Type 2 diabetes has long been associated with excessive sugar and fat intake. However, scientists at the University of Geneva have discovered that fat can help the pancreas adapt to excess sugar, thus slowing the onset of diabetes.
Often touted as a perfect culprit, very bad fat can be rehabilitated. And for good reason. By analyzing the cellular mechanisms at work, scientists at the University of Geneva (UNIGE) have discovered how a fat storage and release cycle enables cells to adapt to excess sugar.
To read these results in, shed light on an unexpected biological mechanism that may act as a liver to delay the onset of type 2 diabetes.
unclear role of fat
In the 1970s, fat was pointed out and the concept of lipotoxicity emerged: exposure of beta cells to fat would be the source of their deterioration. More recently, excess sugar has also been blamed for damaging beta cells and promoting the development of type 2 diabetes.
However, while the guilt of sugar is not in doubt today, the role of fat in beta cell dysfunction remains unclear. What cellular mechanisms are involved?
“To answer this important question, we studied the adaptation of human and murine beta cells to excess sugar and/or fat”, explains Professor Pierre Machler from the Diabetes Center of the UNIGE Faculty of Medicine, who directed this work. Did.
restore insulin secretion
To separate the effects 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 both excess sugar and excess fat, they store fat in the form of droplets in anticipation of a less good time”, explains researcher Lucie Oberhauser of UNIGE’s Faculty of Medicine and first author of this work. Huh. “However, surprisingly, we have shown that this fat store, instead of aggravating the situation, on the contrary, it is possible to restore insulin secretion close to normal.
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By more precisely analyzing the cellular modifications at work, the research team realized that fat droplets do not have stable stores. They were the site of a dynamic cycle of storage and removal.
The release of fat is not really a problem as long as the body uses it as a source of energy.
It is thanks to the released fat molecules that beta cells adapt to the excess of sugar and maintain insulin secretion close to normal. “This release of fat is not really a problem as long as the body uses it as a source of energy”, says Pierre Machler.
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