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A weak heart due to metabolic change

 New Delhi,,Feb 12,(Fast Mail):-- The heart derives its energy primarily from fatty acids. However, if a metabolic shift to other energy sources takes place, this can result in congestive heart failure, scientists from the German Cancer Research Center (DKFZ) and Heidelberg University Hospital have now discovered. This underscores the role of metabolism in heart failure. In addition, these findings are relevant for the use of certain anticancer drugs.

 

Provided everything goes well, by the time a person turns 75, the heart will have pumped almost 180 million liters of blood through his or her body. To do so, it beats approximately 100,000 times a day, precisely and without any rest, in order to supply the body with oxygen and other vital substances down to its tiniest capillaries. However, up to three million people in Germany have a weary pump: They suffer from cardiac insufficiency, also called congestive heart failure, and hence from symptoms such as shortness of breath, buildup of excess watery fluid, and diminished exercise capacity. Eventually, the condition becomes life-threatening.

 

“It has been known for a while that congestive heart failure results in a change in metabolism,” said Andreas Fischer from the German Cancer Research Center (Deutsches Krebsforschungszentrum, DKFZ) in Heidelberg. While healthy hearts produce their energy to more than 75 percent from fatty acids, weak hearts switch to carbohydrates as the preferred energy source. However, this link also works the other way around. In collaboration with other colleagues at the Center and at Heidelberg University Hospital, Fischer has found out that a shift from the metabolism of fatty acids as energy source to carbohydrates causes congestive heart failure.

 

Fischer’s team identified a receptor molecule called Notch-1 as the biochemical key to this effect. The investigators had used a therapeutic antibody that acts primarily in the cells of blood vessel walls to inactivate Notch-1 in mice, thus blocking the downstream signaling pathway. The animals subsequently developed heart failure. In a further experiment, the researchers used a genetic trick and bred mice in whom they could specifically turn off the Notch-1 signaling pathway in endothelial cells, which line the interior surfaces of blood vessels. Again, the animals developed cardiac insufficiency within a few weeks.

 

“This obvious effect came as a surprise, even to us,” said Markus Jabs, who is the first author of the study. But he also has an explanation ready: “For nutrients to travel from the blood vessels into the heart muscle, they must be transported through the endothelial cells.” While the transport processes through the blood vessel wall have been studied relatively well, little is known to date about how they are controlled. The DKFZ researchers have now identified the Notch-1 receptor as a key player controlling the transport of fatty acids from the blood into cardiac muscle tissue.

 

“With Notch-1 inhibited, the heart has less fatty acids available and it must shift to glucose as an energy source,” Jabs said. As a result, another signaling pathway called mTOR is activated. This causes the heart muscle to grow, eventually leading to heart failure. In an experiment, blocking this signaling pathway could prevent the development of heart failure in the mice. A diet that was extremely low in carbohydrates had the same effect.

 

 

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