Medical expert of the article
New publications
Fat cells protect against diabetes mellitus
Last reviewed: 01.07.2025
All iLive content is medically reviewed or fact checked to ensure as much factual accuracy as possible.
We have strict sourcing guidelines and only link to reputable media sites, academic research institutions and, whenever possible, medically peer reviewed studies. Note that the numbers in parentheses ([1], [2], etc.) are clickable links to these studies.
If you feel that any of our content is inaccurate, out-of-date, or otherwise questionable, please select it and press Ctrl + Enter.
Type 2 diabetes is caused by the inability of fat cells to convert glucose into fat. As long as these cells respond to the presence of carbohydrates in the blood, diabetes has no chance.
Over the past ten years, scientists have learned a lot about fat cells: several research groups have discovered that adipocytes control sugar and insulin levels. To do this, fat cells need to sense sugar in the blood, and if the transport of carbohydrates into the cells is disrupted, they stop doing their job. This affects the condition of the entire body: tissues stop responding to insulin, blood glucose levels rise, which ultimately leads directly to diabetes.
A new study by scientists from Beth Israel Deaconess Medical Center at Harvard University (USA) shows how glucose turns on fat cells. In an article published in the journal Nature, the authors describe the ChREBP-β gene, which codes for a protein that helps convert glucose into fatty acids. The scientists first checked the activity of this gene in healthy people. In those who had no problems with glucose absorption, ChREBP-β was active. But, more importantly, this same gene was also active in those who were obese without diabetes. Diabetes is usually considered an inevitable companion of obesity, but this is not entirely true: many people are overweight, but at the same time they are free from severe diabetic metabolic problems.
When we eat, this is what happens. Glucose entering the body is transported into the cell using GLUT4 transporter molecules. These molecules are found not only in adipose tissue, but also in the heart and muscles. When glucose is inside a fat cell, it turns on the ChREBP-β gene, which codes for a transcription factor that affects the cell’s metabolic profile. As a result, the fat cell converts excess glucose into fat. If the number of glucose transporters increased in mice, they developed obesity, but did not develop diabetes. If the level of glucose transporters decreased, the animals developed diabetes, but maintained normal body weight.
Type 2 diabetes occurs due to tissue insensitivity to insulin. Insensitivity of fat cells to insulin means that GLUT4 does not respond to the hormone and does not transport glucose into the cell. The inability of fat tissue to absorb glucose has long been considered one of the earliest signs of diabetes, but the mechanism by which fat cells work has only now been revealed. To activate the metabolic regulator ChREBP-β, mere trifles are needed: only 10% of the glucose entering the body. It turns out that we are literally protected from diabetes by a fat “safety cushion”: the cells keep the glucose level in check, converting it into fatty acids. However, if this conversion is intensive in liver fat cells, then another danger arises: the liver does not tolerate excess fat well, which can lead to fatty metamorphosis.
However, in any case, these results force us to re-evaluate the role of adipose tissue in our body. Apparently, obesity does not necessarily lead to diabetes, if we are talking about type 2 diabetes; perhaps excess weight is the body's way of protecting itself from diabetes. The authors of the work believe that the disease can be defeated if we learn to activate this very ChREBP-β gene in fat cells. Although the question of why the cells become insensitive to insulin remains open.
[