Higher blood levels of indolepropionic acid may help to protect against type 2 diabetes, a new study has found.
The research team from the University of Eastern Finland in Kuopio believes the discovery helps increase our understanding of the important part played by gut bacteria in the relationship between diet, metabolism, and health.
While it is well-known that factors such as genes, lifestyle, and diet can influence the risk of developing type 2 diabetes, what is less clear is what happens at the molecular level to link these factors to the disease.
The new study uses metabolomics, a relatively new technology that allows scientists to quickly assess the metabolite profiles of people.
Metabolites are molecules that cells in the body – including gut bacteria – produce as byproducts of their activity.
Using ‘nontargeted metabolomics analysis’, the researchers assessed the metabolite profiles of 200 participants in the Finnish Diabetes Prevention Study who had impaired glucose tolerance and were overweight when the study began.
The participants fell into two groups. One group developed type 2 diabetes within five years, and the other group did not develop type 2 diabetes during the 15 years of follow-up.
When the researchers compared the metabolite profiles of the two groups, they found that what stood out was differences in levels of indolepropionic acid and certain lipid metabolites.
Further analysis suggested that having high blood levels of indolepropionic acid, a byproduct of gut bacteria that is increased by a fibre-rich diet, appeared to protect against developing type 2 diabetes.
The team confirmed the findings by looking at the link between indolepropionic acid and risk for type 2 diabetes in the data from two other studies: the Finnish metabolic syndrome in men study, and the Swedish Västerbotten intervention project. These also showed that indolepropionic acid appears to protect against type 2 diabetes.
The researchers believe that their study shows that it may be more feasible to use metabolite profiles rather than identifying the bacteria themselves (which is a more complex process) to look at links with diseases such as diabetes.
The study can be found here.