本文選題：脂細胞 + LRP16��； 參考：《中國人民解放軍軍醫(yī)進修學院》2009年碩士論文

【摘要】： LRP16是從健康成人外周血淋巴細胞中克隆的人類基因,它在多種雌激素依賴性腫瘤中高表達。近年腫瘤組織的代謝成為研究熱點,一些促癌基因,并不一定起著促進增殖、抑制凋亡的作用,它們可能通過改變腫瘤組織的代謝模式使其適應乏氧、缺少營養(yǎng)物質(zhì)供給的環(huán)境,從而生存下去。這提示我們,促癌基因也有可能影響機體的代謝模式——目前也已有這方面的證據(jù)。另外已經(jīng)證實,一些肥胖調(diào)節(jié)基因在腫瘤發(fā)生方面起著一定的作用。因此我們假設腫瘤和肥胖可能存在“共同起源”,即某些基因的過度激活(或抑制)可能會導致同時發(fā)生腫瘤和肥胖。LRP16作為與雌激素作用相關的促癌基因,很可能在機體的營養(yǎng)物質(zhì)代謝方面也扮演一定的角色。所以本課題希望在細胞層面上證明LRP16對脂肪細胞分化、胰島素抵抗等方面有影響。 本研究共分為3部分: 一:應用基因芯片技術研究LRP16基因?qū)Τ墒熘炯毎δ苡绊懩康?探討LRP16基因?qū)Τ墒熘炯毎δ苡绊懠捌錆撛诘呐R床意義。方法:(1)經(jīng)典脂肪細胞誘導方案誘導前脂肪細胞為成熟脂肪細胞。(2)應用高通量基因芯片分析技術,通過比較高表達LRP16的成熟脂肪細胞與正常表達組差異表達的基因,分析LRP16可能涉及的信號通路和靶基因,為進一步研究確立方向。結果:實驗組與對照組間差異表達基因共有1222個,其中653個上調(diào),569個下調(diào)。其中涉及多個與脂肪分化、胰島素抵抗以及糖脂代謝相關的信號通路。結論:對脂肪細胞而言,LRP16總體的功能是促進(微)炎癥狀態(tài),對脂肪分化、胰島素抵抗以及糖脂代謝都有影響。 二:LRPl6基因可能通過促進PGC-1α的表達增強細胞的能量代謝目的與方法:通過質(zhì)粒轉染使3T3-L1脂肪細胞過表達LRP16(3T3-16)。通過油紅O染色,在顯微鏡下觀察LRP16對脂肪細胞脂滴形成的影響。使用Real-time PCR技術檢測3T3-16與3T3-3.1(對照組)兩組脂肪細胞與產(chǎn)熱有關的基因mRNA的相對表達量。結果:脂肪細胞誘導成熟后,使用油紅O染色,經(jīng)倒置顯微鏡觀察:3T3-16組細胞著色脂滴明顯少于3T3-3.1組。過表達LRP16組其過氧化物酶體增殖物激活受體共激活因子-1α、解偶聯(lián)蛋白2以及肌肉型肉毒堿棕櫚酰轉移酶1的mRNA水平表達上調(diào)。結論:LRP16可能具有使白色脂肪細胞的能量代謝向棕色脂肪細胞特性轉變的作用。三:LRP16基因?qū)χ疽蜃颖磉_的影響 目的:探討LRP16基因?qū)χ疽蜃拥挠绊憽７椒?使用Real-time PCR技術檢測兩組脂肪細胞的脂聯(lián)素和瘦素mRNA的相對表達量。結果:過表達LRP16組其脂聯(lián)素和瘦素mRNA水平表達上調(diào)。結論:LRP16基因在整體層面上可能有促進能量代謝、改善糖耐量等的作用。 結論 1.LRP16對脂肪細胞總體的效應可能是促進(微)炎癥狀態(tài),對脂肪分化、胰島素抵抗以及糖脂代謝都有影響。 2.LRP16可能具有使白色脂肪細胞的能量代謝向棕色脂肪細胞特性轉變的作用,在細胞層面上促進能量代謝。 3.LRP16基因在整體層面上可能有促進能量代謝、改善糖耐量等的作用。以上研究結果表明:LRP16在脂肪細胞的代謝方面發(fā)揮著重要的作用。
[Abstract]:LRP16 is a human gene cloned from the peripheral blood lymphocytes of healthy adults. It is highly expressed in a variety of estrogen dependent tumors. In recent years, the metabolism of tumor tissues has become a hot spot. Some of the oncogenes do not necessarily play a role in promoting proliferation and inhibiting apoptosis. They can be adapted to adapt the metabolic patterns of tumor tissues to adapt them. Hypoxia, the absence of an environment for the supply of nutrients, can survive. This suggests that the oncogene may also affect the metabolic pattern of the body - and there is now evidence for this. In addition, some obesity regulatory genes have been shown to play a role in the occurrence of cancer. "Common origin", that is, the overactivation (or inhibition) of certain genes may lead to the simultaneous occurrence of tumor and obesity.LRP16 as a oncogene associated with the role of estrogen, and is likely to play a role in the metabolism of nutrients in the body. Therefore, this topic hopes to demonstrate the differentiation of LRP16 on the adipocytes at the cellular level. There is an impact on Isle resistance.
This study is divided into 3 parts:
1: To study the effect of LRP16 gene on the function of mature adipocyte using gene chip technology: To explore the effect of LRP16 gene on the function of mature adipocytes and its potential clinical significance. Methods: (1) the preadipocyte before induction of classical adipocyte induction is mature adipocytes. (2) high throughput gene chip analysis technique, through comparison The differentially expressed genes expressed in the mature adipocytes of LRP16 and the normal expression group, analyzed the possible signal pathways and target genes that LRP16 might involve, and established the direction for further study. Results: there were 1222 differentially expressed genes between the experimental group and the control group, of which 653 were up and 569 down-regulated. Among them, many were associated with fat differentiation and insulin. Resistance and glycolipid signaling pathways. Conclusion: for adipocytes, the overall function of LRP16 is to promote (micro) inflammatory state and affect fat differentiation, insulin resistance, and glycolipid metabolism.
Two: the LRPl6 gene may enhance the energy metabolism of the cells by promoting the expression of PGC-1 A: transfection of 3T3-L1 adipocytes to LRP16 (3T3-16) through plasmid transfection. The effect of LRP16 on lipid droplet formation was observed under microscope by oil red O. Real-time PCR technique was used to detect 3T3-16 and 3T3-3.1 (control group) two. Results: the relative expression of adipocytes and heat producing gene mRNA. Results: after the adipocytes were induced to mature, the fat cells were stained with oil red O and observed by inverted microscope: the coloured lipid droplets in the 3T3-16 group were significantly less than that of the 3T3-3.1 group. The peroxisome proliferator activated receptor co activator -1 alpha, uncoupling protein 2 and muscle were expressed in the LRP16 group. The mRNA expression of botuline palmityl transferase 1 is up-regulated. Conclusion: LRP16 may have the role of energy metabolism in white adipocytes to the transformation of brown adipocytes. Three: the effect of LRP16 gene on the expression of fat factor
Objective: To investigate the effect of LRP16 gene on adipose factors. Methods: Real-time PCR technique was used to detect the relative expression of adiponectin and leptin mRNA in two groups of adipocytes. Results: the expression of adiponectin and leptin mRNA in the LRP16 group was up-regulated. Conclusion: the LRP16 gene may promote energy metabolism and improve the glucose tolerance on the whole layer. The role.
conclusion
The overall effect of 1.LRP16 on adipocytes may be to promote (micro) inflammatory state, and to affect fat differentiation, insulin resistance and glucose and lipid metabolism.
2.LRP16 may play a role in transforming the energy metabolism of white adipocytes into brown adipocytes, and promote energy metabolism at the cellular level.
The 3.LRP16 gene may have the role of promoting energy metabolism and improving glucose tolerance at the overall level. The above results show that LRP16 plays an important role in the metabolism of adipocytes.
【學位授予單位】：中國人民解放軍軍醫(yī)進修學院
【學位級別】：碩士
【學位授予年份】：2009
【分類號】：R329

