本文選題：芹菜素 + 肥胖　； 參考：《合肥工業(yè)大學(xué)》2017年碩士論文

【摘要】：當(dāng)長期的能量攝入遠(yuǎn)遠(yuǎn)大于能量代謝時(shí),機(jī)體的能量平衡出現(xiàn)了紊亂,脂肪組織大量沉積,造成肥胖。肥胖往往伴隨著胰島素抵抗,并最終導(dǎo)致二型糖尿病和高血壓等代謝綜合癥。前人的研究表明,脂肪組織在肥胖及相關(guān)代謝綜合癥的發(fā)生發(fā)展中起首要調(diào)控作用,其脂質(zhì)積累和炎性加劇都會(huì)造成胰島素抵抗。黃酮類化合物在抗炎、抗癌和抗突變等方面具有明確的化學(xué)防御效果,芹菜素作為一種普遍存在于水果和蔬菜中的黃酮類物質(zhì),調(diào)控飲食誘導(dǎo)的肥胖及肥胖相關(guān)胰島素抵抗的作用尚無系統(tǒng)的研究。本論文首先將C57BL/6的雄性小鼠分為三組,分別喂以低脂飲食(LFD)、高脂飲食(HFD)和含0.04%芹菜素的高脂飲食(0.04 HAP)12周。結(jié)果顯示,芹菜素的添加能夠明顯改善高脂飲食所導(dǎo)致的體重增加、脂肪積累及脂肪細(xì)胞增大。其間,芹菜素也改善了肥胖相關(guān)的胰島素抵抗。因此,本文分別在體內(nèi)和體外進(jìn)一步探討了芹菜素改善高脂飲食誘導(dǎo)肥胖及胰島素抵抗的機(jī)制。在脂質(zhì)代謝方面,芹菜素不僅降低了脂質(zhì)合成基因PPARγ和SCD1的表達(dá),而且能夠激活SIRT1/FOXO1/ATGL通路、增加ATGL和HSL基因的表達(dá)來促進(jìn)脂解。此外,芹菜素也顯著增強(qiáng)了產(chǎn)熱調(diào)節(jié)基因UCP-1和PGC-1α的表達(dá)。在炎性調(diào)控方面,流式細(xì)胞術(shù)和Real-time PCR研究顯示,芹菜素的攝入降低了脂肪組織中巨噬細(xì)胞的數(shù)目、抑制了巨噬細(xì)胞的炎性極化,而其作用機(jī)制可能是通過抑制炎性信號(hào)通路NF-κB和MAPK的活化�？偠灾�,我們的研究表明,通過調(diào)控脂質(zhì)代謝和炎性極化,芹菜素的飲食攝入可以改善飲食誘導(dǎo)的肥胖和相關(guān)胰島素抵抗。因此,作為一種天然可食用的黃酮類物質(zhì),芹菜素是一種能夠調(diào)節(jié)肥胖及相關(guān)代謝紊亂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 緯 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 偽. 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.
【學(xué)位授予單位】：合肥工業(yè)大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2017
【分類號(hào)】：TS201.4

【參考文獻(xiàn)】

相關(guān)期刊論文 前1條

1 候麗瓊;趙鐵耘;張伊yN;;黃連素對(duì)肥胖胰島素抵抗大鼠骨骼肌胰島素抵抗的干預(yù)研究[J];四川大學(xué)學(xué)報(bào)(醫(yī)學(xué)版);2015年06期

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本文編號(hào)：2102059