Why phosphate rich foods can increase blood pressure and promote vascular calcifications has been discovered for the first time by scientists at the University of Veterinary Medicine, Vienna. The key is the hormone, FGF23 (Fibroblast Growth Factor 23), which is produced in the bones, and regulates blood levels of calcium and sodium via the kidneys. When the level of FGF23 is raised, as through a high phosphate diet, calcium and sodium accumulate, putting strain on the cardiovascular system. The study appears today in the journal, EMBO Molecular Medicine.
Phosphate rich foods include processed cheese, Parmesan, cola, baking powder and most processed foods. Phosphates are widely used in the food industry as preservatives and pH stabilizers. When large quantities of phosphates are consumed, production of the FGF23 hormone is stimulated, which has a negative effect on the cardiovascular system. Reinhold Erben, the head of the Unit of Physiology, Pathophysiology and Biophysics at the Vetmeduni Vienna, warns that “our phosphate consumption is relevant for our state of health”.
Over 500 million people around the world suffer from chronic kidney disease. Clinical studies have shown that these patients often develop cardiovascular diseases such as high blood pressure and vascular calcification. Until now, the connection between renal disease, the accumulation of the hormone FGF23 which is produced in the bones, and cardiovascular disease was unclear.
FGF23 controls renal excretion of sodium, and so the blood pressure
The researchers showed that FGF23 has a so called sodium conserving effect, meaning it controls the reabsorption of filtered sodium in the kidneys. Mice lacking FGF23 excrete higher amounts of sodium in their urine, resulting in low blood pressure. Animals with high FGF23 levels show high levels of sodium in their blood, and in turn, high blood pressure.
A raised level of FGF23 puts increased strain on the heart. Reinhold Erben explains that, “In patients with chronic renal disease, both the phosphate levels and the levels of FGF23 are chronically high. This often leads to cardiovascular disease.
FGF23 controls calcium, and therefore vascular calcification
A second study, published by Erben’s group in mid-January in EMBO, showed that FGF23 also controls calcium levels. As with sodium, the calcium is filtered in the kidneys and reabsorbed back into the body. If this reabsorption does not take place, the body loses calcium. Too much FGF23 leads to increased take up of calcium by the kidneys, and results in vascular calcification. Olena Andrukhova, the leading author of both studies, is keen to stress that, “Patients with chronic kidney disease often also suffer from cardiovascular disease. Raised FGF23 levels are partly responsible for this. Our results for the first time are able to explain this connection.”
Feedback loop between kidneys and bones
The hormone FGF23 is formed in the bones and controls the excretion of phosphate via the kidneys. When there is too much phosphate present in the body, the FGF23 level rises which leads to the excretion of excess phosphate. If too much phosphate is ingested with food, or if the excretion process via the kidneys does not work correctly, phosphate and FGF23 levels increase. A dangerous spiral begins that can have serious consequences on the overall health.
New critical values of FGF23 in science
The newly discovered functions of the hormone FGF23 were, until recently, attributed to another protein, αKlotho. Several scientific publications had assumed αKlotho to be the crucial factor for calcium conservation in the kidneys. With their newly published work, Erben and his colleagues show for the first time that FGF23 is responsible for this function, and not αKlotho. However, αKlotho is essential for the FGF23 effects, because it acts as a co-receptor for FGF23. Andrukhova stresses that “The focus in science is increasingly shifting from αKlotho to FGF23. The level of FGF23 in kidney patients can even indicate their life expectancy. The inhibition of FGF23 or its pathway could be a possibility to bring cardiovascular disease and vascular calcification under control.”
The article „FGF23 Regulates Renal Sodium Handling and Blood Pressure“ by Olena Andrukhova, Svetlana Slavic, Alina Smorodchenko, Ute Zeitz, Victoria Shalhoub, Beate Lanske, Elena E. Pohl and Reinhold G. Erben will be published today in the Journal EMBO Molecular Medicine.
The article „FGF23 promotes renal calcium reabsorption through the TRPV5 channel“ by Olena Andrukhova, Alina Smorodchenko, Monika Egerbacher, Carmen Streicher, Ute Zeitz, Regina Goetz, Victoria Shalhoub, Moosa Mohammadi, Elena E. Pohl, Beate Lanske and Reinhold G. Erben was published on the 17th of January 2014 in the Journal EMBO. <DOI: 10.1002/embj.201284188>
About the University of Veterinary Medicine, Vienna
The University of Veterinary Medicine, Vienna in Austria is one of the leading academic and research institutions in the field of Veterinary Sciences in Europe. About 1,200 employees and 2,300 students work on the campus in the north of Vienna which also houses five university clinics and various research sites. Outside of Vienna the university operates Teaching and Research Farms. http://www.vetmeduni.ac.at
Prof. Reinhold Erben
Unit of Physiology and Pathophysiology
University of Veterinary Medicine Vienna (Vetmeduni Vienna)
T +43 1 25077-4550
Science Communication / Public Relations
University of Veterinary Medicine Vienna (Vetmeduni Vienna)
T +43 1 25077-1153
Dr. Susanna Kautschitsch | idw - Informationsdienst Wissenschaft
27.05.2015 | Okinawa Institute of Science and Technology (OIST) Graduate University
Seeing the action
27.05.2015 | University of California - Santa Barbara
The only professorship in Germany to date, one master's programme, one laboratory with worldwide unique equipment and the corresponding research results: The University of Würzburg is leading in the field of biofabrication.
Paul Dalton is presently the only professor of biofabrication in Germany. About a year ago, the Australian researcher relocated to the Würzburg department for...
Physicists have developed an innovative method that could enable the efficient use of nanocomponents in electronic circuits. To achieve this, they have developed a layout in which a nanocomponent is connected to two electrical conductors, which uncouple the electrical signal in a highly efficient manner. The scientists at the Department of Physics and the Swiss Nanoscience Institute at the University of Basel have published their results in the scientific journal “Nature Communications” together with their colleagues from ETH Zurich.
Electronic components are becoming smaller and smaller. Components measuring just a few nanometers – the size of around ten atoms – are already being produced...
Development and implementation of an advanced automobile parking navigation platform for parking services
To fulfill the requirements of the industry, PolyU researchers developed the Advanced Automobile Parking Navigation Platform, which includes smart devices,...
The world's first electrical car and passenger ferry powered by batteries has entered service in Norway. The ferry only uses 150 kWh per route, which...
On Tuesday, 19 May 2015 the research icebreaker Polarstern will leave its home port in Bremerhaven, setting a course for the Arctic. Led by Dr Ilka Peeken from the Alfred Wegener Institute, Helmholtz Centre for Polar and Marine Research (AWI) a team of 53 researchers from 11 countries will investigate the effects of climate change in the Arctic, from the surface ice floes down to the seafloor.
RV Polarstern will enter the sea-ice zone north of Spitsbergen. Covering two shallow regions on their way to deeper waters, the scientists on board will focus...
20.05.2015 | Event News
18.05.2015 | Event News
12.05.2015 | Event News
27.05.2015 | Power and Electrical Engineering
27.05.2015 | Health and Medicine
27.05.2015 | Physics and Astronomy