本文選題：CLA + Leptin�。� 參考：《河南農(nóng)業(yè)大學(xué)》2015年碩士論文

【摘要】：瘦素(Leptin)是由脂肪細胞分泌的一種蛋白質(zhì)激素,可以減少能量的攝入,增加能量的消耗。Leptin通過與其受體結(jié)合,通過信號轉(zhuǎn)導(dǎo)發(fā)揮生理學(xué)作用。本實驗以CLA誘導(dǎo)的代謝障礙的小鼠為模型,采取免疫組織化學(xué)的手段研究Leptin干預(yù)動物肝臟代謝相關(guān)基因表達的變化。在飼料中添加CLA后,成功誘導(dǎo)出高血糖、高血脂、脂肪肝等代謝障礙指標。實驗分為對照組亞油酸組(LA組)和實驗組亞油酸組實驗對照組CLA+生理鹽水組(CLA+S)、實驗組CLA+瘦素組(CLA+L)。昆明小鼠在21d斷奶后,開始飼喂添加LA和CLA的鼠糧,飼喂42d后,LA組不做處理,CLA+S組背部皮下加生理鹽水緩釋泵,CLA+L組背部皮下加Leptin(1mg/mL)緩釋泵,作用14d后,取肝臟后做免疫組化試驗。結(jié)果顯示,CLA組小鼠與LA組相比,與糖代謝相關(guān)的Akt、p-AKT、FOXO1的表達量下調(diào),而在CLA+L組,Akt、p-AKT、FOXO1的表達量上調(diào)。由此可知,CLA對這幾個基因表達有所抑制,使胰島素信號通路不能順利的傳導(dǎo),從而出現(xiàn)高血糖和胰島素抵抗的現(xiàn)象。CLA+L組與CLA+S相比,這些基因的表達升高,說明瘦素可以調(diào)節(jié)這些基因的表達從而改善體內(nèi)的糖代謝紊亂。瘦素可以促進胰島素下游信號的傳遞與表達而發(fā)揮調(diào)節(jié)糖代謝的作用。瘦素通過與其受體結(jié)合,通路下游的p-STAT3,CLA+L組與CLA+S相比表達量顯著升高(p0.05),瘦素信號通路信號轉(zhuǎn)導(dǎo)加強。在糖異生方面起重要作用的關(guān)鍵酶G-6-Pase,CLA+S組與LA組相比,表達量顯著下降(p0.05),糖異生活動減弱;CLA+L組與CLA+S組相比,表達量顯著升高(p0.05),糖異生活動增強。脂代謝方面,CLA+S組與LA組相比,CLA+S組SRB1的表達顯著降低(p0.05),CD36的表達顯著升高(p0.05)。表明CLA可以降低SRB1的表達同時可以上調(diào)CD36的表達。推測SRB1參與的膽固的逆轉(zhuǎn)運活動增強,CD36表達量的升高,使長鏈脂肪酸的攝入增加,在肝臟內(nèi)堆積從而形成脂肪肝。CLA+L組與CLA+S組相比,SRB1的表達顯著升高(p0.05),下調(diào)CD36的表達。說明,SRB1參與的膽固的逆轉(zhuǎn)運活動減弱,CD36介導(dǎo)的長鏈脂肪酸的攝入減少。
[Abstract]:Leptin (leptin) is a protein hormone secreted by adipocytes, which can reduce energy intake and increase energy consumption. Leptin plays a physiological role by binding to its receptor and signal transduction. In this study, CLA induced metabolic disorders in mice were used as a model to study the changes of gene expression related to liver metabolism induced by Leptin by immunohistochemical method. Hyperglycemia, hyperlipidemia, fatty liver and other metabolic disorders were successfully induced by adding CLA to feed. The experiment was divided into two groups: control group, linoleic acid group (LA group), experimental group linoleic acid group (experimental control group, CLA normal saline group) and experimental group CLA leptin group. After 21 days weaning, Kunming mice were fed with the diet supplemented with LA and CLA. After 42 days, the rats in the LA group were not treated with hypodermic saline sustained release pump on the back of the CLA group. The mice in the CLAL group were subcutaneously supplemented with Leptin 1 mg / mL. After 14 days of treatment, the mice in the control group were treated with Leptin 1 mg / mL. The liver was taken for immunohistochemistry. The results showed that compared with LA group, the expression of Akttip-AKTnFOXO1 was down-regulated in the CLA L group, but up-regulated in the CLA L group. Therefore, the expression of these genes was inhibited and the insulin signaling pathway could not be transduced smoothly. The expression of these genes in CLA-L group was higher than that in CLA S group, which resulted in hyperglycemia and insulin resistance. Leptin can regulate the expression of these genes and improve the disorder of glucose metabolism in the body. Leptin can promote the transduction and expression of insulin downstream signal and regulate glucose metabolism. By binding to its receptor, the expression of p-STAT3CLAL in the downstream of the pathway was significantly higher than that of CLA S, and the signal transduction of leptin signaling pathway was enhanced. Compared with LA group, the expression of G-6-Pasea-CLA group, the key enzyme that plays an important role in glucose heterogenesis, decreased significantly (p 0.05). The expression level of glucose heterozygosity in CLA L group was significantly higher than that in CLA S group, and that in glucose heterozygosity group was higher than that in CLA S group. In terms of lipid metabolism, the expression of SRB1 in CLAs group was significantly lower than that in LA group. The results showed that CLA could decrease the expression of SRB1 and up-regulate the expression of CD36. It was speculated that the reverse transport of gallbladder solid involved in SRB1 increased the expression of CD36, increased the intake of long chain fatty acids, accumulated in liver and formed fatty liver. Compared with CLA S group, the expression of SRB1 B1 increased significantly, and the expression of CD36 was down-regulated. It indicated that SRB1 involved in reverse transport of bile and solid decreased the intake of long chain fatty acids mediated by CD36.
【學(xué)位授予單位】：河南農(nóng)業(yè)大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2015
【分類號】：S852.2

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