Scholarlink

Background <p>It is widely recognized that dysregulated mineral balance, in the context of disease, has negative health consequences. However, growing evidence shows that imbalances in mineral homeostasis from a sustained high dietary intake of inorganic phosphate/phosphorus (Pi), even when kidney function remains clinically normal, can also cause serious health problems, including bone disease. Western-style diets, which commonly include added Pi salts, contribute significantly to the issue. Despite this, investigations into therapeutic strategies to counter these effects in the absences of disease are limited. This study aimed to determine whether clinically used pharmacologic and nutritional interventions could regulate mineral homeostasis and prevent bone loss while correcting the systemic consequences of chronic high dietary Pi intake.</p> Methods <p>Healthy mice were fed diets with high (HPD), normal (NPD), or low (LPD) levels of Pi additives and constant calcium (Ca). Additional groups were treated with HPD and supplemented with Vitamin D, Lanthanum Carbonate, Cinacalcet, Zoledronic acid, or a strategy of balancing dietary Ca:Pi.</p> Results <p>The therapies that partially or fully corrected serum Pi levels and homeostatic factors, interestingly, corrected the increase in cortical porosity but did not correct the HPD-induced decrease in cortical or trabecular bone volume. Only Zoledronic acid successfully restored the bone volume lost due to HPD but exacerbated the HPD increase in cortical porosity. Surprisingly, many of the treatments generated an inflammatory response in kidney in the context of HPD, suggesting that they can have harmful side effects in the absence of overt kidney disease.</p> Conclusions <p>This work advances the understanding of the health impacts of Pi additives which are common in ultra-processed foods and common in the Western style diet. Specifically, the results produce clinically relevant findings that simply controlling serum Pi and/or Ca levels or Pi responsive endocrine factors such as FGF23, PTH, and osteopontin are not sufficient to block the negative impacts of chronic high dietary Pi consumption on the skeleton. Further, therapeutic strategies to control serum Pi have an impact on the kidneys in the context of high dietary Pi intake.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Correcting serum phosphate homeostasis does not alleviate the health dangers of high phosphate consumption

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年7月22日

查看全文
  • Jamie L. Arnst,
  • Uma D. Alappan,
  • Manjula Viggeswarapu,
  • George R. Beck Jr.

摘要

Background

It is widely recognized that dysregulated mineral balance, in the context of disease, has negative health consequences. However, growing evidence shows that imbalances in mineral homeostasis from a sustained high dietary intake of inorganic phosphate/phosphorus (Pi), even when kidney function remains clinically normal, can also cause serious health problems, including bone disease. Western-style diets, which commonly include added Pi salts, contribute significantly to the issue. Despite this, investigations into therapeutic strategies to counter these effects in the absences of disease are limited. This study aimed to determine whether clinically used pharmacologic and nutritional interventions could regulate mineral homeostasis and prevent bone loss while correcting the systemic consequences of chronic high dietary Pi intake.

Methods

Healthy mice were fed diets with high (HPD), normal (NPD), or low (LPD) levels of Pi additives and constant calcium (Ca). Additional groups were treated with HPD and supplemented with Vitamin D, Lanthanum Carbonate, Cinacalcet, Zoledronic acid, or a strategy of balancing dietary Ca:Pi.

Results

The therapies that partially or fully corrected serum Pi levels and homeostatic factors, interestingly, corrected the increase in cortical porosity but did not correct the HPD-induced decrease in cortical or trabecular bone volume. Only Zoledronic acid successfully restored the bone volume lost due to HPD but exacerbated the HPD increase in cortical porosity. Surprisingly, many of the treatments generated an inflammatory response in kidney in the context of HPD, suggesting that they can have harmful side effects in the absence of overt kidney disease.

Conclusions

This work advances the understanding of the health impacts of Pi additives which are common in ultra-processed foods and common in the Western style diet. Specifically, the results produce clinically relevant findings that simply controlling serum Pi and/or Ca levels or Pi responsive endocrine factors such as FGF23, PTH, and osteopontin are not sufficient to block the negative impacts of chronic high dietary Pi consumption on the skeleton. Further, therapeutic strategies to control serum Pi have an impact on the kidneys in the context of high dietary Pi intake.