State of the microflora affects the risk of obesity and diabetes

The human intestine is lined with a layer of special cells that are interconnected by tight contacts. Normally, this structure acts as a filter.: it allows nutrients to enter the bloodstream and traps potentially dangerous compounds. Beneficial bacteria produce short-chain fatty acids (SCFAs), such as butyrate, which serve as the main source of energy for these cells and maintain the integrity of the barrier.

With dysbiosis, the number of bacteria producing butyrate decreases. This leads to a weakening of the connections between the cells and an increase in the permeability of the intestinal wall. In medicine, this condition is sometimes referred to as “increased epithelial permeability syndrome.” Through the gaps that form, fragments of the outer membranes of dead bacteria, such as lipopolysaccharides (LPS), begin to enter the bloodstream.

Lipopolysaccharides are potent endotoxins. When they enter the bloodstream from the intestines, they are recognized by immune cells as a signal of infection. This triggers a low-intensity systemic inflammatory response. Unlike the usual inflammation in case of injury, this process is hidden and affects all tissues of the body, including the liver and adipose tissue.

Prolonged exposure to pro-inflammatory proteins, such as cytokines, disrupts the functioning of insulin receptors. Cells stop responding effectively to this hormone, which leads to the development of insulin resistance, a key factor in the occurrence of type 2 diabetes. Thus, an imbalance in the intestines becomes the starting point for the disruption of blood sugar regulation and the accumulation of excess fat mass.

The intestinal microflora is actively involved in the processing of food components, converting them into chemical compounds that affect the cardiovascular system. When consuming foods rich in choline and carnitine (red meat, eggs), certain groups of bacteria produce trimethylamine (TMA). In the liver, this compound is oxidized, turning into TMAO — trimethylamine-N-oxide.

Studies confirm that high levels of TMAO in the blood contribute to damage to the inner lining of blood vessels and accelerate the formation of atherosclerotic plaques. Patients with obesity and diabetes often have an excess of bacteria responsible for the synthesis of TMA, which further increases the risk of heart attacks and strokes.

Correcting the composition of the microbiome is an effective tool for improving health indicators. The main method remains a diet high in fiber (dietary fiber). Fiber is not digested by the human body, but it serves as a breeding ground for bacteria that produce beneficial fatty acids. Increasing the proportion of vegetables, whole grains, and legumes in the diet helps strengthen the intestinal barrier and reduce systemic inflammation.

In addition to nutrition, the state of the microflora is influenced by physical activity, sleep quality and stress levels. Regular exercise increases the diversity of beneficial microorganisms, and adherence to circadian rhythms (sleep patterns) maintains the stability of their metabolic activity. In some cases, doctors are considering the use of probiotics and prebiotics, as well as more complex procedures such as fecal microbiota transplantation, to radically change the composition of the intestinal ecosystem.