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Synergistic Treatment of Obesity via Locally Promoting Beige Adipogenesis and Antioxidative Defense in Adipose Tissues
ACS Biomaterials Science & Engineering ( IF 5.8 ) Pub Date : 2021-01-04 , DOI: 10.1021/acsbiomaterials.0c01181
Zhenhua Ding 1 , Maohua Chen 1 , Xinyan Tao 1 , Yuan Liu 1 , Jie He 1 , Tao Wang 1, 2 , Xiaohong Li 1
Affiliation  

Obesity is a primary risk factor for type 2 diabetes, cardiovascular diseases, cancer, and other chronic diseases. Current antiobesity medications need frequent administration and show limited efficacy with severe side effects. Herein, browning agent rosiglitazone (Rsg) and antioxidant manganese tetroxide nanoparticles (MnNPs, around 250 nm) are integrated into electrospun short fibers (SF@Rsg-Mn) with a 1.5 μm width and a 20 μm length. Upon injection into inguinal adipose tissues, SF@Rsg-Mn are well retained in the local depots to sustainably release Rsg in 30 days for adipose tissue browning, while MnNPs on the fiber surface continuously scavenge adipose reactive oxygen species (ROS) for an extended period of time. Synergistic inhibition of fat accumulation through ROS scavenging and white adipocyte browning has been demonstrated for the first time, and the optimal synergistic ratio of Rsg and MnNPs is determined to be 1/14 via combination index examination. SF@Rsg-Mn inhibit lipid accumulation through downregulation of adipogenic gene PPARγ while promoting energy expenditure through upregulation of brown-specific gene UCP1 and mitochondrial function gene COX7A1. In a diet-induced obesity mouse model, a single injection of SF@Rsg-Mn into inguinal adipose tissues has accomplished a synergistic effect on body weight loss, fat reduction, glucose, and lipid metabolic improvement while minimizing adverse effects on other tissues, thereby paving the way to efficacious, safe, and practical treatment of obesity.

中文翻译:

通过局部促进米色脂肪形成和脂肪组织的抗氧化防御作用来协同治疗肥胖。

肥胖是2型糖尿病,心血管疾病,癌症和其他慢性疾病的主要危险因素。当前的抗肥胖药需要频繁施用,并且显示出有限的功效和严重的副作用。在此,将褐变剂罗格列酮(Rsg)和抗氧化剂四氧化锰纳米颗粒(MnNPs,约250 nm)集成到宽度为1.5μm,长度为20μm的电纺短纤维(SF @ Rsg-Mn)中。注射到腹股沟脂肪组织中后,SF @ Rsg-Mn被很好地保留在局部储库中,以在30天之内可持续释放Rsg,从而使脂肪组织褐变,而纤维表面的MnNPs则持续清除脂肪中的活性氧(ROS)较长时间。时间。首次证明了通过清除ROS和白色脂肪细胞褐变对脂肪积累的协同抑制作用,并且通过组合指数检查确定Rsg和MnNPs的最佳协同比例为1/14。SF @ Rsg-Mn通过下调成脂基因PPARγ抑制脂质积累,同时通过上调棕色特异性基因UCP1和线粒体功能基因COX7A1促进能量消耗。在饮食诱发的肥胖小鼠模型中,向腹股沟脂肪组织单次注射SF @ Rsg-Mn已实现了对体重减轻,脂肪减少,葡萄糖和脂质代谢改善的协同作用,同时最大限度地减少了对其他组织的不良影响,从而为肥胖的有效,安全和实际治疗铺平道路。通过结合指数检测,确定Rsg与MnNPs的最佳协同比例为1/14。SF @ Rsg-Mn通过下调成脂基因PPARγ抑制脂质积累,同时通过上调棕色特异性基因UCP1和线粒体功能基因COX7A1促进能量消耗。在饮食诱发的肥胖小鼠模型中,向腹股沟脂肪组织单次注射SF @ Rsg-Mn已实现了对体重减轻,脂肪减少,葡萄糖和脂质代谢改善的协同作用,同时最大限度地减少了对其他组织的不良影响,从而为肥胖的有效,安全和实际治疗铺平道路。通过结合指数检测,确定Rsg与MnNPs的最佳协同比例为1/14。SF @ Rsg-Mn通过下调成脂基因PPARγ抑制脂质积累,同时通过上调棕色特异性基因UCP1和线粒体功能基因COX7A1促进能量消耗。在饮食诱发的肥胖小鼠模型中,向腹股沟脂肪组织单次注射SF @ Rsg-Mn已实现了对体重减轻,脂肪减少,葡萄糖和脂质代谢改善的协同作用,同时最大限度地减少了对其他组织的不良影响,从而为肥胖的有效,安全和实际治疗铺平道路。SF @ Rsg-Mn通过下调成脂基因PPARγ抑制脂质积累,同时通过上调棕色特异性基因UCP1和线粒体功能基因COX7A1促进能量消耗。在饮食诱发的肥胖小鼠模型中,向腹股沟脂肪组织单次注射SF @ Rsg-Mn已实现了对体重减轻,脂肪减少,葡萄糖和脂质代谢改善的协同作用,同时最大限度地减少了对其他组织的不良影响,从而为肥胖的有效,安全和实际治疗铺平道路。SF @ Rsg-Mn通过下调成脂基因PPARγ抑制脂质积累,同时通过上调棕色特异性基因UCP1和线粒体功能基因COX7A1促进能量消耗。在饮食诱发的肥胖小鼠模型中,向腹股沟脂肪组织单次注射SF @ Rsg-Mn已实现了对体重减轻,脂肪减少,葡萄糖和脂质代谢改善的协同作用,同时最大限度地减少了对其他组织的不良影响,从而为肥胖的有效,安全和实际治疗铺平道路。
更新日期:2021-02-08
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