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People who are steamed live longer? It’s not groundless at all.

People

People who are steamed live longer? It’s not groundless at all.

People

There is a saying, “obesity paradox.”

It is commonly known as the myth that a fat person lives longer than a skinny person.

However, this is a phenomenon that the medical community is also paying attention to.

In the short or medium term, the prognosis of obese people can be better than thin people.

Of course, in the long run, there is a greater risk of heart disease in obese people.

Studies have shown that an “obesity paradox” that is hard to accept intuitively may actually be possible.

The point is that fatty tissue sends a “risk signal” to the heart, reducing the damage to the heart tissue caused by obesity.

It has been confirmed that mitochondria are also involved in this signal system.

The results of the study conducted by scientists at the University of Texas’ Southwestern Medical Center were published in the online edition of the journal Cell Metabolism on the 20th (local time.

Metabolic stress builds up due to obesity, causing a gradual abnormality in the function of fatty tissue, which causes mitochondria, a cell power plant, to crumple to die.

Eventually, these fatty tissues lose the ability to accumulate excess calories in food and harm other organizations with the “lipotoxicity” effect.

Some institutions, including the heart, are known to take preemptive defenses.

However, it has not been known until now how these institutions detect abnormalities in the functioning of local tissues.

The UT Southwestern team first manipulated the genes of the mouse model to induce deformation and dysfunction of mitochondria.안전놀이터

After feeding these mice high-fat foods and gaining weight, extracellular vesicles, which were full of dying mitochondrial fragments, began to be released from fat cells.

Some of the mitochondrial fragments we move on to the heart by oxidative stress caused the blood flow.

When driven into this condition, the cell produces harmful free radicals.

However, heart cells have created large amounts of antioxidant molecules in response to these stresses.

The effect of this backlash was very powerful.

When extracellular vesicles containing mitochondrial fragments were injected into mice and they had a heart attack, the tissue damage was significantly smaller than that of mice that did not.

The study also confirmed that fat cells in obese patients also emit these extracellular packages.

This suggests that the ‘risk alert’ effect of fat cells identified in mouse experiments can also be seen in humans.

However, the research team stressed that the “paradox of obesity” does not work to the end.

In the end, obese people can suffer from various diseases at once due to accumulated damage of fat toxicity in organs such as the heart.

Scientists involved in the study are interested in practical applications.

If the defense mechanism of the heart can be artificially induced, it can lead to the development of a treatment that alleviates the negative consequences of obesity.

If successful, the treatment can also help prevent heart damage in skinny people.

“A deeper understanding of the risk signaling system in fatty tissues will help improve heart health, whether you are obese or not,” said Dr. Claire Crew, the first author of the paper.

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