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Scientists at UNIGE have found that fat can help the pancreas adapt to excess sugar, thereby slowing the onset of diabetes
.
Type 2 diabetes is a major public health problem, affecting nearly 10% of the global population
.
An excessively sedentary life>
.
However, fat, which is often considered the ideal culprit, can be remodeled
.
In fact, fat does not necessarily aggravate the disease, and may even play a protective role: by studying insulin-producing pancreatic beta cells, scientists at the University of Geneva (UNIGE) in Switzerland found that these cells were exposed to excessive sugar when previously exposed to fat.
less impact
.
By studying the cellular mechanisms at work, the researchers discovered how the cycle of fat storage and mobilization allows cells to adapt to excess sugar
.
These findings, published in the journal Diabetes, highlight an unexpected biological mechanism that could serve as a lever to delay the onset of type 2 diabetes
.
Type 2 diabetes is caused by dysfunction of the pancreatic beta cells responsible for insulin secretion
.
This impairs the regulation of blood sugar levels and can lead to serious heart, eye and kidney complications
.
In the 1970s, fat was singled out and the concept of lipotoxicity emerged: exposure of cells to fat causes them to deteriorate
.
More recently, excess sugar has also been blamed for damaging beta cells and promoting the development of type 2 diabetes
.
However, while the culpability of sugar has been unquestioned, the role of fat in cellular dysfunction remains unclear
.
What are the cellular mechanisms involved? "To answer this key question, we investigated how human and mouse beta cells adapt to excess sugar and/or fat," explains Pierre Maechler, PhD student in Cell Physiology and the UNIGE Faculty of Medicine.
Professors in the Department of Metabolism and the Diabetes Center, led the work
.
When fat helps beta cells
To distinguish between the effects of fat and sugar, the scientists exposed cells to excess sugar and fat, and then combined the two
.
The toxicity of sugar was first demonstrated: cells exposed to high sugar levels secreted far less insulin than normal
.
"When cells are exposed to too much sugar and too much fat, they store fat droplets in the form of booms" as expected, explains Lucy Oberhauser, researcher at Cell Physiology and Metabolism at UNIGE School of Medicine, and first author of the work
.
"Surprisingly, we have shown that instead of worsening the situation, these fat reserves restore insulin secretion to near-normal levels
.
Cell adaptation to certain fats will help maintain normal blood sugar levels
.
" "
Basic uses of fat
By further analyzing the changes in the cells, the team realized that the fat droplet is not a static reserve, but the site of a dynamic cycle of storage and mobilization
.
Thanks to these released fat molecules, cells adapt to the excess sugar, maintaining near-normal insulin secretion
.
"As long as the body uses fat as a source of energy, the release of fat is not a big deal," adds Pierre Maechler
.
"To avoid developing diabetes, it is important to give this virtuous cycle a chance to be active, such as maintaining regular physical activity.
activity
.
" Scientists are now trying to determine the mechanism by which the released fat stimulates insulin secretion, hoping to discover a way to delay the onset of diabetes
.
Original search:
“Glucolipotoxicity generates high capacity of the glycerolipid – free fatty acid cycle supporting the secretory response of pancreatic ß-cells” 11 January 2022, Diabetologia .
DOI: 10.
1007/s00125-021-05633-x