The effect of sleep impairments on obesity-related microRNAs

Abstract

Introduction: Short sleep duration has been identified as a significant risk factor for obesity, yet the underlying molecular mechanisms remain unclear. This study investigates the expression of key circadian genes and related miRNAs involved in metabolic regulation, including Bmal1, miR-9, miR-17-5p, Ppara, miR-24-3p, Per2, miR-130a, and Pparg, in participants with varying sleep durations and body weights. Methods: Participants were divided into four groups based on sleep duration and weight status: Group A (normal sleepers, normal weight; n = 24), Group B (normal sleepers, obese; n = 24), Group C (short sleepers, normal weight; n = 24), and Group D (short sleepers, obese; n = 24). Blood samples were collected, and the expression levels of interest mRNAs and miRNAs were evaluated using qRT-PCR. One-way ANOVA and Tukey post-hoc analyses were performed to assess differences between groups. Results: The expression of Bmal1 and Pparg genes showed significant differences between groups (p < 0.001), with upregulation observed primarily in short sleepers, particularly in Groups C and D. Per2 expression was significantly decreased across all groups with abnormal sleep or weight status (p < 0.05), especially in Groups C and D. miR-17-5p and miR-130a were significantly downregulated in Groups C and D (p < 0.001), while miR-24-3p was significantly upregulated in these groups (p < 0.001). No significant changes were observed for miR-9 and Ppara expression across the groups. Conclusion: The dysregulation of Bmal1, Per2, and Pparg, along with their regulatory miRNAs, underscores the importance of circadian regulation in maintaining metabolic health. miR-24-3p upregulates during short sleep, inhibiting Per2 expression, while miR-130a downregulates, leading to reduced inhibition of Pparg, promoting adipogenesis. Additionally, Per2 acts as an inhibitor of Pparg, further influencing fat accumulation. miR-24-3p and miR-130a emerge as key modulators of these pathways. These genes provide potential therapeutic targets for mitigating the impact of short sleep duration on obesity and related metabolic disorders.