本文關(guān)鍵詞： 殼聚糖 高脂膳食 氧化應(yīng)激 糖代謝　出處：《江南大學(xué)》2017年碩士論文　論文類型：學(xué)位論文

【摘要】：本文通過長期(16周)對小鼠喂食高脂膳食,研究殼聚糖的添加對由高脂膳食引起的氧化應(yīng)激以及糖代謝紊亂的影響,并對其作用機(jī)理進(jìn)行初步研究,為高脂膳食引發(fā)氧化應(yīng)激和糖代謝紊亂及殼聚糖作為血糖調(diào)節(jié)營養(yǎng)素研究提供理論基礎(chǔ)。選取6周齡SPF級C57BL/6J雄性小鼠60只,隨機(jī)分為5組(每組12只),分別飼喂正常膳食、高脂(無添加、添加低分子量殼聚糖(5%)、高分子量殼聚糖(5%)、二甲雙胍(5%))膳食,飼養(yǎng)過程中測定各組小鼠體重、攝食量、空腹血糖、葡萄糖耐受、胰島素耐受情況,飼養(yǎng)16周后處死,測定血漿中甘油三酯、總膽固醇、高密度脂蛋白膽固醇、低密度脂蛋白膽固醇的含量;檢測肝臟中甘油三酯、總膽固醇、肝脂酶和脂蛋白脂肪酶水平;檢測肝臟中總抗氧化能力、過氧化氫酶和超氧化物歧化酶活性、丙二醛;對肝臟、胰腺的組織結(jié)構(gòu)進(jìn)行觀察;運(yùn)用實(shí)時(shí)相對定量逆轉(zhuǎn)錄聚合酶鏈反應(yīng)(RT-PCR)技術(shù)和Western Blot檢測肝臟中氧化應(yīng)激及糖異生信號通路中相關(guān)基因和蛋白表達(dá)。實(shí)驗(yàn)結(jié)果表明:一、16周的高脂膳食對小鼠日常攝食量無顯著影響,但會(huì)造成體重顯著增加,殼聚糖可有效緩解該現(xiàn)象,高分子量殼聚糖效果略好;二、16周高脂膳食飼喂會(huì)造成小鼠肝臟脂質(zhì)合成相關(guān)酶ACC1表達(dá)水平顯著上升,導(dǎo)致小鼠血清中的總膽固醇、低密度脂蛋白膽固醇含量顯著增加,肝臟中總膽固醇含量顯著增加,殼聚糖可顯著緩解該現(xiàn)象,高分子量殼聚糖效果優(yōu)于低分子量殼聚糖;三、16周高脂膳食對小鼠肝臟和胰腺組織結(jié)構(gòu)有一定破壞,導(dǎo)致組織出現(xiàn)脂肪空泡、脂肪變性,殼聚糖可保護(hù)肝臟和胰腺組織結(jié)構(gòu);四、高脂膳食誘導(dǎo)小鼠氧化還原應(yīng)激,氧化酶(過氧化氫酶、超氧化物歧化酶等)含量降低,丙二醛含量上升,氧化還原環(huán)境的穩(wěn)態(tài)遭到破壞,肝臟轉(zhuǎn)錄因子NF-E2相關(guān)因子-2 mRNA表達(dá)水平略有上升,其調(diào)控的抗氧化酶(血紅素氧合酶1、醌氧化還原酶-1)mRNA表達(dá)水平顯著下降,糖原合成酶激酶-3βmRNA相對表達(dá)量顯著上升。殼聚糖可改善體內(nèi)的氧化應(yīng)激水平,緩解由高脂膳食造成的損傷;五、16周高脂膳食導(dǎo)致的糖代謝紊亂主要是因?yàn)楦闻K氧化應(yīng)激引起磷酸烯醇式丙酮酸羧激酶和葡萄糖6磷酸酶表達(dá)水平上升,最終導(dǎo)致肝臟和肌肉糖代謝紊亂;殼聚糖可調(diào)控叉頭轉(zhuǎn)錄因子-1和肝細(xì)胞核因子-4α等基因表達(dá)水平,下調(diào)磷酸烯醇式丙酮酸羧激酶和葡萄糖6磷酸酶表達(dá)水平。結(jié)論:殼聚糖可改善由高脂膳食造成的氧化應(yīng)激和糖代謝紊亂,高分子殼聚糖效果略好。
[Abstract]:The effects of chitosan supplementation on oxidative stress and glucose metabolism disorder induced by high fat diet were studied in mice fed with high fat diet for a long period of 16 weeks. To provide a theoretical basis for the study of oxidative stress and glucose metabolism disorder induced by high fat diet and chitosan as a glycemic regulating nutrient, 60 SPF grade C57BL / 6J male mice of 6 weeks old were randomly divided into 5 groups (12 rats in each group, fed with normal diet respectively), and 6 weeks old C57BL / 6J male mice were randomly divided into 5 groups (12 rats in each group). High fat diet (no addition, low molecular weight chitosan, high molecular weight chitosan, metformin) diet, body weight, food intake, fasting blood glucose, glucose tolerance, insulin tolerance in each group were measured. The levels of triglyceride, total cholesterol, high density lipoprotein cholesterol, low density lipoprotein cholesterol in plasma, triglyceride, total cholesterol, hepatic lipase and lipoprotein lipase in liver were measured. Total antioxidant capacity, catalase and superoxide dismutase activity, malondialdehyde (MDA), liver and pancreas were observed. Real-time relative quantitative reverse transcription polymerase chain reaction (RT PCR) and Western Blot were used to detect the expression of genes and proteins related to oxidative stress and glycosylated signal pathway in liver. There was no significant effect on regular food intake. However, it could significantly increase body weight, which could be effectively alleviated by chitosan. The effect of high molecular weight chitosan was slightly better, and the level of ACC1 expression of liver lipid-synthase related enzymes was significantly increased in mice fed with high-fat diet for 16 weeks. The results showed that the total cholesterol, low density lipoprotein cholesterol and liver total cholesterol in serum of mice were significantly increased. Chitosan could alleviate this phenomenon, and the effect of high molecular weight chitosan was better than that of low molecular weight chitosan. The liver and pancreas tissue structure of mice was damaged by high fat diet for 16 weeks, resulting in fat vacuole, fatty degeneration, chitosan could protect the liver and pancreas tissue structure. 4, high fat diet induced redox stress in mice. The content of oxidase (catalase, superoxide dismutase, etc.) decreased, the content of malondialdehyde increased, the homeostasis of redox environment was destroyed, and the expression level of liver transcription factor NF-E2 related factor 2 mRNA increased slightly. Its regulated antioxidant enzymes (heme oxygenase 1, quinone redox enzyme -1 mRNA expression level decreased significantly, glycogen synthase kinase-3 尾 mRNA expression increased significantly. Chitosan can improve the oxidative stress level in vivo. The disorder of glucose metabolism caused by high fat diet at the fifth week of 16 weeks was mainly due to the increased expression of phosphoenolpyruvate carboxykinase and glucose-6 phosphatase induced by oxidative stress in liver. Chitosan can regulate the expression level of forkhead transcription factor-1 and liver nuclear factor-4 偽, which leads to the disorder of glucose metabolism in liver and muscle. Conclusion: chitosan can improve oxidative stress and glucose metabolism disorder caused by high fat diet, and the effect of polymer chitosan is better than that of high fat diet, but the expression of phosphoenolpyruvate carboxykinase and glucose-6 phosphatase is down-regulated.
【學(xué)位授予單位】：江南大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2017
【分類號】：R151

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