A recent study reveals that age plays an important role in intermittent fasting results. The researchers at the Technical University of Munich (TUM), the LMU Munich and Helmholtz Munich hospital discovered that chronic intermittent fasting interrupted the development of beta cell producers in insulin in young mice. The results raise concerns about potential risks for humans, especially adolescents.
“It is known that intermittent fasting has benefits, including the impulse of metabolism and helping with weight loss and heart disease. But so far, its possible side effects were not well understood,” says Alexander Bartelt, the other teacher of Kröner Fresenius and president of the nutritional translation Medicine in Tum. In a recently published study, the team shows that intermittent fasting during adolescence could have long -term negative effects on metabolism.
Fasting improves metabolism in major mice, but not in young people
The researchers studied three groups of mice: adolescent animals, adults and older. The mice remained without food for a day and were normally fed in two days. After ten weeks, insulin sensitivity improved in adult and older mice, which means that its metabolism responded better to insulin produced by the pancreas. This is key to regulating blood sugar levels and preventing conditions such as type 2 diabetes.
However, teenage mice showed a worrying decrease in beta cell function, the insulin producing cells of the pancreas. Insufficient insulin production is linked to diabetes and interrupted metabolism. “In general, it is believed that the intermittent fasting benefits beta cells, so we were surprised to discover that young mice produced less insulin after extended fasting,” explains Leonardo Matta by Helmholtz Munich, one of the main authors of the study of the study .
Defective beta cells resemble patients with type 1 diabetes
The researchers used the last sequence of individual cells to discover the cause of the deterioration of beta cells. When examining the pancreas plan, the team discovered that beta cells in younger mice could not mature correctly. “At some point, the cells of the teenage mice stopped developing and produced less insulin,” says Peter Weber of Helmholtz Munich, also a lead author. The major mice, whose beta cells were already mature before fasting began, were not affected.
The team compared its mouse findings with human tissue data. They found that patients with type 1 diabetes, where beta cells are destroyed by an autoimmune response, showed similar signs of deteriorated cell maturation. This suggests that mouse study findings could also be relevant to humans. “Our study confirms that intermittent fasting is beneficial for adults, but could come with risks for children and adolescents,” says Stephan Herzig, professor of Tum and director of the Helmholtz Munich Institute of Diabetes and Cancer. “The next step is to deepen the molecular mechanisms underlying these observations. If we better understand how to promote the healthy development of beta cells, it will open new ways to treat diabetes restoring insulin production.”