Gut bacteria may play a role in diabetes

One type of bacteria found in the gut may contribute to the development of type 2 diabetes, while another may protect against the disease, according to the first results of an ongoing prospective study led by Cedars-Sinai researchers.

The study, published in the peer-reviewed journal Diabetesfound people with higher levels of a bacterium called coprococo tended to have higher insulin sensitivity, while those whose microbiomes had higher levels of the bacteria flavonifractor tended to have lower insulin sensitivity.

For years, researchers have sought to understand why people develop diabetes by studying the composition of the microbiome, which is a collection of microorganisms including fungi, bacteria, and viruses that live in the digestive tract. The microbiome is thought to be affected by medications and diet. Studies have also found that people who don’t process insulin properly have lower levels of a certain type of bacteria that produces a type of fatty acid called butyrate.

Mark Goodarzi, MD, PhDDirector of Cedars-Sinai’s Endocrine Genetics Laboratory, he is leading an ongoing study that is tracking and looking at people at risk for diabetes to learn whether those with lower levels of these bacteria develop the disease.

“The big question we hope to address is: did the differences in the microbiome cause the diabetes, or did the diabetes cause the differences in the microbiome?” said Goodarzi, lead author of the study and principal investigator of the multicenter study called the Microbiome and Insulin Longitudinal Evaluation Study (MILES).

Researchers involved in MILES have been collecting data from participating black and non-Hispanic white adults ages 40 to 80 since 2018. A previous cohort study of the MILES trial found that cesarean delivery is associated with an increased risk of developing prediabetes and diabetes.

For the most recent study to emerge from this ongoing trial, the researchers analyzed data from 352 people without known diabetes who were recruited from Wake Forest Baptist Health System in Winston-Salem, North Carolina.

Study participants were required to attend three clinic visits and collect stool samples prior to the visits. The researchers analyzed the data collected at the first visit. They performed genetic sequencing on the stool samples, for example, to study the participants’ microbiomes and look specifically for bacteria that previous studies had found to be associated with insulin resistance. Each participant also filled out a diet questionnaire and took an oral glucose tolerance test, which was used to determine the ability to process glucose.

The researchers found that 28 people had oral glucose tolerance results that met criteria for diabetes. They also found that 135 people had prediabetesa condition in which a person’s blood sugar levels are higher than normal but not high enough to meet the definition of diabetes.

The research team looked at associations between 36 butyrate-producing bacteria found in stool samples and a person’s ability to maintain normal insulin levels. They controlled for factors that could also contribute to a person’s risk of diabetes, such as age, gender, body mass index and race. coprococo and related bacteria formed a network of bacteria with beneficial effects on insulin sensitivity. Despite being a producer of butyrate, flavonifractor was associated with insulin resistance; previous work by others has found higher levels of flavonifractor in the feces of people with diabetes.

The researchers continue to study samples from patients who participated in this study to learn how insulin production and microbiome composition change over time. They also plan to study how diet can affect the bacterial balance of the microbiome.

Goodarzi stressed, however, that it’s too soon to know how people can change their microbiome to reduce diabetes risk.

“As far as the idea of ​​taking probiotics, that would really be kind of experimental,” said Goodarzi, who is also the Eris M. field chair in diabetes research at Cedars-Sinai. “We need more research to identify the specific bacteria that we need to modulate to prevent or treat diabetes, but that will probably come in the next five to 10 years.”

Jinrui Cui, a biostatistician at the Goodarzi Laboratory at Cedars-Sinai, was the first author of the study.

Funding: The study was funded by the National Institutes of Health (R01-DK109588), the National Institute of Diabetes and Digestive and Kidney Diseases (P30-DK063491), the National Center for the Advancement of Translational Sciences (grants UL1TR001420, UL1TR001881) .

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