David E. Lee1, Jacob L. Brown1, Megan E. Rosa1, Lemuel A. Brown1, Richard A. Perry, Jr.1, Mats I. Nilsson2, Tyrone A. Washington1, James D. Fluckey2 & Nicholas P. Greene1

1University of Arkansas, Fayetteville, Arkansas; 2Texas A&M University, College Station, Texas

MicroRNAs are an emerging post-transcriptional modifier of protein expression. Some microRNAs are tissue specific including miRNA-1, -133, and -206, which are skeletal muscle specific. Skeletal muscle protein synthesis and metabolic health are vital in situations of atrophy and insulin resistance as seen with sarcopenic obesity and type II diabetes, respectively. PURPOSE: The purpose of this study was to investigate the changes in muscle specific microRNAs in healthy and diabetic rats and their responses to resistance exercise training (RE) METHODS: Zucker rats (16 healthy, 14 diabetic) were sedentary (sed, 8 healthy, 6 diabetic) subjected to a RE protocol (8 healthy, 8 diabetic) involving a high-volume, weighted squat-jump-like movement. After 4 progressive bouts, animals were euthanized and gastrocnemus muscles were removed and later processed for microRNA and mRNA gene targets, various protein contents and protein fractional synthetic rates (FSR). Data were analyzed by 2X2 ANOVA (phenotype [healthy vs diabetic] vs. exercise [sed vs. RE]), correlations were assessed using Pearson’s product moment, α = 0.05. RESULTS: miRNA-1 significantly increased in the diabetic condition ~4-fold (pp<0.05) compared to healthy sed. In healthy groups, no difference was seen with RE on miRNA-133a levels while in the diabetic phenotype miRNA-133a content in RE was 113% greater than sed (pp<0.05) compared to healthy sed. No significant differences were seen in levels of microRNA-206. miRNA-1 was negatively correlated with FSR in RE groups but not sed. miRNA-133b showed a negative correlation with mitochondrial FSR in healthy but not diabetic animals. CONCLUSION: Control of protein synthesis and mitochondrial health is under complex control involving many factors. The alteration of muscle specific microRNAs in diabetes and RE and the relationships to targeted mRNAs suggests that the control of protein expression by microRNAs is at least partially responsible for protein synthetic and metabolic dysfunctions. Further research into the direct mechanisms and microRNA targets is warranted.

The investigation was funded, in part, by the University of Arkansas, and the Sydney and J. L. Huffines Institute of Texas A&M University

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