New research from the University of Utah suggests that the microbiome plays a pivotal role in the development of insulin-producing cells during infancy, potentially influencing long-term metabolic health and diabetes risk. The study in mice could offer new avenues for preventing Type 1 diabetes and even restoring pancreatic function in adults.
The research highlights the critical window of early life, revealing that exposure to broad-spectrum antibiotics during a 10-day period shortly after birth leads to poorer metabolic health later in life. Mice treated with antibiotics during this crucial developmental phase developed fewer insulin-producing beta cells in the pancreas, which are vital for regulating blood sugar levels. These mice also showed elevated blood sugar levels and reduced insulin production as adults.
“This finding was both shocking and concerning,” said June Round, a professor of pathology at University of Utah Health and senior author of the study. “It underscores the importance of the microbiota during this brief but essential period of development.”
Through further investigation, the team identified specific microbes that positively impacted insulin production. Among these was the relatively understudied fungus Candida dubliniensis, which, though uncommon in healthy adults, appears to be more prevalent in infants. Not only did this fungus increase the presence of insulin-producing tissue, but it also reduced the risk of Type 1 diabetes in male mice genetically predisposed to the condition. Mice exposed to C. dubliniensis developed diabetes in less than 15% of cases, compared to a 90% incidence in those given a neutral microbe.
Moreover, the study found that exposure to C. dubliniensis helped regenerate insulin-producing cells in adult mice whose pancreatic cells had been destroyed. This regeneration of cells is highly unusual, as beta cells typically do not grow in adulthood.
“If these results translate to humans, microbe-derived treatments could eventually help restore pancreatic function in those with diabetes,” said Jennifer Hill, first author of the study and a former postdoctoral scientist at the University of Utah. However, Hill noted that similar treatments in mice have not yet been successful in humans.
The beneficial effects of C. dubliniensis appear to be linked to its influence on the immune system. Previous studies showed that immune cells in the pancreas can encourage the development of insulin-producing cells. Mice without a microbiome had fewer immune cells in the pancreas and poorer metabolic health. However, when these mice were exposed to C. dubliniensis early in life, both their immune cell levels and metabolic function returned to normal. The fungus promoted growth in the pancreas only in mice with macrophages, indicating that the immune system plays a key role in the fungus’s beneficial effects.
The researchers believe other microbes may offer similar benefits, and their findings open the door to further exploration of how gut microbes impact early-life development and long-term metabolic health. Understanding this relationship could eventually lead to preventive strategies against Type 1 diabetes by harnessing the power of specific microbes.
“Our hope is to identify these important microbes and provide them to infants, potentially preventing the onset of diabetes entirely,” Round concluded.
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