Research Article: Phosphorus restriction does not prevent the increase in fibroblast growth factor 23 elicited by high fat diet

Date Published: June 1, 2018

Publisher: Public Library of Science

Author(s): Rafael Rios, Carmen Pineda, Ignacio Lopez, Juan Muñoz-Castañeda, Mariano Rodriguez, Escolastico Aguilera-Tejero, Ana I. Raya, Michael Bader.

http://doi.org/10.1371/journal.pone.0198481

Abstract

This study was designed to evaluate the influence of phosphorus (P) restriction on the deleterious effects of high fat diets on mineral metabolism. Twenty-four rats were allotted to 3 groups (n = 8 each) that were fed different diets for 7 months. Rats in group 1 were fed normal fat-normal P (0.6%) diet (NF-NP), rats in group 2 were fed high fat- normal P diet (HF-NP) and rats in group 3 were fed high fat-low P (0.2%) diet (HF-LP). Blood, urine and tissues were collected at the end of the experiments. When compared with the control group (NF-NP), rats fed HF diets showed increases in body weight, and in plasma concentrations of triglycerides and leptin, and decreased plasma calcitriol concentrations. In rats fed HF-NP plasma fibroblast growth factor 23 (FGF23) was higher (279.6±39.4 pg/ml vs 160.6±25.0 pg/ml, p = 0.018) and renal klotho (ratio klotho/GAPDH) was lower (0.75±0.06 vs 1.06±0.08, p<0.01) than in rats fed NF-NP. Phosphorus restriction did not normalize plasma FGF23 or renal klotho; in fact, rats fed HF-LP, that only ingested an average of 22.9 mg/day of P, had higher FGF23 (214.7±32.4 pg/ml) concentrations than rats fed NF-NP (160.6±25.0 pg/ml), that ingested and average of 74.4 mg/day of P over a 7 month period. In conclusion, our results demonstrate that severe P restriction over a prolonged period of time (7 months) does not normalize the increase in circulating FGF23 induced by HF diets. These data indicate that the deleterious effects of high fat diet on the FGF23/klotho axis are not eliminated by reduced P intake.

Partial Text

Obesity and its related metabolic complications represent a major health concern, not only due to their influence on morbidity and mortality but also for the high healthcare cost associated to this disease [1,2]. A major factor in the development of obesity is excessive caloric intake which is favored by the ingestion of energy-dense processed foods (fast food). In addition to their high caloric concentration, processed foods are often rich in phosphate (P) [3]. Phosphate is a common food additive and the inorganic P added to processed foods is more readily absorbed than organic P [4]. Moreover, the high fat content of many fast foods also enhances intestinal P absorption [5]. Therefore, individuals eating fast food often ingest an overload of P that must be excreted by the kidney to maintain P homeostasis.

At the beginning of the study all rats had similar body weight that ranged between 239.4±1.7 and 251.2±3.3 g. During the 7 months that lasted the experiment rats experienced an increase in body weight that was more accentuated in the groups fed a HF diet. Phosphorus restriction attenuated the increase in body weight in rats fed HF, but the differences were small and non-significant (Fig 1). Mean daily intake of P (mg/day) was not influenced by the amount of ingested fat but, obviously, was much lower (p<0.001) in the P restricted group: NF-NP = 74.4±6.3, HF-NP = 77.9±3.7, HF-LP = 22.9±1.4. This study was designed to investigate the effect of restricting P intake on the changes in mineral metabolism elicited by HF diets. Our results demonstrate that marked P restriction over a prolonged period of time (7 months) does not normalize the elevated circulating FGF23 levels induced by HF diets. These data indicate that the deleterious effects of high fat diet on the FGF23/klotho axis are not eliminated by reduced P intake.   Source: http://doi.org/10.1371/journal.pone.0198481

 

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