeding period was similar. In the LH and HL groups, endothelial-dependent vasodilation significantly decreased plasma 8-(OH)dG level significantly increased, and the expression of inflammatory factors such as MCP-1 increased in the endothelium as compared with the control group. These data indicate that repetitive fluctuations of plasma P caused by varying dietary P intake can impair endothelial function via increased oxidative stress and inflammatory response. Taken together, these results suggest that habitual fluctuation of dietary P intake might be a cause of cardiovascular disease through endothelial dysfunction, especially in chronic kidney disease patients.

No MeSH data available.


Related in: MedlinePlus

Daily P intake (A) and daily plasma P level (B) in the low P (open circle), control (hatched circle), high P (closed circle) groups during the experimental period. Daily P intake was calculated from daily food intake and the P content in each experimental diet. Blood samples were taken from the tail vein. Results are expressed as mean ± SEM (n = 5).
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Figure 2: Daily P intake (A) and daily plasma P level (B) in the low P (open circle), control (hatched circle), high P (closed circle) groups during the experimental period. Daily P intake was calculated from daily food intake and the P content in each experimental diet. Blood samples were taken from the tail vein. Results are expressed as mean ± SEM (n = 5).

Mentions: Continuous administration of the CP diet, LP diet or HP diet led to different daily dietary P intake during the experimental period (Fig. 2A). The LP diet group showed lower plasma P levels as compared with the CP diet group immediately after beginning ingestion of LP diet; on the other hand, ingestion of the HP diet did not increase plasma P levels during the experimental period (Fig. 2B). In the alternating diet groups, when the rats were fed the HP diet, both daily P intake and plasma P levels were elevated (Fig. 3). Conversely, when the rats were fed the LP diet, both daily P intake and plasma P levels were decreased (Fig. 3). Importantly, total P intake during the experimental period in the alternating diet groups was almost same as that of CP diet group. Thus, the alternating diet groups showed a clear fluctuation of dietary P intake and plasma P levels.


Fluctuating plasma phosphorus level by changes in dietary phosphorus intake induces endothelial dysfunction.

Watari E, Taketani Y, Kitamura T, Tanaka T, Ohminami H, Abuduli M, Harada N, Yamanaka-Okumura H, Yamamoto H, Takeda E - J Clin Biochem Nutr (2014)

Daily P intake (A) and daily plasma P level (B) in the low P (open circle), control (hatched circle), high P (closed circle) groups during the experimental period. Daily P intake was calculated from daily food intake and the P content in each experimental diet. Blood samples were taken from the tail vein. Results are expressed as mean ± SEM (n = 5).
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4306666&req=5

Figure 2: Daily P intake (A) and daily plasma P level (B) in the low P (open circle), control (hatched circle), high P (closed circle) groups during the experimental period. Daily P intake was calculated from daily food intake and the P content in each experimental diet. Blood samples were taken from the tail vein. Results are expressed as mean ± SEM (n = 5).
Mentions: Continuous administration of the CP diet, LP diet or HP diet led to different daily dietary P intake during the experimental period (Fig. 2A). The LP diet group showed lower plasma P levels as compared with the CP diet group immediately after beginning ingestion of LP diet; on the other hand, ingestion of the HP diet did not increase plasma P levels during the experimental period (Fig. 2B). In the alternating diet groups, when the rats were fed the HP diet, both daily P intake and plasma P levels were elevated (Fig. 3). Conversely, when the rats were fed the LP diet, both daily P intake and plasma P levels were decreased (Fig. 3). Importantly, total P intake during the experimental period in the alternating diet groups was almost same as that of CP diet group. Thus, the alternating diet groups showed a clear fluctuation of dietary P intake and plasma P levels.

Bottom Line: Here we examined whether fluctuating plasma P caused by changes in dietary P intake may be involved in endothelial dysfunction, resulting in increased cardiovascular risk.In the LH and HL groups, endothelial-dependent vasodilation significantly decreased plasma 8-(OH)dG level significantly increased, and the expression of inflammatory factors such as MCP-1 increased in the endothelium as compared with the control group.These data indicate that repetitive fluctuations of plasma P caused by varying dietary P intake can impair endothelial function via increased oxidative stress and inflammatory response.

View Article: PubMed Central - PubMed

Affiliation: Department of Clinical Nutrition, Institute of Health Biosciences, University of Tokushima Graduate School, 3-18-15, Kuramoto-cho, Tokushima 770-8503, Japan.

ABSTRACT
High serum phosphorus (P) impairs endothelial function by increasing oxidative stress and decreasing nitric oxide production. Serum P levels fluctuate due to circadian rhythms or dietary P intake in healthy people and due to dialysis in end-stage chronic kidney disease patients. Here we examined whether fluctuating plasma P caused by changes in dietary P intake may be involved in endothelial dysfunction, resulting in increased cardiovascular risk. Rats were fed a diet containing 0.6% P for 16 days (control group), or a diet alternating between 0.02% P and 1.2% P (LH group) or between 1.2% P and 0.02% P (HL group) every 2 days; the total amount of P intake among the groups during the feeding period was similar. In the LH and HL groups, endothelial-dependent vasodilation significantly decreased plasma 8-(OH)dG level significantly increased, and the expression of inflammatory factors such as MCP-1 increased in the endothelium as compared with the control group. These data indicate that repetitive fluctuations of plasma P caused by varying dietary P intake can impair endothelial function via increased oxidative stress and inflammatory response. Taken together, these results suggest that habitual fluctuation of dietary P intake might be a cause of cardiovascular disease through endothelial dysfunction, especially in chronic kidney disease patients.

No MeSH data available.


Related in: MedlinePlus