本文關(guān)鍵詞：短期灌服丁酸鈉緩解小鼠肥胖的功效與機(jī)制研究　出處：《南京農(nóng)業(yè)大學(xué)》2016年博士論文　論文類(lèi)型：學(xué)位論文

  更多相關(guān)文章： 線(xiàn)粒體 脂肪分解 脂聯(lián)素 丁酸 小鼠 肥胖

【摘要】：丁酸是膳食纖維在結(jié)腸經(jīng)發(fā)酵而產(chǎn)生的短鏈脂肪酸之一,它天然存在于黃油和奶酪中。丁酸不僅可以為機(jī)體提供能量,還可以作為信號(hào)分子通過(guò)激活G蛋白耦聯(lián)受體41 (G protein-coupled receptor 41,GPR41)和 43 (G protein-coupled receptor 43, GPR43 )或抑制組蛋白去乙�；�(Histone deacetylase,HDAC )來(lái)發(fā)揮生物學(xué)功能。丁酸具有抗炎、抗癌、抗氧化和免疫調(diào)節(jié)等生理作用。目前,大多數(shù)研究都是在誘導(dǎo)肥胖的模型過(guò)程中將丁酸長(zhǎng)期添加到高脂日糧中,研究其對(duì)肥胖的預(yù)防作用,丁酸對(duì)已建立的肥胖模型的治療作用僅在一項(xiàng)研究報(bào)道中簡(jiǎn)單的提及,并且缺乏深入的分子機(jī)制研究。因此,我們以高脂誘導(dǎo)的肥胖小鼠為模型,研究短期灌服丁酸鈉對(duì)肥胖的緩解作用,并對(duì)其作用機(jī)制進(jìn)行了研究。1短期灌服丁酸鈉緩解肥胖的功效3周齡SPF級(jí)雄性C57BL/6J小鼠(n = 36),購(gòu)于揚(yáng)州大學(xué)比較醫(yī)學(xué)中心,飼養(yǎng)于江蘇省中西醫(yī)結(jié)合醫(yī)院實(shí)驗(yàn)動(dòng)物中心,適應(yīng)一周后,小鼠隨機(jī)分為兩組,高脂組小鼠(High-fat diet, HF, n = 24)飼喂高脂日糧(脂肪供能45%)誘導(dǎo)肥胖,對(duì)照組小鼠(Con,n= 12)飼喂正常脂肪含量日糧(脂肪供能10%), 12h光照,12h黑暗,恒溫恒濕,自由采食和飲水,記錄每周體重增長(zhǎng)情況。實(shí)驗(yàn)發(fā)現(xiàn),飼喂8周后,高脂組小鼠相對(duì)于對(duì)照組小鼠體重極顯著升高(P 0.01 ),并且高脂組相比對(duì)照組體重增加20%以上,達(dá)到了肥胖小鼠模型建立的基本要求。此外,葡萄糖耐量實(shí)驗(yàn)(Glucose tolerance test, GTT)測(cè)試結(jié)果顯示相比Con組,HF組中小鼠無(wú)論是空腹血糖(0min)還是在腹腔注射葡萄糖15 min、30min、60min、90 min和120 min血糖含量均極顯著升高(P 0.01 )。說(shuō)明高脂日糧飼喂8周后小鼠發(fā)生了葡萄糖不耐受。飼喂8周肥胖模型建立成功后,將高脂日糧飼喂小鼠隨機(jī)均分為2組:處理組灌胃 1 mL 水含 80 mg 丁酸鈉(High-fat diet with sodium butyrate,HFB);高脂對(duì)照組和空白對(duì)照組灌服等體積的水。每?jī)商旃辔敢淮?灌胃時(shí)間下午5點(diǎn),共灌胃5次。在丁酸鈉灌胃的10天里,小鼠采食的日糧仍然與處理前保持一致。實(shí)驗(yàn)發(fā)現(xiàn),與HF組小鼠相比,HFB組中小鼠的體重(P 0.05 )和肝臟重(P 0.05 )顯著降低;腓腸肌重、腓腸肌重/體重和肝重/體重沒(méi)有變化。HFB組中小鼠無(wú)論是空腹血糖(P= 0.001),還是在腹腔注射葡萄糖15 min (P= 0.163)、30 min(P= 0.091)、60 min (P = 0.263 )、90 min (P = 0.105 )和 120 min (P = 0.000)的血糖含量均有一定程度的降低,表明短期丁酸鈉灌胃能夠一定程度緩解小鼠高脂日糧造成的葡萄糖不耐受。與HF組相比,HFB組小鼠血清中葡萄糖(P0.05)、胰島素(P0.05)、瘦素(P0.05)的水平顯著降低,但血清中總甘油三酯、總膽固醇、高低密度脂蛋白膽固醇和游離脂肪酸的含量沒(méi)有變化。此外,與HF組相比,HFB組小鼠肝臟中總甘油三酯和總膽固醇的含量沒(méi)有顯著變化。以上結(jié)果表明,高脂日糧飼喂小鼠8周后造肥胖模型成功。當(dāng)丁酸鈉短期灌服后,緩解了高脂日糧導(dǎo)致的肥胖和葡萄糖不耐受。2 丁酸鈉對(duì)脂肪組織的影響及作用機(jī)制丁酸鈉短期灌服后,HE染色結(jié)果顯示,與HF組相比,HFB組中脂肪組織脂肪細(xì)胞的大小(P0.05)、附睪脂重(P0.05)以及附睪脂重/體重(P0.05)顯著降低。實(shí)驗(yàn)發(fā)現(xiàn),與HF組相比,HFB組中脂肪分解的關(guān)鍵酶激素敏感酯酶(Hormone sensitive lipase, HSL)和甘油三酯水解酶(Adipose triglyceride lipase, ATGL)的 mRNA表達(dá)水平?jīng)]有變化,但HSL (P0.05)和ATGL (P0.05)的蛋白表達(dá)水平顯著升高。HFB組小鼠脂肪組織中13個(gè)線(xiàn)粒體自身編碼基因中的4個(gè)(P 0.05 X ND2, ND4,ND4L和COX1)的mRNA表達(dá)顯著升高,另外3個(gè)(ND6, CYTB和ATP6 )有升高的趨勢(shì)。與HF組相比,HFB組中編碼線(xiàn)粒體解耦聯(lián)蛋白的基因(Uncoupling protein 2,UCP2 )和(Uncoupling protein 3, UCP3 ),脂肪棕色化的標(biāo)志基因(PR domain containing 16,PRDM16)以及線(xiàn)粒體 β 氧化相關(guān)基因(Peroxisomal acyl-coenzyme A oxidase 1,ACOX1)的mRNA表達(dá)水平?jīng)]有變化,卻顯著升高了調(diào)控線(xiàn)粒體功能的關(guān)鍵基因(Peroxisome proliferator-activated receptor gamma coactivator 1-alpha, PGC1α) (P 0.05 )的mRNA和蛋白表達(dá)水平以及與線(xiàn)粒體功能相關(guān)的蛋白(Cytochrome c oxidase IV,COX4)(P 0.05 )的蛋白表達(dá)水平。此外,HFB組中蛋白激酶A (Protein kinase A,PKA)(P 0.05)的蛋白表達(dá)水平以及環(huán)磷腺苷效應(yīng)元件結(jié)合蛋白(cAMP-response element binding protein, CREB )(P 0.05 )的磷酸化水平顯著升高。