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New Insights Into How Microbiome Helps Cause Type 2 Diabetes
- June 26, 2024
- Dennis Thompson HealthDay Reporter
A person's gut microbiome appears to increase their risk of developing type 2 diabetes, researchers claim.
Specific strains of gut microbes are more commonly found in people with type 2 diabetes, and these strains seem to heighten the risk of developing the metabolic disorder, they say.
"We believe that changes in the gut microbiome cause type 2 diabetes,"said researcher Dr. Daniel Wang, an assistant professor of nutrition at the Harvard T.H. Chan School of Public Health in Boston.
If that's true, "we can find a way to change the microbiome and reduce type 2 diabetes risk,"Wang added in a Harvard news release. "The microbiome is amenable to intervention -- meaning you can change your microbiome, for example, with dietary changes, probiotics or fecal transplants."
Every healthy gut contains trillions of bacteria, fungi, parasites and viruses, all of which constitute the gut microbiome.
The microbiome plays a number of key roles in a person's health. It stimulates the immune system, helps digest potentially toxic foods and produces key vitamins, enzymes and amino acids.
Research has previously linked changes in the gut microbiome to the development of type 2 diabetes, researchers said in background notes.
However, these prior studies have not been large enough to say in which direction the relationship runs -- does the microbiome contribute to diabetes, or does diabetes alter the microbiome?
In the new study, "we asked two questions. One is, 'What are the roles of species and strains that make up the gut microbiome in type 2 diabetes?' The other question is, 'What are these microbes doing?'" Wang said.
Researchers analyzed genetic data on the gut microbiomes of more than 8,100 people from around the world, including healthy people, people with prediabetes and folks who had developed type 2 diabetes.
The team found that certain microbe strains had functions that could be linked to type 2 diabetes risk.
For example, a strain of Prevotella copri -- a common gut microbe that produces large amounts of branched-chain amino acids (BCAAs) -- was more commonly found in diabetes patients.
People with chronically high blood levels of BCAAs have a higher risk of obesity and type 2 diabetes, earlier studies have shown.
The researchers also found evidence that bacteriophages"viruses that infect bacteria"could be driving some of these changes in gut bacteria.
"Our findings related to bacteriophages were very surprising," Wang said. "This could mean that the virus infects the bacteria and changes its function in a way that increases or decreases type 2 diabetes risk, but more work is needed to understand this connection."
The research team then focused on a smaller set of samples from patients newly diagnosed with type 2 diabetes, to look at microbiomes that hadn't yet been affected by either long-term elevated blood sugar levels or the drugs used to treat diabetes.
They found results similar to what they saw in the larger sample, suggesting that the gut microbiome differences contribute to diabetes, rather than the other way around.
However, Wang said more research is needed to prove this relationship more firmly, including studies that look at the link over an extended period and focus on the specific functions of different microbe strains.
The new study was published June 25 in the journal Nature Medicine.
"A benefit and a challenge of the human microbiome is that it is highly personalized," said researcher Curtis Huttenhower, a professor of computational biology and bioinformatics at the Harvard T.H. Chan School of Public Health.
"The fact that we each have highly distinct microbial communities and microbial genetics means that very large population studies are needed to find consistent patterns,"Huttenhower added. "But once we do, individual microbiomes have the potential to be reshaped to help reduce disease risk."
More information
The National Institutes of Health has more about the microbiome.
SOURCE: Harvard University, news release, June 25, 2024
