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The consumption of phosphorus in Western populations largely exceeds the recommended intake, while vitamin D supply is often insufficient. Both situations are linked to an increased cardiovascular risk. A 17-week two-factorial study with Ldl receptor -/-  mice was conducted to investigate the cardiovascular impact of dietary phosphorus [adequate (0.3%; P 0.3 ) vs. high (1.5%; P 1.5 )] in combination with a low (50 IU/kg; D 50 ) or adequate vitamin D diet (1000 IU/kg; D 1000 ). The data demonstrate that mice fed the P 1.5  vs. P 0.3  diets developed smaller vascular lesions ( p  = 0.013) and cardiac hypotrophy ( p  = 0.011), which were accompanied by diminished IGF1 and insulin signalling activity in their hearts. Vitamin D showed no independent effect on atherogenesis and heart morphology. Feeding P 1.5  vs. P 0.3  diets resulted in markedly reduced serum triacylglycerols ( p  < 0.0001) and cholesterol ( p  < 0.0001), higher faecal lipid excretion ( p  < 0.0001) and a reduced mRNA abundance of hepatic sterol exporters and lipoprotein receptors. Minor hypocholesterolaemic and hypotriglyceridaemic effects were also found in mice fed the D 1000  vs. D 50  diets ( p  = 0.048,  p  = 0.026). To conclude, a high phosphorus intake strongly affected the formation of vascular lesions, cardiac morphology, and lipid metabolism, although these changes are not indicative of an increased cardiovascular risk.

High-phosphorus diets reduce aortic lesions and cardiomyocyte size and modify lipid metabolism in Ldl receptor knockout mice