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Skeletal Muscle Mitochondrial Function in Goto‐Kakizaki Rat Model of Type 2 Diabetes

Type 2 diabetes (T2D) presents with significant comorbidities and reported exercise intolerance affecting over 30 million people in the US alone. Aerobic metabolism is the predominant pathway for fueling exercise and utilizing glucose, therefore mitochondrial oxidative phosphorylation (MOP) is important in diabetes and the future of diabetic interventions. However, studies in T2D have conflicting reports regarding the functional status of the mitochondrial pool suggesting deficits are an inherent cause of the disease but a comprehensive study has yet to be done. The Goto‐Kakizaki (GK) rat model of T2D was used to measure both mitochondrial function and density in vitro and in vivo over a broad range of metabolic challenges. Mitochondrial densities were similar in red (RG) and white gastrocnemius (WG) muscles of the GK rat (Cyt c oxidase, RG: 22.2 ± 1.6 versus 23.3 ± 1.7 μmol/min/g, WG: 10.8 ± 1.1 versus 12.1 ± 0.9 μmol/min/g; n=7–8). Mitochondria isolated from the muscles of GK rats and their Wistar controls showed no difference in mitochondrial respiration in vitro as measured by high resolution respirometry. Mitochondrial function in vivo, measured by 31Phosphorus magnetic resonance spectroscopy, was similar between GK and Wistar controls determined from phosphocreatine dynamics reaching similar exercise steady states at submaximal workloads with no difference in recovery time constant (72 ± 6 s GK vs. 71 ± 2 s Wistar). However, at exercise intensities beyond what can be sustained aerobically, the GK rat exhibited bioenergetic deficits suggesting something other than mitochondrial function is responsible at these workloads. The current work demonstrates normal mitochondrial function in a non‐obese non‐sedentary rat model of T2D in vitro and in vivo and no change in mitochondrial content. Taken together these results show when considering both density and function of mitochondria no deficit in MOP is present in the GK T2D rat model and may not be in T2D patients but these studies remain to be done.