Muscle Molecular Pathway Explains Effectiveness of Type 2 Diabetes Interventions

For the first time researchers at the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) demonstrated in the mouse model that skeletal muscle cells, cultured in a low-calorie environment refrain from differentiating an energy-demanding process by which cells mature and specialize. The study was published in the Developmental Cell.

The discovery is also important for the diabetes researchers. Calorie-restriction diets, as well as the drug metformin, are both treatments for type 2 diabetes and a related condition, metabolic syndrome. The treatments help the body better regulate the body’s uptake of sugar, a nutrient that people with these conditions have trouble regulating. But the exact mechanism of action of these treatments is unclear.

Vittorio Sartorelli of the research team expressed his hope that this discovery will be helpful to find out the better molecular understanding of the lifestyle and drug interventions function in the treatment of type 2 diabetes and metabolic syndrome.

In their project, Sartorelli and his colleagues set out to investigate the relationship between skeletal muscle cells, calorie restriction, metformin and SIRT1 in mice. They cultured skeletal muscle cells from normal mice in a low-glucose environment to restrict calories and treated others with metformin. As expected, in each intervention the cells failed to mature and form myocytes, cells that are the building blocks of muscle fibers. What was new in their findings, however, was that metformin and calorie restriction both promoted the activation of two proteins, AMPK and Nampt, which in turn made SIRT1 more active and capable of suppressing cell differentiation.

Source: NIH NEWS

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