Pancreatic beta cell underneath digital microscopy. The white circles seen in the centre of the cell correspond to fats storage droplets. Credit: © UNIGE – laboratoire Maechler
Scientists at UNIGE have found that fats might assist the pancreas adapt to extra sugar, thereby slowing down the onset of diabetes.
With practically 10% of the world’s inhabitants affected, sort 2 diabetes is a serious public health difficulty. An excessively sedentary life-style and a too-caloric weight loss program encourage the event of this metabolic illness by altering the functioning of pancreatic cells and making blood sugar regulation much less efficient. However, fats, which is usually cited as the perfect perpetrator, may very well be rehabilitated. Indeed, fats doesn’t essentially worsen the illness and will even play a protecting position: by finding out insulin-producing pancreatic beta cells, scientists from the University of Geneva (UNIGE), Switzerland, have proven that these cells suffered much less from extra sugar once they had beforehand been uncovered to fats. By investigating the mobile mechanisms at work, the researchers found how a cycle of fats storage and mobilization permits cells to adapt to extra sugar. These outcomes, printed in the journal Diabetologia, spotlight an sudden organic mechanism that may very well be used as a lever to delay the onset of sort 2 diabetes.
Type 2 diabetes outcomes from a dysfunction of pancreatic beta cells, that are answerable for insulin secretion. This impairs the regulation of blood sugar ranges and might result in severe coronary heart, eye, and kidney problems. In the 1970s, fats was singled out and the idea of lipotoxicity emerged: publicity of beta cells to fats would trigger their deterioration. More just lately, extra sugar has additionally been blamed for damaging beta cells and selling the event of sort 2 diabetes. However, whereas the culpability of sugar is not in doubt, the position of fats in beta cell dysfunction stays ambiguous. What are the mobile mechanisms concerned? “To answer this key question, we studied how human and murine beta cells adapt to an excess of sugar and/or fat”, explains Pierre Maechler, a Professor in the Department of Cell Physiology and Metabolism and in the Diabetes Centre of the UNIGE Faculty of Medicine, who led this work.
When fats lends a hand to beta cells
In order to distinguish the impact of fats from that of sugar, the scientists uncovered beta cells to an extra of sugar, of fats, after which to a mixture of the 2. The toxicity of sugar was first confirmed: beta cells uncovered to high sugar ranges secreted a lot much less insulin than regular. “When cells are exposed to both too much sugar and too much fat, they store the 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 on the UNIGE Faculty of Medicine, and first writer of this work. “Surprisingly, we have shown that this stock of fat, instead of worsening the situation, allows insulin secretion to be restored to near-normal levels. The adaptation of beta cells to certain fats would thus contribute to maintain normal blood sugar levels.”
The essential use of fats
By additional analyzing the mobile modifications at stake, the analysis workforce realised that fats droplets weren’t static reserves, however have been the positioning of a dynamic cycle of storage and mobilization. And thanks to those launched fats molecules, beta cells adapt to the surplus sugar and preserve a near-normal insulin secretion. “This release of fat is not really a problem as long as the body uses it as a source of energy”, provides Pierre Maechler. “To avoid developing diabetes, it is important to give this beneficial cycle a chance to be active, for example by maintaining regular physical activity.”
Scientists at the moment are attempting to find out the mechanism by which this launched fats stimulates insulin secretion, in the hope of discovering a method to delay the onset of diabetes.
Reference: “Glucolipotoxicity generates high capability 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