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A new scientific study conducted by researchers from the University of Reading suggests that high fat diets increase the risk of heart disease by triggering a protein that causes destructive growth in the heart.

The team of researchers conducted a study in which they observed the effects of high fat diets on heart cells and oxidative stress levels in mice. The team observed that cells from mice fed on high fat foods had twice the level of oxidative stress compared to mice fed on healthy diets. As a result, the mice on a high fat diet experienced cardiac hypertrophy, causing their heart cells to be 1.8 times bigger than normal.

“Our research shows one way in which a high fat diet can cause damage to the muscle cells that make up our hearts,” stated Dr. Sunbal Naureen Bhatti, the lead author in the study.

The lead author added that there appears to be a switch in the cells of mice on high fat diets which over-activity in a protein called Nox2 which is usually harmless. Once the protein becomes overactive, it leads to oxidative damage while triggering destructive hypetrophy. He also added that researchers are still trying to understand how diet causes the switch in Nox2 protein. However, the existing research as per the latest study highlights the mechanism through which a high fat diet increases the risk of heart disease and heart damage.

How researchers narrowed down the Nox2 protein as the culprit involved

Scientists wanted to find out whether the Nox2 protein was indeed responsible for cardiac stress and damage in subjects who consume high fat foods. They bred some mice that were genetically engineered such that Nox2 protein was eliminated. These mice were also studied alongside the mice with the protein while being fed the same high fat diet.

The fascinating results showed that the mice with no Nox2 protein had very little or no raised oxidative stress levels compared to their counterparts. The researchers also treated the high oxidative stress mice with three pipeline treatments that are designed to reduce the production of reactive oxygen species (ROS) associated with Nox2. All three developmental treatments yielded promising results in reducing the heart damaging effects of ROS.