NAFLD外周血Ghrelin、脂联素与炎性细胞因子变化的临床意义

发布时间：2018-05-19 05:54

本文选题：Ghrelin + 脂联素　；参考：《吉林大学》2010年硕士论文

【摘要】： 目的:探讨外周血清中Ghrelin、脂联素、炎性细胞因子与非酒精性脂肪性肝病及糖脂代谢障碍的关系及临床意义。方法:采用酶联免疫吸附实验(ELISA)方法检测对照组及实验组患者血浆中Ghrelin、脂联素、空腹胰岛素及TNF-α水平。结果:Ghrelin及脂联素在所有实验组中表达均较对照组明显减低,差异均有统计学意义(P0.01);其中,Ghrelin及脂联素表达在脂肪性肝炎组、脂肪肝合并IGT组以及脂肪肝合并血脂异常组间无显著意义(P0.05),但三组均较单纯性脂肪肝组减低,差异具有显著性意义(P0.05)。与之相反,TNF-a在各实验组均较对照组表达明显增高(P0.01);在脂肪性肝炎组、脂肪肝合并IGT组以及脂肪肝合并血脂异常组间无显著意义(P0.05);但三组均较单纯性脂肪肝组升高,差异具有显著性意义(P0.05)。所有实验组中患者BMI及HOMA-IR较健康对照组均升高,差异具有显著性意义(P0.01)。脂肪肝合并糖耐量减低组中HOMA-IR高于单纯性脂肪肝组、脂肪性肝炎组及脂肪肝合并血脂异常组,差异具有显著性意义(P0.05)。HOMA-IR在单纯性脂肪肝组、脂肪性肝炎组及脂肪肝合并血脂异常组中无明显差异(P0.05)。在4个实验组中,以脂联素为因变量,以Ghrelin、TNF-α、BMI和HOMA-IR为自变量行多元逐步回归分析,均发现脂联素与TNF-α、BMI和HOMA-IR呈负相关,与Ghrelin呈正相关。结论:在NAFLD及代谢综合征发生发展中,由多种因素共同参与,尤其是始动因素胰岛素抵抗在发病机制中起了重要作用。Ghrelin及脂联素在患者外周血明显降低,这与胰岛素抵抗密切相关。TNF-α与脂联素同为脂肪因子,结构相似,但作用相反,互相拮抗。TNF-α作为炎性细胞因子加重胰岛素抵抗。本次研究的创新之处就是同时探讨脂联素及Ghrelin在不同NAFLD患者中的变化和意义,以及脂联素在同一疾病组与其它细胞因子的相关性。研究体内这些细胞因子失衡为设想通过增加内源性Ghrelin表达、上调脂联素受体、加强外源性Ghrelin干预、开发脂联素受体激动剂及增强Ghretin敏感性等手段,从而改善抗炎细胞因子在病理状态下表达失衡,充分发挥各种细胞因子的生物学活性来达到治疗目的,这具有深远的临床意义。
[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- 伪 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- 伪 BMI were used as independent variables for stepwise regression analysis. It was found that adiponectin was negatively correlated with TNF- 伪 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- 伪 and adiponectin are both adiponectin and adiponectin, the structure is similar, but the opposite effect, mutual antagonism. TNF- 伪 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.
【学位授予单位】：吉林大学
【学位级别】：硕士
【学位授予年份】：2010
【分类号】：R363

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