New Delhi: Scientists have identified a protein that may make it harder for muscles to respond to insulin, potentially contributing to insulin resistance. The findings could help researchers explore new treatment targets for type 2 diabetes.
The study, published in Nature Communications on 19 October, found that the relatively little-known protein Miro1 accumulated in the skeletal muscles of people with type 2 diabetes. The researchers discovered that putting these patients through regular exercise reduced the levels of Miro1 in their muscles. In animal experiments, removing the protein improved insulin sensitivity.
Type 2 diabetes develops when the body becomes resistant to insulin, the hormone that regulates blood sugar, and the pancreas can no longer produce enough insulin to compensate. As senior author John P. Kirwan told ScienceDaily: “Insulin resistance in muscle is at the heart of Type 2 diabetes, and its molecular causes have remained frustratingly unclear.”
How Miro1 affects insulin resistance
Miro1 is typically found on the outer membrane of mitochondria, the structures that produce energy in cells. It helps regulate mitochondrial activity, but the new study points to its role in type 2 diabetes.
The researchers examined muscle tissue from people with and without type 2 diabetes, and conducted additional experiments using lab-grown cells and animals.
They found elevated Miro1 levels in the muscle tissue of people with both type 2 diabetes and obesity, but not in people with obesity alone.
Further experiments suggested that the protein’s accumulation may interfere with insulin signalling. A protein called AKT, which helps regulate glucose uptake by cells, was unable to interact properly with Miro1.
When the researchers reduced or removed Miro1 from mouse muscle tissue, glucose uptake and mitochondrial function improved.
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What exercise changed
The researchers also conducted a randomised trial involving participants whose muscle tissue had been examined.
They were divided into two groups: one received standard medical care, while the other followed a 12-week aerobic exercise programme. The programme involved supervised treadmill walking or jogging for an hour a day, five days a week.
Participants in the exercise group showed improvements in insulin sensitivity and mitochondrial function, alongside a reduction in Miro1 levels in their muscles.
Kirwan said Miro1 could become “a new therapeutic target” and that the findings could help explain why exercise helps in managing diabetes.
Could Miro1 become a target for treatment?
Although removing Miro1 from mouse muscle tissue and human muscle samples in laboratory experiments improved insulin sensitivity, it remains to be seen whether targeting the protein in people would be safe or effective.
The exercise trial also found that lower Miro1 levels occurred alongside improvements in insulin sensitivity and cellular function. However, the findings do not establish that the reduction in Miro1 directly caused these improvements.
The researchers plan to investigate the protein further and explore whether it could be targeted in future diabetes treatments.
“Ultimately, we are looking for cures, and we hope these recent findings could be part of the solution,” Kirwan said.
(Edited by Maryam Hassan)