本文選題：丁酸 + 肥胖��； 參考：《中國生物化學(xué)與分子生物學(xué)報》2017年12期

【摘要】：丁酸可以預(yù)防高脂日糧誘導(dǎo)的小鼠肥胖和胰島素抵抗,但是否有治療作用尚不清楚。本研究證明,高脂日糧誘導(dǎo)小鼠肥胖模型后,用80 mg/mL丁酸鈉水溶液灌胃能夠緩解肥胖。表觀指標(biāo)檢測發(fā)現(xiàn),丁酸鈉顯著降低肥胖小鼠的肝重(1.24 g±0.03 g至1.08 g±0.04 g)、體重(32.46 g±0.50 g至28.35 g±0.58 g)和附睪脂重(1.33 g±0.13 g至0.81 g±0.08 g)及其與體重的比(4.06%±0.37%至2.83%±0.22%)。葡萄糖耐受實(shí)驗(yàn)和血液激素含量檢測表明,丁酸鈉部分緩解由高脂引起的葡萄糖不耐受,并顯著降低血液中瘦素(3.71 ng/mL±0.62 ng/mL至1.50ng/m L±0.26 ng/mL)和胰島素(2.39 ng/mL±0.30 ng/mL至1.25 ng/mL±0.09 ng/mL)的水平。肝中脂質(zhì)和糖原的生化檢測表明,丁酸鈉對肝中的甘油三酯、膽固醇和糖原的含量沒有顯著影響。通過RT-PCR實(shí)驗(yàn)發(fā)現(xiàn),丁酸鈉顯著上調(diào)線粒體β氧化和解耦聯(lián)相關(guān)的關(guān)鍵基因以及線粒體自身編碼的8個基因的mRNA水平的表達(dá),Western印跡檢測表明,丁酸鈉顯著升高肝葡萄糖轉(zhuǎn)運(yùn)蛋白GLUT2和調(diào)控線粒體功能的關(guān)鍵蛋白PGC-1α的表達(dá)。上述結(jié)果提示,丁酸鈉可能通過增強(qiáng)肝線粒體功能緩解食源性小鼠肥胖。
[Abstract]:Butyric acid can prevent obesity and insulin resistance induced by high fat diet in mice. This study demonstrated that the obesity model of mice induced by high fat diet could be alleviated by oral administration of 80 mg/mL sodium butyrate solution. It was found that sodium butyrate significantly decreased the liver weight of obese mice from 1.24 g 鹵0.03 g to 1.08 g 鹵0.04 g, weight of 32.46 g 鹵0.50 g to 28.35 g 鹵0.58 g) and epididymal lipid weight of 1.33 g 鹵0.13 g to 0.81 g 鹵0.08 g), and the ratio to body weight was 4.06% 鹵0.37% to 2.83% 鹵0.22g. Glucose tolerance test and determination of serum hormones showed that sodium butyrate partially alleviated glucose intolerance induced by hyperlipidemia, and significantly decreased the levels of leptin in blood from 3.71 鹵0.62 ng/mL to 1.50ng/m L 鹵0.26 ng / mL) and insulin (2.39 鹵0.30 ng/mL to 1.25 ng/mL 鹵0.09 ng / mL). Biochemical analysis of lipids and glycogen in the liver showed that sodium butyrate had no significant effect on the contents of triglycerides, cholesterol and glycogen in the liver. RT-PCR assay showed that sodium butyrate upregulated the expression of mRNA in mitochondrial 尾 -oxidation and decoupling related genes and 8 genes encoded by mitochondria. Sodium butyrate significantly increased the expression of hepatic glucose transporter GLUT2 and PGC-1 偽, a key protein regulating mitochondrial function. These results suggest that sodium butyrate may alleviate obesity by enhancing the function of liver mitochondria.
【作者單位】： 南京農(nóng)業(yè)大學(xué)農(nóng)業(yè)部動物生理生化重點(diǎn)實(shí)驗(yàn)室;鹽城師范學(xué)院海洋與生物工程學(xué)院;
【基金】：江蘇省高校自然科學(xué)研究面上項(xiàng)目(No.17KJB230004) 國家自然科學(xué)青年基金項(xiàng)目(No.31402161)資助~~
【分類號】：R589.2

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