Lack of an immune-responsive protein in the intestine can lead to metabolic disorders

Scientists in the United States have experimentally found that

The lack of an immune-responsive protein in the intestinal epithelium can lead to metabolic syndrome and

This increases the risk of obesity, metabolic disorder diabetes and cardiovascular disease.

The use of drugs to regulate intestinal flora can help prevent the development of metabolic syndrome.

Metabolic syndrome is a common pathological condition that involves the metabolic dysfunction of multiple substances such as fats, sugars and proteins.

Typical symptoms include abdominal obesity, hyperglycemia and hypertension.

The immune protein TLR4 may be associated with this condition, but the exact mechanism of its work is not clear.

Johns researchers at Hopkins Medical Center found that even under a normal diet, mice lacking TLR4 in the intestinal epithelium would rapidly gain weight and observe metabolic disorders, such as increased body fat and insulin.

Such as increased body fat and insulin resistance; when fed a high-fat diet, their weight and body fat increases were significantly higher than those of normal mice.

The lack of this protein in intestinal epithelial cells alone can cause metabolic syndrome, but not in other somatic cells.

The lack of TLR4 in intestinal epithelial cells affects intestinal bacteria, and the use of antibiotics to regulate intestinal flora prevents metabolic syndrome in experimental mice.

The lack of this protein in intestinal epithelial cells also suppressed some metabolic genes in experimental mice.

The ability to control intestinal flora with antibiotics or to activate the body's own metabolic genes with specific substances is expected to be used for the prevention and treatment of metabolic syndrome.