肥胖发展过程中皮下白色脂肪组织中一些mirna的表达谱和分析。

Elham M Youssef, Asmaa M Elfiky, BanglySoliman, Nourhan Abu-Shahba, Mahmoud M Elhefnawi
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引用次数: 12

摘要

背景:MicroRNAs正在成为调节脂肪细胞生理的新介质,并已被批准在肥胖中发挥作用。尽管有几项研究关注了microRNA在不同代谢组织中的表达谱和功能,但人们对它们在肥胖阶段对白色脂肪组织营养干预的反应知之甚少,而且它们对减肥策略的反应是否不同也知之甚少。我们的目的是研究在体重变化、扩张/缩小过程中,腹股沟皮下白色脂肪组织中一些mirna的失调;方法:将100只6周龄雄性Wister大鼠随机分为正常饮食组(N.D)、高脂肪饮食组(H.F.D)和转换为正常饮食组(H.F.D/N.D)。采用双能x线吸收仪(DEXA)记录试验开始时和每隔2周的血脂、激素水平、体脂量和腹股沟皮下白色脂肪组织量(WAT)。采用实时荧光定量PCR技术检测microrna的表达水平。结果:在肥胖发展的早期阶段,观察到血清葡萄糖,脂质谱和脂肪因子激素的显著变化。在多个时间点观察到rno-mir 30a-5p、rno-mir 133a-5p和rno-mir 107-5p表达水平的改变。而在连续喂养10周后的2 - 4周内,rno-let-7a-5p、rno-mir 193a-5p和rno-mir125a-5p在所有时间点均下调,rno-mir130a-5p上调。转换到正常饮食的影响对脂质谱、脂肪因子激素水平和一些mirna有相反的影响。生物信息学的结果已经确定了一个新的和重要的途径相关的炎症信号。结论:我们的研究表明,在短时间的高热量饮食消耗后,一些脂肪细胞表达的mirna发生了显著变化。这进一步证明了营养作为一种表观遗传因子,通过调节相关的关键mirna,在脂质和糖代谢基因的调控中发挥重要作用。因此,我们建议mirna可以作为饮食性肥胖过程中肥胖的生物标志物。也许限制卡路里的摄入是控制肥胖和相关代谢紊乱的一种方法。需要进一步的研究来充分阐明microrna在肥胖发展中的作用。
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Expression profiling and analysis of some miRNAs in subcutaneous white adipose tissue during development of obesity.

Background: MicroRNAs are emerging as new mediators in the regulation of adipocyte physiology and have been approved to play a role in obesity. Despite several studies have focused on microRNA expression profiles and functions in different metabolic tissues, little is known about their response to nutritional interventions in white adipose tissue during obesity stages, and whether they differ in this response to weight-reduction strategy is poorly understood. Our objectives were to study the dysregulation of some miRNAs in subcutaneous inguinal white adipose tissue during weight change, expansion/reduction; in response to both a high-fat diet and switching to a normal diet feeding, and to evaluate them as potential biomarkers and therapeutic targets for early obesity management METHOD: A hundred 6-week-old male Wister rats were randomly divided into a normal diet group (N.D), a high-fat diet group (H.F.D), and a switched to a normal diet group (H.F.D/N.D). At the beginning and at intervals 2 weeks, serum lipid, hormone levels, total body fat mass, and inguinal subcutaneous white adipose tissue mass (WAT) measurements were recorded using dual-energy X-ray absorptiometry (DEXA). The expression levels of microRNAs were evaluated using real-time PCR.

Results: Significant alterations were observed in serum glucose, lipid profile, and adipokine hormones during the early stages of obesity development. Alteration in rno-mir 30a-5p, rno-mir 133a-5p, and rno-mir 107-5p expression levels were observed at more than one time point. While rno-let-7a-5p, rno-mir 193a-5p, and rno-mir125a-5p were downregulated and rno-mir130a-5p was upregulated at all time points within 2 to 4 weeks in response to H.F.D feeding for 10 weeks. The impact of switching to normal diet has a reversed effect on lipid profile, adipokine hormone levels, and some miRNAs. The bioinformatics results have identified a novel and important pathway related to inflammatory signalling.

Conclusion: Our research demonstrated significant alterations in some adipocyte-expressed miRNAs after a short time of high caloric diet consumption. This provides further evidence of the significant role of nutrition as an epigenetic factor in regulation of lipid and glucose metabolism genes by modulating of related key miRNAs. Therefore, we suggest that miRNAs could be used as biomarkers for adiposity during diet-induced obesity. Perhaps limitation in calories intake is a way to manipulate obesity and associated metabolic disorders. Further studies are needed to fully elucidate the role of microRNAs in the development of obesity.

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