Sleep deprivation induced fat accumulation in the visceral white adipose tissue by suppressing SIRT1/FOXO1/ATGL pathway activation.

IF 3.7 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Journal of physiology and biochemistry Pub Date : 2024-08-01 Epub Date: 2024-06-10 DOI:10.1007/s13105-024-01024-z
Wei Wang, Kun Liu, Huan Xu, Chongchong Zhang, Yifan Zhang, Mengnan Ding, Chen Xing, Xin Huang, Qing Wen, Chunfeng Lu, Lun Song
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Abstract

Sleep is critical for maintaining overall health. Insufficient sleep duration and poor sleep quality are associated with various physical and mental health risks and chronic diseases. To date, plenty of epidemiological research has shown that sleep disorders are associated with the risk of obesity, which is usually featured by the expansion of adipose tissue. However, the underlying mechanism of increased fat accumulation upon sleep disorders remains unclear. Here we demonstrated that sleep deprivation (SD) caused triglycerides (TG) accumulation in the visceral white adipose tissue (vWAT), accompanied by a remarkable decrease in the expression of adipose triglyceride lipase (ATGL) and other two rate-limiting lipolytic enzymes. Due to the key role of ATGL in initiating and controlling lipolysis, we focused on investigating the signaling pathway leading to attenuated ATGL expression in vWAT upon SD in the following study. We observed that ATGL downregulation resulted from the suppression of ATGL transcription, which was mediated by the reduction of the transcriptional factor FOXO1 and its upstream regulator SIRT1 expression in vWAT after SD. Furthermore, impairment of SIRT1/FOXO1/ATGL pathway activation and lipolysis induced by SIRT1 inhibitor EX527 in the 3 T3-L1 adipocytes were efficiently rescued by the SIRT1 activator resveratrol. Most notably, resveratrol administration in SD mice revitalized the SIRT1/FOXO1/ATGL pathway activation and lipid mobilization in vWAT. These findings suggest that targeting the SIRT1/FOXO1/ATGL pathway may offer a promising strategy to mitigate fat accumulation in vWAT and reduce obesity risk associated with sleep disorders.

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睡眠不足会抑制SIRT1/FOXO1/ATGL途径的激活,从而诱导内脏白色脂肪组织的脂肪堆积。
睡眠对保持整体健康至关重要。睡眠时间不足和睡眠质量差与各种身心健康风险和慢性疾病有关。迄今为止,大量流行病学研究表明,睡眠障碍与肥胖风险有关,而肥胖通常以脂肪组织扩张为特征。然而,睡眠障碍导致脂肪堆积增加的内在机制仍不清楚。在这里,我们证明了睡眠剥夺(SD)会导致甘油三酯(TG)在内脏白色脂肪组织(vWAT)中积累,并伴随着脂肪甘油三酯脂肪酶(ATGL)和其他两种限速脂肪分解酶表达的显著下降。鉴于 ATGL 在启动和控制脂肪分解中的关键作用,我们在接下来的研究中重点探讨了 SD 导致 vWAT 中 ATGL 表达减少的信号通路。我们观察到,ATGL的下调源于ATGL转录的抑制,而转录因子FOXO1及其上游调节因子SIRT1在SD后vWAT中的表达减少则介导了ATGL转录的抑制。此外,SIRT1抑制剂EX527诱导的SIRT1/FOXO1/ATGL通路激活和脂肪分解在3个T3-L1脂肪细胞中的损伤可被SIRT1激活剂白藜芦醇有效挽救。最值得注意的是,在SD小鼠体内施用白藜芦醇可恢复SIRT1/FOXO1/ATGL通路的活化和vWAT的脂质动员。这些研究结果表明,以 SIRT1/FOXO1/ATGL 通路为靶点可能是一种很有前景的策略,它可以缓解 vWAT 中的脂肪积累,降低与睡眠障碍相关的肥胖风险。
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来源期刊
Journal of physiology and biochemistry
Journal of physiology and biochemistry 生物-生化与分子生物学
CiteScore
6.60
自引率
0.00%
发文量
86
审稿时长
6-12 weeks
期刊介绍: The Journal of Physiology and Biochemistry publishes original research articles and reviews describing relevant new observations on molecular, biochemical and cellular mechanisms involved in human physiology. All areas of the physiology are covered. Special emphasis is placed on the integration of those levels in the whole-organism. The Journal of Physiology and Biochemistry also welcomes articles on molecular nutrition and metabolism studies, and works related to the genomic or proteomic bases of the physiological functions. Descriptive manuscripts about physiological/biochemical processes or clinical manuscripts will not be considered. The journal will not accept manuscripts testing effects of animal or plant extracts.
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