The effect of acute thermotherapy on type 2 diabetic skeletal muscle gene expression




Galvan, Felicite
Griffin, Makalah
Newmire, Daniel E.
Sparks, Jean
Omoruyi, Felix
Gonzales, Xavier F.

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Type 2 Diabetes (T2D) is among the chronic diseases increasingly affecting the human population. This disease potentially results in the interruption in the production of insulin and/or the dysregulation of insulin signaling which may facilitate skeletal muscle mass loss. Exercise is a known stimulus of muscle mass gain or retention. During exercise, skeletal muscle temperature increases (~39°C), however, it is unknown if this in- crease in temperature alone may influence the transcriptome related to skeletal muscle growth. PURPOSE: The aim of this study was to identify if thermotherapy (heat stress mimetic) may influence genes related to muscle growth and atrophy. METHODS: Human Skeletal Muscle Myoblasts (HSMM) and Diabetic Type 2 Human Skeletal Myoblast (D-HSMM) were purchased from Lonza Inc. (Lonza Inc, Walkersville, MS). HSMM and D-HSMM were cultured until reaching a confluency of 70-80%. Both D-HSMM and HSMM were exposed to an acute bout of thermotherapy (40°C) in experimental well plates. All well plates were treated at a one-time for 30 min. Control well plates were kept at 37°C. The experimental well plates were treated for 24 hours following an initial 48-hour incubation at 37°C. Post-thermotherapy treatment consisted of cell observation, cell viability, and preparation for gene expression. To perform gene expres- sion, RNA was isolated from D-HSMM and HSMM, converted to cDNA, and a real-time polymerase chain reaction (qRT-PCR) was used to assess Activin-A Receptor Type 2B (ACVR2B) and b-catenin (CTNNB1) to a housekeeping gene (GAPDH). RESULTS: Following gene expression analysis, it was determined that ACVR2B yielded the highest change (~1-fold) in D-HSMM. For HSMM, CTNNB1 yielded the highest change (~1-fold). CONCLUSION: These preliminary results suggest that ACVR2B expression, which is the prime myostatin receptor during thermotherapy could potentially facilitate greater muscle atrophy in T2D skeletal muscle. However, the thermotherapy-induced increase in CTNNB1 expression in the normal, healthy skeletal muscle cells may suggest greater androgen receptor (AR) activation and a role in skeletal muscle growth due to the reported actions of b-catenin on AR activation.



type ii diabetic muscle cells, heat-stress, muscle hypertrophy, thermotherapy, gene expression



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