本文選題：Ghrelin + 脂聯(lián)素�。� 參考：《吉林大學(xué)》2010年碩士論文

【摘要】： 目的:探討外周血清中Ghrelin、脂聯(lián)素、炎性細(xì)胞因子與非酒精性脂肪性肝病及糖脂代謝障礙的關(guān)系及臨床意義。方法:采用酶聯(lián)免疫吸附實(shí)驗(yàn)(ELISA)方法檢測對照組及實(shí)驗(yàn)組患者血漿中Ghrelin、脂聯(lián)素、空腹胰島素及TNF-α水平。結(jié)果:Ghrelin及脂聯(lián)素在所有實(shí)驗(yàn)組中表達(dá)均較對照組明顯減低,差異均有統(tǒng)計(jì)學(xué)意義(P0.01);其中,Ghrelin及脂聯(lián)素表達(dá)在脂肪性肝炎組、脂肪肝合并IGT組以及脂肪肝合并血脂異常組間無顯著意義(P0.05),但三組均較單純性脂肪肝組減低,差異具有顯著性意義(P0.05)。與之相反,TNF-a在各實(shí)驗(yàn)組均較對照組表達(dá)明顯增高(P0.01);在脂肪性肝炎組、脂肪肝合并IGT組以及脂肪肝合并血脂異常組間無顯著意義(P0.05);但三組均較單純性脂肪肝組升高,差異具有顯著性意義(P0.05)。所有實(shí)驗(yàn)組中患者BMI及HOMA-IR較健康對照組均升高,差異具有顯著性意義(P0.01)。脂肪肝合并糖耐量減低組中HOMA-IR高于單純性脂肪肝組、脂肪性肝炎組及脂肪肝合并血脂異常組,差異具有顯著性意義(P0.05)。HOMA-IR在單純性脂肪肝組、脂肪性肝炎組及脂肪肝合并血脂異常組中無明顯差異(P0.05)。在4個(gè)實(shí)驗(yàn)組中,以脂聯(lián)素為因變量,以Ghrelin、TNF-α、BMI和HOMA-IR為自變量行多元逐步回歸分析,均發(fā)現(xiàn)脂聯(lián)素與TNF-α、BMI和HOMA-IR呈負(fù)相關(guān),與Ghrelin呈正相關(guān)。結(jié)論:在NAFLD及代謝綜合征發(fā)生發(fā)展中,由多種因素共同參與,尤其是始動(dòng)因素胰島素抵抗在發(fā)病機(jī)制中起了重要作用。Ghrelin及脂聯(lián)素在患者外周血明顯降低,這與胰島素抵抗密切相關(guān)。TNF-α與脂聯(lián)素同為脂肪因子,結(jié)構(gòu)相似,但作用相反,互相拮抗。TNF-α作為炎性細(xì)胞因子加重胰島素抵抗。本次研究的創(chuàng)新之處就是同時(shí)探討脂聯(lián)素及Ghrelin在不同NAFLD患者中的變化和意義,以及脂聯(lián)素在同一疾病組與其它細(xì)胞因子的相關(guān)性。研究體內(nèi)這些細(xì)胞因子失衡為設(shè)想通過增加內(nèi)源性Ghrelin表達(dá)、上調(diào)脂聯(lián)素受體、加強(qiáng)外源性Ghrelin干預(yù)、開發(fā)脂聯(lián)素受體激動(dòng)劑及增強(qiáng)Ghretin敏感性等手段,從而改善抗炎細(xì)胞因子在病理狀態(tài)下表達(dá)失衡,充分發(fā)揮各種細(xì)胞因子的生物學(xué)活性來達(dá)到治療目的,這具有深遠(yuǎn)的臨床意義。
[Abstract]:Objective: to investigate the relationship between ghrelin, adiponectin, inflammatory cytokines in peripheral serum and nonalcoholic fatty liver disease and impaired glucose and lipid metabolism. Methods: the levels of ghrelin, adiponectin, fasting insulin and TNF- 偽 in plasma of patients in control group and experimental group were detected by enzyme linked immunosorbent assay (Elisa). Results the expression of w ghrelin and adiponectin in all the experimental groups was significantly lower than that in the control group, and the difference was statistically significant (P 0.01), and the expression of ghrelin and adiponectin in the adipose hepatitis group was significantly lower than that in the control group. There was no significant difference between fatty liver with IGT and fatty liver with dyslipidemia, but the three groups were lower than simple fatty liver group (P 0.05). On the contrary, the expression of TNF-a in each experimental group was significantly higher than that in the control group, while in the fatty hepatitis group, there was no significant difference between the fatty liver combined with IGT group and the fatty liver combined with dyslipidemia group, but the expression of TNF-a in the three groups was higher than that in the simple fatty liver group. The difference was significant (P 0.05). The levels of BMI and HOMA-IR in all the experimental groups were higher than those in the healthy control group, and the difference was significant (P 0.01). The HOMA-IR in fatty liver with impaired glucose tolerance group was higher than that in simple fatty liver group, fatty hepatitis group and fatty liver complicated with abnormal blood lipid group, the difference was significant (P 0.05). HOMA-IR was significantly different in simple fatty liver group. There was no significant difference between fatty hepatitis group and fatty liver with dyslipidemia group (P 0.05). In four experimental groups, adiponectin was used as dependent variable, and HOMA-IR and TNF- 偽 BMI were used as independent variables for stepwise regression analysis. It was found that adiponectin was negatively correlated with TNF- 偽 BMI and HOMA-IR, and positively correlated with Ghrelin. Conclusion: in the development of NAFLD and metabolic syndrome, many factors are involved, especially the initiation factor insulin resistance plays an important role in the pathogenesis. Ghrelin and adiponectin are significantly decreased in the peripheral blood of the patients. This is closely related to insulin resistance. TNF- 偽 and adiponectin are both adiponectin and adiponectin, the structure is similar, but the opposite effect, mutual antagonism. TNF- 偽 as an inflammatory cytokine exacerbates insulin resistance. The innovation of this study is to explore the changes and significance of adiponectin and Ghrelin in different NAFLD patients and the correlation between adiponectin and other cytokines in the same disease group. The study of these cytokines imbalance in vivo is supposed to increase endogenous Ghrelin expression, up-regulate adiponectin receptor, enhance exogenous Ghrelin intervention, develop adiponectin receptor agonists and enhance Ghretin sensitivity, etc. It is of profound clinical significance to improve the imbalance of the expression of anti-inflammatory cytokines in the pathological state and to give full play to the biological activities of various cytokines to achieve the therapeutic purpose.
【學(xué)位授予單位】：吉林大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2010
【分類號(hào)】：R363

【參考文獻(xiàn)】

相關(guān)期刊論文 前2條

1 ;非酒精性脂肪性肝病診療指南[J];中華肝臟病雜志;2006年03期

2 梁曉萍;韓全水;文錦麗;林小蘭;楊夏敏;李嵐;;超重和肥胖人群血清脂聯(lián)素水平與2型糖尿病的關(guān)系[J];中國糖尿病雜志;2006年05期

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本文編號(hào)：1908963