西格列汀對肥胖合并非酒精性脂肪肝大鼠的代謝調節(jié)作用及機制的探討
發(fā)布時間：2018-12-30 16:27
【摘要】：目的:背景:隨著社會經(jīng)濟發(fā)展以及生活水平不斷提高生活方式的轉變,人們日常餐飲中攝入更高的熱量,且靜坐的生活方式越來越普遍,從而導致體內能量過剩、脂肪堆積。肥胖癥是指體內脂肪堆積過多和(或)分布異常、體重增加,是遺傳因素、環(huán)境因素等多種因素相互作用所引起的慢性代謝性疾病。超重和肥胖在全球流行,已經(jīng)成為嚴峻的公共衛(wèi)生危機之一。肥胖癥作為代謝綜合征的主要組分之一,與多種疾病如2型糖尿病、血脂異常、高血壓、冠心病、卒中、腫瘤等密切相關。過多的脂肪沉積在內臟器官,則造成內臟器官的脂肪樣變,最常見的為肝臟脂肪樣變,稱之為脂肪肝。脂肪樣變的肝細胞在凝血因子及白蛋白的合成方面、毒素降解、膽紅素的循環(huán)等生命活動中重要代謝過程不能順利進行,進而引發(fā)一系列代謝疾病的發(fā)生和發(fā)展。因此本文擬初步探討西格列汀對肥胖合并非酒精性脂肪肝大鼠糖脂代謝及氧化應激的影響。方法:將實驗SD大鼠隨機分為正常飲食組(ND組)、高脂飲食組,高熱量高脂飲食喂養(yǎng)高脂飲食組大鼠16周,成功構建肥胖合并非酒精性脂肪肝模型;隨機將高脂飲食組大鼠等量分至肥胖對照組(OB組)、西格列汀干預組(ST組),以上三組每組各8只。16周后西格列汀干預組大鼠予西格列汀10 mg/(kg·d)干預6周,正常飲食組及肥胖對照組予等量生理鹽水干預6周。測定各組實驗大鼠干預前后空腹血糖(FPG)、空腹血清胰島素(FINS)、血清甘油三酯(TG)及氧化應激指標血清超氧化物歧化酶(SOD)、血清丙二醛(MDA)、血清谷胱甘肽過氧化物酶(GSH-Px)的水平及干預后10%肝臟組織勻漿氧化應激指標GSH-Px、SOD、MDA及TG水平,同時計算胰島素抵抗指數(shù)(HOMA-IR);油紅O染色觀察肝臟組織病理切片脂肪樣變程度。結果:1).干預前,OB組與ST組大鼠各指標無統(tǒng)計學差異(P0.05);OB組、ST組與ND組比較各指標有統(tǒng)計學差異,ND組FPG、FINS、TG、MDA水平較低(P0.05),血清SOD、GSH-Px水平較高(P0.05)。2).干預后,ST組與ND組比較,ST組肝臟組織TG及MDA濃度升高(P0.05),FPG、FINS、血清TG、HOMA-IR、血清MDA、血清及肝臟組織中SOD、GSH-Px濃度差異無統(tǒng)計學意義(P0.05),肝臟脂肪變樣的程度升高;與OB組比較,ST組FPG、FINS、HOMA-IR、血清及肝臟組織MDA、TG濃度降低,血清及肝臟組織中GSH-Px、SOD濃度升高,差異具有統(tǒng)計學意義(P0.05),肝臟脂肪樣變的程度降低。結論:西格列汀可調節(jié)肥胖合并非酒精性脂肪肝大鼠的糖代謝和脂代謝,并降低肝臟脂肪樣變程度,可能是通過調節(jié)氧化應激反應來實現(xiàn)上述調節(jié)。
[Abstract]:Objective: with the development of social economy and the change of living style, people eat more calories in their daily meals, and the life style of sit-ins is more and more common, which leads to excess energy and fat accumulation in the body. Obesity is a chronic metabolic disease caused by excessive fat accumulation and / or abnormal distribution and weight gain in the body. It is a chronic metabolic disease caused by the interaction of genetic factors, environmental factors and other factors. Overweight and obesity have become one of the severe public health crises in the world. As one of the main components of metabolic syndrome, obesity is closely related to many diseases such as type 2 diabetes, dyslipidemia, hypertension, coronary heart disease, stroke, tumor and so on. Too much fat deposits in the visceral organs, causing the visceral organs, the most common fatty liver, called fatty liver. The important metabolic processes such as coagulation factor and albumin synthesis, toxin degradation and bilirubin circulation in lipopolysaccharide hepatocytes can not be carried out smoothly, which leads to the occurrence and development of a series of metabolic diseases. Therefore, the effect of siglitatin on glucose and lipid metabolism and oxidative stress in obese rats with non-alcoholic fatty liver was studied. Methods: the experimental SD rats were randomly divided into normal diet group (ND group), high-fat diet group, high-calorie high-fat diet group and high-fat diet group for 16 weeks. The rats in high-fat diet group were randomly divided into obese control group (OB group) and siglitatin intervention group (ST group). Normal diet group and obese control group were treated with saline for 6 weeks. Fasting blood glucose (FPG), fasting serum insulin (FINS), serum triglyceride (TG) and serum superoxide dismutase (SOD), serum malondialdehyde (MDA), were measured before and after intervention in each group of experimental rats. The level of serum glutathione peroxidase (GSH-Px) and the levels of GSH-Px,SOD,MDA and TG in 10% liver homogenate after intervention were calculated, and insulin resistance index (HOMA-IR) was calculated. Oil red O staining was used to observe the degree of fatty degeneration in pathological sections of liver. Results: 1). Before intervention, there was no statistical difference between OB group and ST group (P0.05). In OB group, ST group and ND group, the FPG,FINS,TG,MDA level was lower (P0.05) and the serum SOD,GSH-Px level was higher (P0.05). After intervention, the concentrations of TG and MDA in liver tissue of ST group were higher than those in ND group (P0.05), but there was no significant difference in FPG,FINS, serum TG,HOMA-IR, serum MDA, serum and liver tissue SOD,GSH-Px concentration (P0.05). The degree of liver fat variant was increased. Compared with OB group, the concentration of MDA,TG in serum and liver of ST group was decreased, the concentration of GSH-Px,SOD in serum and liver tissue was increased, the difference was statistically significant (P0.05), and the degree of hepatic fatty degeneration was decreased. Conclusion: siglitatin can regulate the metabolism of glucose and lipid in obese rats with non-alcoholic fatty liver and decrease the degree of hepatic fatty degeneration, which may be achieved by regulating the oxidative stress reaction.
