Creatine kinase M2 (CKMT2) plays a key role in mitochondrial dysfunction in type 2 diabetes, affecting energy metabolism in skeletal muscle.
By Dr. Priyom Bose, Ph.D.Reviewed by Benedette Cuffari, M.Sc.Oct 10 2024 Discover how CKMT2 controls energy balance and mitochondrial health in skeletal muscles, revealing a new link between metabolism and type 2 diabetes management.
Creatine serves as an energy shuttle due to its ability to store and transport ATP across the cell membrane. Creatine metabolism is associated with various pathophysiological functions, including immune responses to macrophages. To rapidly hydrolyze ATP into adenosine diphosphate to phosphorylate creatine, CKMT2 functionally co-localizes with the adenine nucleotide translocator . Although some studies have indicated that CKMT2 is a vital regulator of mitochondrial respiration and oxidative phosphorylation in skeletal muscle, the functional role of CKMT2 in skeletal muscle metabolism in type 2 diabetes remains unclear.
Study findings Higher circulating fasting creatine levels were observed in plasma samples of men with type 2 diabetes and negatively correlated with the expression of the creatine transporter solute carrier family 6 member 8 in skeletal muscles. Reduced phosphocreatine levels were also observed, along with elevated intramuscular creatine content, both of which correlated with CKMT2 expression in skeletal muscles.
Mitochondria Muscle Type 2 Diabetes Adenosine Adenosine Triphosphate Adipose Biopsy Brain Cell Cell Membrane Creatine Diet Fasting Genes Glucose Insulin Insulin Resistance Intracellular Kinase Macrophage Medicine Membrane Metabolism Nitric Oxide
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