芹菜素对小鼠高脂饮食诱导肥胖的作用及相关调控机制的研究

发布时间：2018-07-06 07:56

本文选题：芹菜素 + 肥胖　；参考：《合肥工业大学》2017年硕士论文

【摘要】：当长期的能量摄入远远大于能量代谢时,机体的能量平衡出现了紊乱,脂肪组织大量沉积,造成肥胖。肥胖往往伴随着胰岛素抵抗,并最终导致二型糖尿病和高血压等代谢综合症。前人的研究表明,脂肪组织在肥胖及相关代谢综合症的发生发展中起首要调控作用,其脂质积累和炎性加剧都会造成胰岛素抵抗。黄酮类化合物在抗炎、抗癌和抗突变等方面具有明确的化学防御效果,芹菜素作为一种普遍存在于水果和蔬菜中的黄酮类物质,调控饮食诱导的肥胖及肥胖相关胰岛素抵抗的作用尚无系统的研究。本论文首先将C57BL/6的雄性小鼠分为三组,分别喂以低脂饮食(LFD)、高脂饮食(HFD)和含0.04%芹菜素的高脂饮食(0.04 HAP)12周。结果显示,芹菜素的添加能够明显改善高脂饮食所导致的体重增加、脂肪积累及脂肪细胞增大。其间,芹菜素也改善了肥胖相关的胰岛素抵抗。因此,本文分别在体内和体外进一步探讨了芹菜素改善高脂饮食诱导肥胖及胰岛素抵抗的机制。在脂质代谢方面,芹菜素不仅降低了脂质合成基因PPARγ和SCD1的表达,而且能够激活SIRT1/FOXO1/ATGL通路、增加ATGL和HSL基因的表达来促进脂解。此外,芹菜素也显著增强了产热调节基因UCP-1和PGC-1α的表达。在炎性调控方面,流式细胞术和Real-time PCR研究显示,芹菜素的摄入降低了脂肪组织中巨噬细胞的数目、抑制了巨噬细胞的炎性极化,而其作用机制可能是通过抑制炎性信号通路NF-κB和MAPK的活化。总而言之,我们的研究表明,通过调控脂质代谢和炎性极化,芹菜素的饮食摄入可以改善饮食诱导的肥胖和相关胰岛素抵抗。因此,作为一种天然可食用的黄酮类物质,芹菜素是一种能够调节肥胖及相关代谢紊乱的重要功能性食品因子。
[Abstract]:When the long-term energy intake is far greater than the energy metabolism, the energy balance of the body appears disorder, fat tissue deposition, resulting in obesity. Obesity is often accompanied by insulin resistance, which ultimately leads to metabolic syndrome such as type 2 diabetes and hypertension. Previous studies have shown that adipose tissue plays an important role in the development of obesity and related metabolic syndrome, and its lipid accumulation and inflammatory exacerbation will lead to insulin resistance. Flavonoids have definite chemical defense effects in anti-inflammatory, anti-cancer and anti-mutation aspects. Apigenin is a common flavonoid in fruits and vegetables. The regulation of diet-induced obesity and obesity-related insulin resistance has not been systematically studied. C57BL / 6 male mice were divided into three groups: low fat diet (LFD), high fat diet (HFD) and high fat diet containing 0.04% apigenin (0.04 HAP) for 12 weeks. The results showed that the addition of apigenin could significantly improve the weight gain, fat accumulation and adipocyte increase induced by high fat diet. Meanwhile, apigenin also improves insulin resistance associated with obesity. Therefore, the mechanism of apigenin on obesity and insulin resistance induced by high fat diet was further investigated in vivo and in vitro. In the aspect of lipid metabolism, apigenin not only reduced the expression of PPAR 纬 and SCD1, but also activated the SIRT1 / FOXO1 / ATGL pathway, and increased the expression of ATGL and HSL genes to promote lipid hydrolysis. In addition, apigenin also significantly enhanced the expression of heat production genes UCP-1 and PGC-1 伪. In terms of inflammatory regulation, flow cytometry and Real-time PCR showed that apigenin intake decreased the number of macrophages in adipose tissue and inhibited the inflammatory polarization of macrophages. The mechanism may be by inhibiting the activation of NF- 魏 B and MAPK. All in all, our studies have shown that by regulating lipid metabolism and inflammatory polarization, apigenin dietary intake can improve diet-induced obesity and related insulin resistance. Therefore, as a natural edible flavonoid, apigenin is an important functional food factor which can regulate obesity and related metabolic disorders.
【学位授予单位】：合肥工业大学
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：TS201.4

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