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Energy-dense diets increase FGF23, lead to phosphorus retention and promote vascular calcifications in rats.

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2016-07-29

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Raya, Ana I.
Rios, Rafael
Pineda, Carmen
Rodriguez-Ortiz, Maria E.
Diez, Elisa
Almaden, Yolanda
Muñoz-Castañeda, Juan R.
Rodriguez, Mariano
Aguilera-Tejero, Escolastico
Lopez, Ignacio

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Nature
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Rats with normal renal function (Experiment 1, n=12) and uninephrectomized (1/2Nx) rats (Experiment 2, n=12) were fed diets with normal P (NP) and either normal (NF) or high fat (HF). Rats with intact renal function (Experiment 3, n=12) were also fed NF or HF diets with high P (HP). Additionally, uremic (5/6Nx) rats (n=16) were fed HP diets with NF or HF. Feeding the HF diets resulted in significant elevation of plasma FGF23 vs rats fed NF diets: Experiment 1, 593±126 vs 157±28pg/ml (p<0.01); Experiment 2, 538±105 vs 250±18pg/ml (p<0.05); Experiment 3, 971±118 vs 534±40pg/ml (p<0.01). Rats fed HF diets showed P retention and decreased renal klotho (ratio klotho/actin) vs rats fed NF diets: Experiment 1, 0.75±0.06 vs 0.97±0.02 (p<0.01); Experiment 2, 0.69±0.07 vs 1.12±0.08 (p<0.01); Experiment 3, 0.57±0.19 vs 1.16±0.15 (p<0.05). Uremic rats fed HF diet showed more severe vascular calcification (VC) than rats fed NF diet (aortic Ca=6.3±1.4 vs 1.4±0.1mg/g tissue, p<0.001). In conclusion, energy-rich diets increased plasma levels of FGF23, a known risk factor of cardiovascular morbidity and mortality. Even though FGF23 has major phosphaturic actions, feeding HF diets resulted in P retention, likely secondary to decreased renal klotho, and aggravated uremic VC

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Animals
Body Weight
Dietary Fats
Fibroblast Growth Factors
Gene Expression Regulation
Glucuronidase
Kidney
Klotho Proteins
Male
Phosphorus
Rats
Uremia
Vascular Calcification

DeCS Terms

Calcificacion vascular
Factores de crecimiento de fibroblastos
Regulacion de la expresion genica
Uremia
Proteinas Klotho
Fosforo
Peso corporal

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Raya AI, Rios R, Pineda C, Rodriguez-Ortiz ME, Diez E, Almaden Y, et al. Energy-dense diets increase FGF23, lead to phosphorus retention and promote vascular calcifications in rats. Sci Rep. 2016 Nov 14;6:36881