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Type 2 diabetes is a major public health problem, with almost 10% of the world’s population affected. An excessively sedentary lifestyle and an excessively caloric diet favor the development of this metabolic disease by altering the functioning of the pancreatic cells and making the regulation of blood sugar less effective.
However, fat, which is often seen as the big culprit, might be reused to fight disease. In fact, this not necessarily it aggravates the ailment and might even play a protective role.
By studying insulin-producing pancreatic beta cells, scientists from the
Geneva University
(UNIGE), Switzerland, have shown that these cells suffered less excess sugar when they had been previously exposed to fat.
By investigating the cellular mechanisms at work, the researchers discovered how a cycle of fat storage and mobilization allows cells to adapt to excess sugar.
These results, published in the journal
«Diabetology»Describe an unexpected biological mechanism that might be used as a mechanism to delay the onset of type 2 diabetes.
Type 2 diabetes results from a dysfunction of the pancreatic beta cells, which are responsible for the secretion of insulin. This affects the regulation of blood sugar levels and can lead to serious complications in the heart, eyes, and kidneys.
In the 1970s, fat was highlighted and the concept of lipotoxicity: Exposure of beta cells to fat would cause their deterioration. More recently, excess sugar has also been blamed for damaging beta cells and promoting the development of type 2 diabetes.
However, although the negative role of sugar is no longer in doubt, the role of fat in beta cell dysfunction remains ambiguous. What are the cellular mechanisms involved?
“To answer this key question, we studied how human and murine beta cells adapt to excess sugar and / or fat,” explains Pierre Maechler, professor of the Department of Cellular Physiology and Metabolism and the Diabetes Center of the
UNIGE Faculty of Medicine, who directed this work.
To differentiate the effect of fat from sugar, the scientists exposed beta cells to excess sugar, excess fat, and then a combination of both. Sugar toxicity was confirmed for the first time: beta cells exposed to high levels of sugar secreted much less insulin than normal.
“When cells are exposed to too much sugar and too much fat, they store fat in the form of droplets in anticipation of less prosperous times, explains Lucie Oberhauser, a researcher in the Department of Cell Physiology and Metabolism at the Faculty.
UNIGE»Of Medicine, and first author of this work.
“Surprisingly, we have shown that this stock of fat, instead of making the situation worse, allows the insulin secretion is restored to near normal levels. The adaptation of beta cells to certain fats would thus help maintain normal blood sugar levels. ‘
The essential use of fat
By further analyzing the cellular changes at play, the research team realized that the fat droplets were not static reserves, but the site of a dynamic storage and mobilization cycle. And thanks to these released fat molecules, beta cells adapt to excess sugar and maintain almost normal insulin secretion.
“This release of fat is not really a problem as long as the body uses it as an energy source,” adds Pierre Maechler. “To avoid developing diabetes, it is important to give this beneficial cycle the opportunity to be active, for example by maintaining regular physical activity.”
Scientists are now trying to determine the mechanism by which this released fat stimulates insulin secretion, hoping to discover a way to delay the onset of diabetes.
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