HFB組脂肪組織中GPR43的mRNA表達(dá)水平?jīng)]有變化,GPR43 (P 0.05 )的蛋白表達(dá)水平顯著升高,對(duì) β3 腎上腺素受體(β3-adrenergic receptor,AR-β3 ), HFB 組中其 mRNA (P 0.05 )和蛋白(P0.05)表達(dá)水平同時(shí)顯著升高。染色質(zhì)免疫共沉淀技術(shù)(Chromatin Immunoprecipitation, ChIP)檢測(cè) GPR43 和AR-β3啟動(dòng)子上的乙�；�,結(jié)果發(fā)現(xiàn),與HF組相比,HFB組中GPR43基因啟動(dòng)子上的H3K9Ac的含量沒(méi)有影響,卻顯著提高了 AR-β3基因啟動(dòng)子上的H3K9Ac富集程度(P 0.05)。以上結(jié)果說(shuō)明,在脂肪組織中丁酸鈉通過(guò)增強(qiáng)GPR43和AR-β3信號(hào)通路,促進(jìn)脂肪組織的脂解作用和增強(qiáng)線(xiàn)粒體功能,從而降低脂肪含量。3 丁酸鈉對(duì)骨骼肌的影響及作用機(jī)制丁酸鈉短期灌服后,顯著降低了 HFB組小鼠骨骼肌中甘油三酯(P 0.05)和膽固醇(P 0.05)的含量,顯著升高了 HFB組小鼠骨骼肌中二磷酸腺苷(Adenosine diphosphate,ADP)(P 0.05)和一磷酸腺苷(Adenosine monophosphate,AMP)(P 0.05)的含量,但對(duì)三磷酸腺苷(Adenosine tiphosphate,ATP)的含量和能荷值沒(méi)有影響。實(shí)驗(yàn)發(fā)現(xiàn),與HF組相比,HFB組骨骼肌中脂解的關(guān)鍵酶HSL (P0.05)和脂蛋白脂酶(Lipoprotein lipase,LPL)(P 0.05 )的mRNA表達(dá)水平顯著升高,并且與線(xiàn)粒體功能相關(guān)基因UCP2 (P 0.05)、UCP3 (P 0.05)、肉毒堿棕櫚酰轉(zhuǎn)移酶(Carnitine palmitoyl transferase Ib,CPT1b)(P 0.05 )和 PGC1a (P 0.05 )的 mRNA和蛋白表達(dá)水平都顯著升高,同時(shí)骨骼肌中13個(gè)線(xiàn)粒體自身編碼基因中的12個(gè)基因(P 0.05 )的mRNA表達(dá)水平和與線(xiàn)粒體功能相關(guān)的蛋白COX4 (P 0.05 )的蛋白表達(dá)水平均顯著升高。與HF組相比,HFB組骨骼肌中過(guò)氧化物酶體增殖激活受體α(Peroxisome proliferator-activated receptor alpha, PPARα)(P 0.05)的 mRNA 表達(dá)水平顯著升高,但其蛋白的表達(dá)沒(méi)有影響,并且骨骼肌中蛋白激酶(Adenosine 5'-monophosphate (AMP)-activated protein kinase, AMPK)的蛋白磷酸化水平(P 0.05)顯著升高。此外,HFB組骨骼肌中瘦素受體(Leptinreceptor,LeptinR) (P0.05)的mRNA表達(dá)水平顯著升高了,但其蛋白水平?jīng)]有變化,同時(shí)脂聯(lián)素受體1 (Adiponectin receptor 1,AdipoR1)和 2 (Adiponectin receptor 2, AdipoR2)的 mRNA (P 0.05 )和蛋白(P 0.05)表達(dá)水平顯著升高,但血液和骨骼肌中脂聯(lián)素(Adiponectin)的蛋白表達(dá)水平?jīng)]有變化。HFB組骨骼肌中丁酸的兩個(gè)主要受體GPR41和GPR43的蛋白表達(dá)都沒(méi)有變化,但組蛋白去乙�；�1 (Histone deacetylase 1, HDAC1)的蛋白表達(dá)水平(P0.05)顯著降低。染色質(zhì)免疫共沉淀技術(shù)(ChIP)檢測(cè)發(fā)現(xiàn),與HF組相比,HFB組中UCP2 (P 0.05)、UCP3 (P0.05)、AdipoR1 (P0.05)和 AdipoR2 (P0.05)基因啟動(dòng)子上H3K9Ac的含量顯著提高。以上結(jié)果說(shuō)明,在骨骼肌中丁酸鈉通過(guò)促進(jìn)脂聯(lián)素信號(hào)通路和增強(qiáng)線(xiàn)粒體β氧化來(lái)促進(jìn)脂肪酸的代謝。綜上所述,丁酸鈉短期灌服可以通過(guò)促進(jìn)脂肪組織和骨骼肌中的能量代謝以及線(xiàn)粒體功能來(lái)緩解高脂日糧誘導(dǎo)的肥胖。
[Abstract]:Butyric acid (butyric acid) is one of the short chain fatty acids produced by the dietary fiber in the colonic fermentation. It is naturally found in butter and cheese. Butyric acid can not only provide energy for the body, but also can be used as a signal molecule through the activation of G protein coupled receptor 41 (G protein-coupled 41 receptor, GPR41) and 43 (G protein-coupled 43 receptor, GPR43) or inhibition of histone deacetylase (Histone deacetylase, HDAC) to play the biological functions. Butyric acid has some physiological functions, such as anti-inflammatory, anticancer, antioxidation and immunoregulation. At present, most of the studies are in the process of the long-term model of obesity induced by butyrate added to high fat diet, to study its preventive effect on obesity, therapeutic effect of butyrate on obesity model has been established only in a study reported in the simple mention, and lack of in-depth study on the molecular mechanism. Therefore, we used high fat induced obese mice as a model to study the effect of sodium butyrate on obesity in short term, and the mechanism of its action was studied. 