A study published in Nature Communications linked high Miro1 levels in skeletal muscle to insulin resistance in type 2 diabetes and found that removing the protein improved insulin response in preclinical models; exercise was also linked to lower Miro1 levels in people with the disease.
Miro1 is a protein on the outer covering of mitochondria, which help cells make energy. The researchers examined muscle from humans and mice, as well as cells and animal models, and found that Miro1 built up in muscle affected by obesity and diabetes. Their results suggest that problems in insulin signaling involving the molecule AKT may help explain this buildup.
In mice and cell models, removing Miro1 only from muscle helped insulin work better and improved how mitochondria functioned. The study also included a randomized 12-week trial involving 24 people with type 2 diabetes. Participants assigned to exercise training had lower muscle Miro1 levels, responded better to insulin and had greater mitochondrial capacity to use oxygen to produce energy.
The human findings link exercise with changes in Miro1, but do not show that lowering the protein caused all the improvements observed. Because the direct removal experiments were in preclinical models and the human trial was small, Miro1 remains a research lead, not an available diabetes treatment.