New Breakthrough Study Targets the Cause of Muscle Loss in Diabetes Patients

The new study sheds light on what causes muscle atrophy and could offer insights into how to prevent it.
Donovan Alexander

Across the planet, 422 million people suffer from diabetes. For the uninitiated diabetes is a chronic metabolic disease characterized by elevated levels of blood glucose, or what is known as blood sugar. This can lead to serious health issues like damage to the heart, blood vessels, eyes, kidneys, and nerves.


However, diabetes is also associated with a loss of muscle mass. Led by Professor Wataru Ogawa of the Kobe University Graduate School of Medicine, researchers may have gained further insight into what causes this phenomenon of muscle atrophy when blood sugar levels are elevated.

Diabetes and Muscle Loss

Aside from looking good, muscle mass plays a vital role in your overall health, protecting your organs, stabilizing your metabolism, and even extending your life. Even more so, the proper amount of muscle mass can help you age gracefully, allowing your body to maintain certain physical tasks.

Understanding the correlation between diabetes and muscle loss could help inform those who live with diabetes stay healthier.  According to the Kobe study, the proteins WWP1 and KLF15 are what causes muscle atrophy.

Diabetes mellitus is a disease caused by insufficient action of the hormone insulin. Think of insulin as the regulator of your blood sugar levels, making sure your body’s glucose level is not too high.


However, insulin plays another role, promoting the growth and proliferation of cells. It was originally believed that this lack of growth is what led to a decline in skeletal muscle mass. Professor Ogawa begs to differ.

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A major insight into this phenomenon, Professor Ogawa discovered that among diabetic mice muscle atrophy was attributed to the protein mentioned above KLF15. Elevated blood sugar levels slow down the degradation of the KLF15 protein. The protein WWP1 also expedites this process contributing to the slow degradation of KLF15.

This study is the first for those studying diabetes and its relation to muscle loss. Though there is currently no viable medical treatments that prevent muscle loss, this new insight could lay the framework for future drugs.

As mentioned in the study, "If we develop a drug that strengthens the function of WWP1 or weakens the function of KLF15, it would lead to a groundbreaking new treatment".

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