Scientists have found out what connection between obesity and inflammatory processes

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Employees of the Faculty of Fundamental Medicine of the MV Lomonosov Moscow State University, the National Medical Research Center for Cardiology and the Endocrinology Research Center analyzed the prospects for anti-inflammatory therapy of type 2 diabetes, the main cause of which is obesity, RIA Novosti reported . The work was carried out within the framework of a  project supported by a grant from the Russian Science Foundation, and its results were published in the journal  International Journal of Endocrinology .

Obesity is the main risk factor for the development of type 2 diabetes. This disease is now observed in 30% of the inhabitants of the Earth. Its development burdens the course of cardiovascular diseases and increases the likelihood of oncological diseases in patients, therefore, scientists note that the social significance of the study of the problem of the development of type 2 diabetes is extremely high.

There are two types of diabetes – a disease associated with high blood glucose. Normally, liver cells synthesize the hormone insulin in response to an increase in blood glucose levels. Insulin promotes glucose uptake by cells. If this hormone is not released (usually due to damage to the liver cells), a person’s blood glucose rises and then he develops type 1 diabetes. And if insulin is released in too much, but not perceived by tissues (such a condition is called insulin resistance), blood glucose will also be increased – diabetes of the second type will develop.

Russian scientists have studied patients who are obese. Such people often have an inflammatory process. Excess nutrients are stored in the form of lipids inside the cells of adipose tissue. As a result, these cells gradually increase in volume and become so large that oxygen-supplied oxygen is not sufficient to ensure their entire volume. Since aerobic respiration is the main source of energy in the cell, it eventually begins to be missed. Nevertheless, the flow of nutrients entering the cell does not decrease (and sometimes increases), and it can no longer cope with it. As a result, the stress of the endoplasmic reticulum, organelles, is involved in the processes of protein, fat and carbohydrate processing. When the fat cell lacks energy,

This abnormal behavior of the cell leads to inflammation: the body tries to repair the damage. Adipose tissue secretes anti-inflammatory cytokines – substances that attract immune cells that promote inflammation. Cytokines, migrating to adipose tissue, do not kill its cells, but themselves begin to secrete mediators of inflammation.

Thus, they maintain a high inflammatory background first of the tissue, and then of the body. This process can be called a latent inflammation. As a result, a person with obesity has an increased inflammatory background, but not so strong as to cause a fever and other symptoms of an acute inflammatory process.

Ученые выяснили, что участник воспалительного процесса протеинкиназа IKK (фермент, способный модифицировать белки) действует на рецепторы мембраны жировой клетки, которые активируются инсулином, и блокирует проведение сигнала от инсулина. В результате клетка “не чувствует”, что на нее действует инсулин.

“To stop the inflammatory process, it is necessary to learn how to control protein kinase IKK,” explains Yury Stafeev, a postgraduate student at the Department of Biochemistry and Molecular Medicine at the Faculty of Basic Medicine of the Moscow State University named after MV Lomonosov, “IKK is in the body always, in all organs and Without protein kinase IKK, the body can not protect itself against many infections, but its constant activation under conditions that do not require it can cause including the type 2 diabetes mellitus.The main protein kinase IKK, responsible for the development of insulin resistance, is IKKbeta, however, it can not be removed and blocked, otherwise it will destroy immunity,

The current state of research on the role of inflammatory protein kinase IKK in the pathogenesis of type 2 diabetes mellitus is reviewed. In the article hypotheses about possible prospects of development of anti-inflammatory therapy of type 2 diabetes mellitus, including in the direction of personalized medical influence, are expressed.

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