Mitochondrial open reading frame of the 12S rRNA-c (MOTS-c) is a mitochondrial-derived peptide that attenuates weight gain and hyperinsulinemia when administered to high fat-fed mice. MOTS-c is therefore a potential regulator of metabolic homeostasis under conditions of high-energy supply. However, the effect of insulin resistance and obesity on plasma MOTS-c concentration in humans is unknown. To gain insight into MOTS-c regulation, we measured plasma MOTS-c concentration and analyzed its relationship with insulin sensitivity surrogates, in lean and obese humans (n=10 per group). Obese individuals had impaired insulin sensitivity as indicated by low Matsuda and high Homeostatic Model Assessment (HOMA) indexes. Although plasma MOTS-c concentration was similar in lean and obese individuals (0.48±0.16 and 0.52±0.15 ng/mL; p=0.60), it was correlated with HOMA (r=0.53; p<0.05) and Matsuda index (r=−0.46; p<0.05). Notably, when the groups were analyzed separately, the associations remained only in lean individuals. We conclude that plasma MOTS-c concentration is unaltered in human obesity. However, MOTS-c associates positively with insulin resistance mostly in lean individuals, indicating that plasma MOTS-c concentration depends on the metabolic status in this population. Such dependence seems altered when obesity settles. The implications of plasma MOTS-c for human metabolic homeostasis deserve future examination.
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LRC and RF-V contributed equally.
Contributors JEG, LRC and JLS conceived the study. All authors participated in data analysis and interpretation. JEG, LRC and RF-V wrote the manuscript, which was approved by all the co-authors.
Funding Fondo Nacional de Desarrollo Científico y Tecnológico (Fondecyt; #1130217, #1170117 and #1150416) funded the study.
Competing interests None declared.
Patient consent Obtained.
Ethics approval The Ethical Board at Pontificia Universidad Católica de Chile approved the protocol (Reference number: 12-201, 2012).
Provenance and peer review Not commissioned; externally peer reviewed.