Partial Pancreatectomized Diabetic Rats Present with Altered Skeletal Muscle Contractility and Phenotype

People with long‐term type 1 diabetes (T1D) often have skeletal muscle complications (myopathy). Studies on T1D and skeletal muscle are limited and often use animal models that induce T1D with streptozotocin, which causes myopathy independent of hyperglycemia. The objective of this study was to characterize diabetic myopathy in a partially pancreatectomized (Px) model of T1D. Male Sprague Dawley rats were randomly assigned to either Px or sham surgery groups. Following 8 weeks of diabetes, Px had significantly lower body and gastrocnemius‐plantaris‐soleus (GPS) mass compared to shams (349.1±21 vs 484.4±10 g; 1.8±0.1 vs 3.3±0.1 g/g mass, respectively). In situ muscle stimulation of the GPS revealed a lower maximal force (Fmax) in Px vs shams (12.1±1.3N vs 22.6±1.8N, p<0.01), but was similar when corrected for muscle mass. During a 2 minute fatigue protocol, stimulating the GPS at ~50% Fmax (3 sec stimulation, 3 sec rest), Px had a lower rate of decline in force than shams (52.8±3.4% vs 69.7±7.2%, p<0.05). Histochemical analysis of the GPS demonstrates that Px have reduced myofiber area irrespective of fiber type and an increase in type IIa fiber number. These data suggest that sustained hyperglycemia/hypoinsulinemia induced by Px is characterized by changes in the skeletal muscle phenotype that result in compromised function. This research was funded by NSERC.

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