Study Shows Decreased Mitochondrial Creatine Kinase Impairs Muscle Function Independently of Insulin in Type 2 Diabetes

Published in Science Translational Medicine

Researchers from Karolinska Institutet have uncovered a key factor contributing to impaired muscle energy production in individuals with type 2 diabetes. The study reveals that people with type 2 diabetes have reduced levels of creatine kinase, a protein responsible for metabolizing and converting creatine in muscle cells. This deficiency hampers mitochondrial function—the "powerhouses" of cells—leading to decreased energy production and increased cellular stress.

Creatine, a compound naturally produced by the body and found in foods like meat and fish, is critical for muscle function. Although creatine supplementation is popular for enhancing exercise performance, elevated blood creatine levels have been linked to an increased risk of type 2 diabetes. This study demonstrates that the reduced levels of creatine kinase observed in people with type 2 diabetes lead to impaired creatine metabolism, explaining the accumulation of creatine in their bloodstream.

“Our findings suggest that impaired creatine metabolism is a consequence of type 2 diabetes rather than a cause,” says Professor Anna Krook from the Department of Physiology and Pharmacology at Karolinska Institutet, the study’s principal investigator.

Moreover, the study shows that reduced creatine kinase levels directly affect mitochondrial function, independent of creatine availability. This discovery highlights the multifaceted role of creatine kinase in cellular energy production.

“This is consistent with the poorer energy metabolism seen in people with type 2 diabetes,” adds Professor Krook. “In the future, regulating creatine kinase could be explored as a potential treatment strategy for metabolic diseases like obesity and diabetes.”

The next phase of research will focus on identifying the molecular mechanisms linking creatine kinase levels to mitochondrial function.

Source: https://www.eurekalert.org/news-releases/1060405