Fat cells protect against diabetes mellitus
Last reviewed: 23.04.2024
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Diabetes mellitus type 2 is associated with the inability of fat cells to convert glucose into fat. While these cells react to the presence of carbohydrates in the blood, diabetes has no chance.
Over the past decade, scientists have learned about fat cells many new things: several research groups have discovered that adipocytes control the level of sugar and insulin. To do this, fat cells need to feel sugar in the blood, and if the transport of carbohydrates into the cells is broken, then they stop doing their work. This affects the condition of the whole body: tissues stop reacting to insulin, the blood glucose level rises, which in sum leads directly to diabetes.
A new study of scientists from the deaconess Beth Israel Medical Center at Harvard University (USA) shows how glucose includes fat cells. In an article published in the journal Nature, the authors describe the ChREBP-β gene, which encodes a protein that helps convert glucose to fatty acids. First, scientists checked the activity of this gene in healthy people. In those who did not know the problems with the assimilation of glucose, ChREBP-β worked actively. But, more importantly, the same gene also acted in those who had obesity without diabetes. Usually, diabetes is considered to be an inevitable companion of obesity, but this is not quite true: many people are overweight, but they are spared from severe diabetic problems with metabolism.
When we eat, events develop as follows. The incoming glucose is transported to the interior of the cell with the help of GLUT4 carrier molecules. These molecules are not only in adipose tissue, but also in the heart and muscles. When glucose is inside a fat cell, it includes the ChREBP-β gene, which encodes a transcription factor that affects the metabolic profile of the cell. As a result, the fat cell transports excess glucose into fat. If the number of glucose carriers in mice increased, they developed obesity, but there was no diabetes. If the level of glucose carriers fell, then the animals developed diabetes, but the normal body weight remained.
Diabetes of the second type is due to insensitivity of tissues to insulin. Insensitivity of fat cells to insulin means that GLUT4 does not react to the hormone and does not transfer glucose into the cell. The inability of fatty tissue to absorb glucose has long been considered one of the earliest signs of diabetes, but the mechanism of fat cells was only revealed right now. To activate the metabolic regulator ChREBP-β, you need a total trifle: only 10% of the incoming glucose. It turns out that the diabetes protects us literally from the fatty "airbag": the cells keep the glucose level in check, turning it into fatty acids. However, if this transformation intensively goes on in the liver fat cells, then there is another danger: the liver does not tolerate excess fat, which can lead to fat metamorphosis.
However, in any case, these results force a new assessment of the role of adipose tissue in our body. Obviously, obesity does not necessarily lead to diabetes, when it comes to type 2 diabetes; perhaps overweight is the body's way of protecting itself from diabetes. The authors of the paper believe that the disease can be defeated if one learns to activate the same ChREBP-β gene in fat cells. Although the question remains open, because of what all the same the cells become insensitive to insulin.
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