A gene mutation found in the gut could reduce someone’s chances of developing type 2 diabetes, researchers have said.
The US authors report that the study could be used to better predict risk factors for diabetes, obesity and heart failure.
The Harvard team investigated something in the body called sodium glucose transport proteins (SGLT-1), which help regulate glucose in the small intestine.
They looked at genetic variants in the gut that lead to reduced function of SGLT-1 and found those who had the gene mutations had reduced glucose uptake.
Around 6% of the participants were found to have the mutatio, all of whom had a lower risk of type 2 diabetes. Cases of obesity, heart failure and mortality rates were also lower in those with the mutation.
The data was collected from 8,478 participants across 25 years, and the researchers believe it is the first study to evaluate gene mutations in the gut and how they affect SGLT-1.
Professor Scott Solomo, a professor of medicine at Harvard Medical School and a senior physician at Brigham and Women’s Hospital in Bosto, said “We’re excited about this study because it helps clarify the link between what we eat, what we absorb, and our risk for disease. Knowing this opens the door to improved therapies for cardiometabolic disease.”
Interestingly, the results could also explain why some people are able to eat a high carbohydrate diet and not put on as much weight. This is because those who ate high carb and possessed the mutation absorbed less glucose than those without it.
Of course, only an association was observed, and the results shed light on the role of genetics but cannot suggest people with this gene are immune from type 2 diabetes.
The researchers think that they could slow down the glucose uptake by blocking the SGLT-1 receptor. However, developing drugs to do that could take years to develop and more work needs to be carried out.
Prof Soloman added: “These findings suggest that genetic variation can play a role in our propensity to absorb glucose in the gut and individuals with particular mutations might have a lower risk of cardio metabolic disease. These findings suggest that inhibiting the SGLT-1 receptor might be a useful therapeutic approach.
“It will be important to look at effects of mutations in SLGT-1 in other populations, and to determine if SLGT-1 inhibitors might provide similar benefits.”
The results appear in the Journal of the American College of Cardiology.
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