1 short term gavage of sodium butyrate to alleviate the obesity effect SPF 3 week old male C57BL/6J mice (n = 36), purchased from Yangzhou University medical center, raised in Jiangsu province combining traditional Chinese and Western Medicine Experimental Animal Center Hospital, after one week adaptation, mice were randomly divided into two groups, high fat group (High-fat diet, HF n = 24), fed with high fat diet (45% fat) induced obese mice in control group (Con, n= 12) with a normal fat diet (10% fat), 12h light, 12h dark, constant temperature and humidity, free feeding and drinking water, record weekly weight gain. The experiment found that after 8 weeks of feeding, the body weight of the high-fat group was significantly higher than that of the control group (P 0.01), and the body weight of the high-fat group increased by more than 20% compared with the control group, which reached the basic requirement of establishing the obesity mouse model. In addition, the results of Glucose tolerance test (GTT) test showed that compared with the Con group, the fasting plasma glucose (0min) or the intraperitoneal injection of glucose 15 min, 30min, 60min, 90 min and 120 60min blood glucose levels in the HF group were significantly increased (0.01). It was suggested that glucose intolerance occurred in mice after 8 weeks of high fat diet feeding. After feeding for 8 weeks, the obesity model was established successfully, and the mice fed high-fat diet were randomly divided into 2 groups: the treatment group was gavaged 1 mL water containing 80 mg sodium butyrate (High-fat diet with sodium butyrate, HFB); the high-fat control group and the blank control group were given equal volume of water. Every two days, the stomach was gavage, and the time of gavage was 5 p.m. and gavage was 5 times. In the 10 day of sodium butyrate gavage, the diet of the mice was still consistent with that before treatment. It was found that compared with group HF, body weight (P 0.05) and liver weight (P 0.05) of mice in HFB group were significantly reduced, gastrocnemius muscle weight, gastrocnemius muscle weight / body weight and liver weight / weight did not change. The mice in the HFB group both fasting blood glucose (P= 0.001), or in the intraperitoneal injection of glucose 15 min (P= 0.163), 30 min (0.091 P=), 60 min (P = 0.263), 90 min (P = 0.105) and 120 min (P = 0) reduced blood sugar content to a certain extent, the short-term intragastric administration of sodium butyrate can alleviate to some extent of high-fat diet mice caused by glucose intolerance. Compared with group HF, the levels of serum