【學位授予單位】：安徽醫(yī)科大學
【學位級別】：碩士
【學位授予年份】：2017
【分類號】：R575;R589.2
本文編號：2395824
[Abstract]:Objective: with the development of social economy and the change of living style, people eat more calories in their daily meals, and the life style of sit-ins is more and more common, which leads to excess energy and fat accumulation in the body. Obesity is a chronic metabolic disease caused by excessive fat accumulation and / or abnormal distribution and weight gain in the body. It is a chronic metabolic disease caused by the interaction of genetic factors, environmental factors and other factors. Overweight and obesity have become one of the severe public health crises in the world. As one of the main components of metabolic syndrome, obesity is closely related to many diseases such as type 2 diabetes, dyslipidemia, hypertension, coronary heart disease, stroke, tumor and so on. Too much fat deposits in the visceral organs, causing the visceral organs, the most common fatty liver, called fatty liver. The important metabolic processes such as coagulation factor and albumin synthesis, toxin degradation and bilirubin circulation in lipopolysaccharide hepatocytes can not be carried out smoothly, which leads to the occurrence and development of a series of metabolic diseases. Therefore, the effect of siglitatin on glucose and lipid metabolism and oxidative stress in obese rats with non-alcoholic fatty liver was studied. Methods: the experimental SD rats were randomly divided into normal diet group (ND group), high-fat diet group, high-calorie high-fat diet group and high-fat diet group for 16 weeks. The rats in high-fat diet group were randomly divided into obese control group (OB group) and siglitatin intervention group (ST group). Normal diet group and obese control group were treated with saline for 6 weeks. Fasting blood glucose (FPG), fasting serum insulin (FINS), serum triglyceride (TG) and serum superoxide dismutase (SOD), serum malondialdehyde (MDA), were measured before and after intervention in each group of experimental rats. The level of serum glutathione peroxidase (GSH-Px) and the levels of GSH-Px,SOD,MDA and TG in 10% liver homogenate after intervention were calculated, and insulin resistance index (HOMA-IR) was calculated. Oil red O staining was used to observe the degree of fatty degeneration in pathological sections of liver. Results: 1). Before intervention, there was no statistical difference between OB group and ST group (P0.05). In OB group, ST group and ND group, the FPG,FINS,TG,MDA level was lower (P0.05) and the serum SOD,GSH-Px level was higher (P0.05). After intervention, the concentrations of TG and MDA in liver tissue of ST group were higher than those in ND group (P0.05), but there was no significant difference in FPG,FINS, serum TG,HOMA-IR, serum MDA, serum and liver tissue SOD,GSH-Px concentration (P0.05). The degree of liver fat variant was increased. Compared with OB group, the concentration of MDA,TG in serum and liver of ST group was decreased, the concentration of GSH-Px,SOD in serum and liver tissue was increased, the difference was statistically significant (P0.05), and the degree of hepatic fatty degeneration was decreased. Conclusion: siglitatin can regulate the metabolism of glucose and lipid in obese rats with non-alcoholic fatty liver and decrease the degree of hepatic fatty degeneration, which may be achieved by regulating the oxidative stress reaction.
【學位授予單位】：安徽醫(yī)科大學
【學位級別】：碩士
【學位授予年份】：2017
【分類號】：R575;R589.2
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