Fatty liver disease also affects the brain

Fatty liver disease also affects the brain

Non-alcoholic fatty liver disease (or Nash), an accumulation of fat in the liver, leads to reduced oxygen in the brain and inflammation of brain tissue. However, the partial invalidation of a protein would protect against the disease and the brain dysfunction associated with it.

Non-alcoholic fatty liver disease (Nash), also called “fatty liver disease”, is a severe form of fatty liver disease. Independent of consumptionalcoholalcoholthis metabolic syndromemetabolic syndrome — which affects more than 80% of people suffering fromobesityobesity morbid — includes at least two of the following factors: high rate of triglyceridestriglycerides (fats), low level of “good” cholesterol, arterial pressurearterial pressure high and high blood sugar.

Building on previous work, researchers at the Roger Williams Institute of Hepatology (affiliated with the king of college of London and the University of Lausanne) have highlighted the pathophysiology of the liver-brain axis, in a new study on the link between Nash and brain dysfunction. The results published in Journal of Hepatology show that the accumulation of fat in the liverliver results in decreased oxygen to the brain and inflammation of brain tissue, which can lead to serious brain disease.

Dieted mice were divided into two groups. Half of the mice consumed a diet with a caloric intake consisting of 55% fat, while the calorie intake of the other half of the mice contained no more than 10% fat. This research was carried out in collaboration with Inserm and the University of Poitiers.

Oxygen deficiency and brain dysfunction

The researchers compared the effect of these two diets on the liver and the brain after 16 weeks. All the mice subjected to the most caloric consumption were obese and affected by a Nash, a insulin resistanceinsulin resistance and brain dysfunction. To explain the latter, the researchers measured tissue oxygenation, cerebrovascular reactivity, as well as the volumevolume cerebral blood.

Indeed, we know that the brain depends on the continuous supply of oxygen and substratessubstrates energy for its operation. ” The cerebral vasculature is well suited for this purpose, and additional mechanisms have evolved to tightly regulate blood flow, matching oxygen supply to demand. Therefore, any changes in these mechanisms or in the structure of the cerebral vasculature can have adverse effects on brain tissue oxygenation and overall physiology. write the authors of the study.

In fact, the brains of mice subjected to the fattest diet suffered from a lack of oxygen: Nash affects the number and thickness of cerebral blood vessels, which then bring less oxygen to the tissues. In addition, the inflammation of the brain caused by the disease can induce greater oxygen consumption. These mice were also more anxious and showed signs of depression.

MCT1 as a potential therapeutic target to prevent or treat Nash

None of the above-mentioned problems was found in the mice subjected to the low-calorie diet. However, researchers have spotted a potential therapeutic target against Nash. The MCT1 protein (for Monocarboxylate Transporter 1) is specialized in the transport of energy substrates used by various cells to function. Presenting lower than usual levels of this protein to mice consuming the same high-fat diet protects them from Nash and related brain dysfunction.

While waiting for a targeted treatment, a suitable diet and physical activity can improve biomarkers in case of Nash or benign metabolic steatosis.

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