A high-fat diet may over-activate the activity of destructive heart disease proteins

A high-fat diet may over-activate the activity of destructive heart disease proteins.  In a research report published in the international journal “Biochemical and Biophysical Research Communications”, scientists from the University of Reading in the United Kingdom and other institutions found through research that eating a high-fat diet may activate reactions in the heart, leading to destructive Growth and increased risk of heart attack.

In this study, the researchers analyzed the effect of a high-fat diet in mice on the oxidative stress level of the heart cells of the body. The results found that the oxidative stress level of the heart cells in the mouse body doubled, and the heart The size of the cells increased by 1.8 times, which may be attributed to cardiac hypertrophy associated with heart attacks.

Researcher Sunbal Naureen Bhatti said that a high-fat diet can cause damage to the cardiomyocytes that make up the heart; when mice eat a high-fat diet, it induces a normally harmless protein, Nox2, to become over-activated. It seems that this conversion occurs. At the cellular level; however, researchers currently do not know how the Nox2 protein causes oxidative damage and destructive hypertrophy of cells.

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Researchers said that we may just “touch” the surface of protein Nox2’s response to diet, but current research clearly shows that a high-fat diet seems to cause major damage to the heart. The researchers focused on the Nox2 protein, which they believe is related to increased oxidative stress in the heart; in addition, the activity of Nox2 in mice fed a high-fat diet doubled, which would lead to the production of similar levels of reactive oxygen species , And reactive oxygen species is a kind of free radicals related to the pathological damage of the body.

In order to analyze whether Nox2 is involved in the process of heart damage, the researchers compared the results of studies conducted in mice that specifically knocked out Nox2. Knockout of Nox2 will block the activation of the protein at the cellular level; researchers It was found that after feeding these mice a high-fat diet, their bodies did not show an increase in the level of oxidative stress.

In addition, the researchers also used three experimental therapies that can reduce the production of reactive oxygen species related to Nox2, and found that all therapies can reduce the production and effects of reactive oxygen species in the hearts of injured mice. Of the calories in mice fed a high-fat diet, 45% came from fat, 20% came from protein, and 35% came from carbohydrates.

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