A recent research study indicates that individuals with type 2 diabetes exhibit decreased levels of a specific protein that is responsible for breaking down and converting creatine in their muscles. This reduction hampers the functioning of mitochondria, which are often referred to as the cell’s ‘powerhouses.’
A recent investigation from Karolinska Institutet, published in Science Translational Medicine, reveals that people diagnosed with type 2 diabetes have diminished levels of a protein that is vital for metabolizing and converting creatine in muscle tissues. This condition results in compromised functioning of the mitochondria, which are known as the ‘powerhouses’ of our cells.
Creatine is a natural substance produced by the body and is also found in certain foods like fish and meat. It is commonly used as a supplement to enhance exercise performance, as it enables muscles to perform better and endure longer before tiring out. However, despite the acknowledged benefits of creatine, earlier research has hinted at a potential association between elevated blood creatine levels and a heightened risk of developing type 2 diabetes, prompting inquiries about whether creatine supplementation could elevate that risk.
Recent findings from studies involving both humans and mice indicate that those with type 2 diabetes have lesser amounts of the protein known as creatine kinase, which plays a key role in the metabolism and conversion of creatine in muscle tissues.
“The decline in this protein leads to disrupted creatine metabolism within the muscles, potentially elucidating the reason why individuals with type 2 diabetes experience increased creatine levels in their bloodstream,” states Anna Krook, Professor at the Department of Physiology and Pharmacology at Karolinska Institutet and lead investigator of the study.
While scientists are still uncertain about the implications of elevated creatine levels in blood, it is known to affect various functions outside of cells.
“The results suggest that impaired creatine metabolism arises as a result of type 2 diabetes, rather than being a triggering factor for the disease,” Anna Krook adds.
The research further indicates that lower levels of creatine kinase are correlated not just with heightened blood creatine levels, but also lead to the dysfunction of mitochondria in muscle cells. Since mitochondria are responsible for converting nutrients into energy, their reduced efficiency due to lower creatine kinase levels results in diminished energy production and heightened cellular stress.
“This aligns well with the observation that individuals with type 2 diabetes often experience suboptimal energy metabolism. In the future, a potential approach could involve modulating creatine kinase as a means to treat metabolic disorders like obesity and diabetes,” Anna Krook suggests.
Another intriguing outcome of the study was the finding that alterations in creatine kinase levels influenced not only the structure of mitochondria but also their energy-producing capabilities, irrespective of the creatine levels present.
“This indicates that while the primary function of creatine kinase is to metabolize creatine, it also impacts mitochondrial functions in other significant ways,” explains David Rizo-Roca, the first author of the study.
“Our forthcoming objective is to unveil the molecular processes driving these outcomes,” he adds.
The study was a collaborative effort with Danderyd Hospital and Karolinska University Hospital Huddinge. Major funding sources include the European Association for the Study of Diabetes (EASD), the Knut and Alice Wallenberg Foundation, the Swedish Research Council for Health, Working Life and Welfare, the Diabetes Foundation, and the Novo Nordisk Foundation. The researchers assert that they hold no conflicting interests.
