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Study reveals surprising benefits of fat in type 2 diabetes

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Fat may help the pancreas adapt to increased sugar, hence delaying diabetes onset, according to researchers.

Type 2 diabetes affects almost 10% of the world’s population, making it a major public health concern. A sedentary lifestyle and a high-calorie diet promote the development of this metabolic disorder by changing pancreatic cell function and making blood sugar management less effective.

Fat could be used as a lever to delay the onset of type 2 diabetes

Fat, which is frequently cited as the ideal culprit, could, however, be rehabilitated. Indeed, fat does not always aggravate the condition and may even serve a protective role: researchers from the University of Geneva (UNIGE), Switzerland, discovered that when insulin-producing pancreatic beta cells were previously exposed to fat, they suffered less from excess sugar.

By looking at the cell mechanisms at work, the researchers found out how a cycle of fat storage and mobilization helps cells adapt to too much sugar.

These findings, which were published in the journal Diabetologia, shed light on a previously unknown molecular process that may be employed to delay the onset of type 2 diabetes.

Type 2 diabetes is caused by a malfunction of pancreatic beta cells, which are in charge of insulin secretion. This disrupts blood sugar homeostasis and can result in significant heart, eye, and renal issues.

‘Fat’ was singled out in the 1970s, and the concept of lipotoxicity was born: beta cells would deteriorate if they were exposed to fat.

More recently, high sugar has been linked to beta cell damage and the development of type 2 diabetes. While the role of sugar in beta cell dysfunction is no longer debatable, the involvement of fat in beta cell dysfunction remains a mystery. What cellular mechanisms are at play?

“To answer this key question, we studied how human and murine beta cells adapt to an excess of sugar and/or fat,” said Pierre Maechler, lead author of this work.

To distinguish the effect of fat from that of sugar, the scientists subjected beta cells to an excess of sugar, fat, and then a mixture of the two. Sugar’s toxicity was first demonstrated when beta cells exposed to high sugar levels released significantly less insulin than normal.

“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”, added Lucie Oberhauser, the first author 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.”

By examining the cellular processes involved in greater detail, the research team discovered that fat droplets were not static reserves, but rather were the location of a dynamic cycle of storage and mobilization. And, as a result of the fat molecules produced, beta cells adjust to the excess sugar and maintain near-normal insulin output.

“This release of fat is not really a problem as long as the body uses it as a source of energy”, added 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.”

Researchers are now trying to figure out how this released fat triggers insulin secretion in the hopes of finding a technique to prevent diabetes from developing.

Source: 10.1007/s00125-021-05633-x 

Image Credit: © UNIGE – laboratoire Maechler

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