glucose, P0.05, P0.05 and leptin (P0.05) in group HFB were significantly decreased, but the total triglycerides, total cholesterol, high-density lipoprotein cholesterol and free fatty acids in serum did not change. In addition, there was no significant change in total triglyceride and total cholesterol in the liver of HFB mice compared with the HF group. The above results showed that high fat diet fed mice 8 weeks after the successful model of obesity. When sodium butyrate was administered in a short period of time, obesity and glucose intolerance caused by high fat diet were relieved. 2, the effect and mechanism of sodium butyrate on adipose tissue. After short-term administration of sodium butyrate, HE staining showed that the adipocyte size (P0.05), epididymal fat weight (P0.05) and epididymal fat / body weight (P0.05) in HFB group were significantly lower than those in HF group. Experiments show that, compared with the HF group, the key enzyme hormone sensitive lipase lipolysis in group HFB (Hormone sensitive lipase HSL (Adipose triglyceride) and triglyceride hydrolase lipase, ATGL) did not change the expression level of mRNA, but HSL (P0.05) and ATGL (P0.05) protein expression levels were significantly increased. MRNA expression of 13 mitochondrial self coding genes (P 0.05 X ND2, ND4, ND4L and COX1) in HFB adipose tissue of group 4 increased significantly, and the other 3 (ND6, CYTB and ATP6) increased. Compared with group HF, the gene encoding mitochondrial uncoupling protein in the HFB group (Uncoupling protein 2, UCP2 (Uncoupling) and protein 3, UCP3), the brown fat mark gene (PR domain containing 16, PRDM16) and mitochondrial beta oxidation related genes (Peroxisomal acyl-coenzyme A oxidase 1, ACOX1) did not change the expression level the mRNA was significantly increased in the key genes regulating mitochondrial function (Peroxisome proliferator-activated receptor gamma coactivator 1-alpha, PGC1 alpha) (P 0.05) mRNA and protein expression level and protein related to mitochondrial function (Cytochrome c oxidase IV, COX4) (P 0.05) protein expression levels. In addition, the protein expression level of protein kinase A (Protein kinase A, PKA) (P 0.05) and the phosphorylation level of cyclic adenosine effect element binding protein (cAMP-response element binding protein, binding 0.05) increased significantly in group HFB. The expression level of GPR43 mRNA in adipose tissue of HFB group did not change. The protein expression level of GPR43 (P 0.05) increased significantly, and the expression level of mRNA (P 0.05) and protein (HFB) increased significantly in beta 3 adrenergic receptor (3-adrenergic receptor, AR- beta 3) and HFB group. Detection of GPR43 and AR- beta 3 by chromatin immunoprecipitation (Chromatin Immunoprecipitation, ChIP)
【學(xué)位授予單位】：南京農(nóng)業(yè)大學(xué)
【學(xué)位級(jí)別】：博士
【學(xué)位授予年份】：2016
【分類(lèi)號(hào)】：S859.7

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