from the Watching-What-You-Eat dept.
With nearly 10% of the world's population affected, type 2 diabetes is a major public health issue. An excessively sedentary lifestyle and a too-caloric diet encourage the development of this metabolic disease by altering the functioning of pancreatic cells and making blood sugar regulation less effective. However, fat, which is often cited as the ideal culprit, could be rehabilitated. Indeed, fat does not necessarily aggravate the disease and could even play a protective role: by studying insulin-producing pancreatic beta cells, scientists from the University of Geneva (UNIGE), Switzerland, have shown that these cells suffered less from excess sugar when they had previously been 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 Diabetologia, highlight an unexpected biological mechanism that could be used as a lever to delay the onset of type 2 diabetes.
Type 2 diabetes results from a dysfunction of pancreatic beta cells, which are 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 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, while the culpability 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 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.
[...] By further analyzing the cellular changes at stake, the research team realised that fat droplets were not static reserves, but were the site of a dynamic cycle of storage and mobilization. And thanks to these released fat molecules, beta cells adapt to the excess sugar and maintain a near-normal insulin secretion.
Lucie Oberhauser, Cecilia Jiménez-Sánchez, Jesper Grud Skat Madsen, et al. Glucolipotoxicity promotes the capacity of the glycerolipid/NEFA cycle supporting the secretory response of pancreatic beta cells, Diabetologia (DOI: 10.1007/s00125-021-05633-x)