Effects of aerobic exercise training on C1q tumor necrosis factor α-related protein isoform 5 (myonectin): Association with insulin resistance and mitochondrial DNA density in women

Abstract

Context: The C1q TNF α-related protein (C1QTNF) families exhibit a C-terminal complement factor C1q globular domain similar to that of TNF. However, their clinical implications are largely unknown. We recently found that the C1q TNF α-related protein isoform 5 (C1QTNF5 or myonectin) level was increased in insulin-resistant rodents and mitochondrial DNA (mtDNA)-depleted myocytes. Objective: We aimed to determine the effects of aerobic exercise training on C1QTNF5 level and its association with insulin resistance and mtDNA density in young and old healthy women. Design and Setting: Fourteen healthy young women aged 22.5 ± 2.7 yr and 14 healthy older womenaged 60.3 ± 5.2 yr performed aerobic exercise at 60-80%of maximal oxygen consumption (VO 2max) over three 1-h sessions perweekfor 10 wk. Insulin resistance was assessed by homeostasis model assessment of insulin resistance and adiponectin concentration. Serum C1QTNF5 level was estimated by immunoblotting. The mtDNA/28S rRNA ratio was used to determine mtDNA density. Results: VO 2max increased significantly after the exercise training from 33.1 ± 6.2 to 35.3 ± 5.3 ml/kg·min in younger women and from 23.2 ± 3.1 to 27.2 ± 4.8 ml/kg·min in older women (P < 0.05). The C1QTNF5 level and homeostasis model assessment of insulin resistance decreased significantly after exercise training and were correlated positively (r = 0.462; P < 0.01). There were negative correlations between the changes in C1QTNF5 level and the changes in VO 2max, mtDNA density, and adiponectin level (r = -0.495, -0.672, and -0.569, respectively; all P < 0.01). Conclusion: These findings suggest a physiological function for C1QTNF5 (myonectin) in linking insulin resistance with quantitative changes in mtDNA. Further research exploring the role of C1QTNF5 in the development of insulin resistance is warranted. Copyright © 2012 by The Endocrine Society.