【參考文獻】

相關期刊論文 前6條

1 于力,韓為東,樓方定,王全順,趙瑜,MichaelACaligiuri;新的白血病相關基因LRP16的克隆[J];軍醫(yī)進修學院學報;2000年02期

2 韓為東,樓方定,于力,韓小平,王全順,李楠,周春喜;LRP16編碼蛋白的信息學分析及亞細胞定位研究[J];軍醫(yī)進修學院學報;2002年04期

3 韓為東,于力,樓方定,王全順,趙瑜,史子江,焦宏遠,周建軍;一個新的白血病相關基因LRP16全長cDNA的克隆、序列分析及表達特征[J];中國生物化學與分子生物學報;2001年02期

4 苗艷君;石建華;項平;;解偶聯(lián)蛋白與能量代謝[J];實用全科醫(yī)學;2007年05期

5 韓為東,母義明,盧學春,徐周敏,李續(xù)建,于力,宋海靜,李明,陸菊明,潘長玉;雌激素通過其受體α上調(diào)LRP16 mRNA表達并促進MCF-7細胞增殖[J];中華內(nèi)分泌代謝雜志;2004年02期

6 周麗斌;陳名道;;脂肪因子和代謝綜合征[J];中國醫(yī)學科學院學報;2006年06期

，

本文編號：1949276