Sugar consumption leads to obesity, destroying the normal intestinal microflora

(ORDO NEWS) — Experiments on mice have shown that a diet high in sugar dramatically changes the composition of the microflora.

This causes a drop in the number of leukocytes in the intestine, leading to the development of metabolic disorders and obesity.

It is no secret that a diet rich in fats and sugar leads to a host of disorders and even diseases, including obesity and diabetes.

But the point here is not only the excess intake of calories that the body does not have time to use and stores.

New animal studies have shown that such a diet affects the intestinal microflora, causing changes in many metabolic processes, which ultimately lead to the development of various disorders.

The group, led by Professor Ivaylo Ivanov, experimented with laboratory mice that were kept for four weeks on a diet enriched with fats and sugar, in the spirit of the “Western diet”.

As might be expected, by the end of this period, the animals were not only overweight, but also showed signs of other disorders, including glucose intolerance and insulin resistance. However, their microflora has also changed a lot.

The numbers of segmented filamentous bacteria , common inhabitants of the rodent intestines, have plummeted. But there are much more microbes, which should normally be few in number.

To find out how this affects the health of animals, biologists studied their Th17 lymphocytes. This is a special type of T-helpers, immune cells that play an important role in protecting the body from pathogenic bacteria.

They are active in the intestines, also preventing the absorption of unhealthy fats. Decreased amounts of Th17 are indicative of metabolic disorders and inflammation.

This is exactly what scientists found in mice overfed with fat and sugar. Experiments have shown that the main culprit for such changes is sugar.

This is most likely due to changes in the microflora and a decrease in the number of filamentous bacteria that stimulate the production of Th17.

Indeed, if the same mice were transferred to a “dietary” diet with a minimum amount of fat and sugar, but at the same time fed with the necessary microbes, the number of Th17 cells was restored in them, and signs of metabolic disorders disappeared.

But in rodents that did not receive beneficial mouse bacteria, all the problems persisted.

The work of Ivanov’s team could help treat similar disorders in humans. She has already shown that ideally this requires proper nutrition and bacterial probiotics.

True, segmented filamentous bacteria in the human intestinal microflora should not normally be: their role is probably played by some other species. Which ones, exactly, remains to be seen.


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