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Study On The Effect And The Mechanism Of Anti-metabolic Syndrome Of β-glucan To Experimental SD Metabolic Syndrome

Posted on:2008-09-08Degree:DoctorType:Dissertation
Country:ChinaCandidate:P Y WuFull Text:PDF
GTID:1104360218958867Subject:Military Preventive Medicine
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BackgroundThe morbidity of obesity,atherogenic dyslipidemia and diabetes is increase year by year,Accompanying with the development of society economic and change of life style,These non-communicable chronicity disease are interaction. And often cluste in an individual ,which named metabolic syndrome.The cross-sectional,epidemiological study in 15540 Chinese aged 35~74yr,the morbidity of metabolic syndrome in men and women was 9.8% and 7.8%,respectively. The survey in 2048 resident aged 20~74yr in Caoyang and Huayang community in 1999~2001 in Shanghai : The morbidity of metabolic syndrome was 17.14%,A clustering of obesity,hyperglycemia,hypertension and hyperlipemia were constitute to multiplicities risk of cerebrovascular disease besides detrimenting to healthy by itself. So,the research of metabolic syndrome research is imperative to health.It was confirm that metabolic syndrome is relative to unreasonable dietary ,high fat and high sugar animal feeds can induce metabolic syndrome and accelerate proceeding,It is very important to explore functionality foods to prevention and treatment metabolic syndrome.β-glucan is a sort of glycans extracted from barley and oat. It belongs to soluble dietary fiber. Experiments have proved thatβ-glucan have anti-oxidate effectiveness. It can decrease blood lipid,decrease blood glucose,protect liver cell,facilitate the growing of intestinal beneficial bacteria. but it is still not clear thatβ-glucan prevent and treat metabolic syndrome .Our research was based on the newest researching of metabolic syndrome.,We adopted high fat and high sugar animal feeds to replicate the SD rat metabolic syndrome model,Then,we performed the experiment ofβ-glucan intervention for 4 weeks based on this model. We observed the effects ofβ-glucan to metabolic syndrome rats which includes weigh,blood lipid,fasting blood glucose,hepatic function,renal function etc. We particularly focused on the anti-oxidation and inhibition inflammatory reaction ofβ-glucan to metabolic syndrome rats. We used the real-time fluorogenetic quantitative PCR(FQ-PCR) technology to detect the regulation ofβ-glucan to the expression of TNF-αmRNA,PPAR-γmRNA of viscero-fat of metabolic syndrome rat. To study the benefit effects ofβ-glucan to experimental animal metabolic syndrome and the mechanism,which will provide a theory foundation to develop functional and health protection food to prevent and treat metabolic syndrome.Objectives1. Prepare metabolic syndrome animal model with high fat and high sugar animal feeds.2. To observe the treatment ofβ-glucan to metabolic syndrome rats.3. To explore the mechanism ofβ-glucan inhibiting metabolic syndrome.4. To provide the theory foundation to develop functional food to prevent and treat metabolic syndrome.Methods1. Animal experiments(1) Animal model setting80 male SD rat were divided into 8 groups randomly: pre-control group and post-control group,Pre-model group and post-model group,β-glucan intervention group (high,medium,lower) and Rosiglitazone treatment group.Rats in model group(includingβ-glucan intervention group and Rosiglitazone treatment group) were feed with high fat and high sugar animal feeds (10kg animal feeds including: animal fat 1.5kg,cane-sugar 2kg,cholesterin 0.25kg,bile salt 0.05kg,salt 0.5kg,additives 0.2kg,common animal feeds 5.5kg),and rats in control group were feed with common animal feeds. We perform fasting blood glucose and blood lipid randomly in the time of 4 week,6 week and 8 week to ascertain the formation of metabolic syndrome. At the end of 12 week,rats in pre-control and pre-model were execute to collection serum and fat sample to experiment. (2)Experimental methodsβ-glucan high dose group(560mg/kg.d-1),β-glucan medium dose group(280mg/kg.d-1),β-glucan lower dose group(140mg/kg.d-1),Rosiglitazone treatment group.(0.1% Rosiglitazone,4 mg/kg.d-1) ,5%β-glucan intragastric administration every day,Rats were feed with high fat and high sugar animal feeds except the rats of the post control group,The experimental took 4 week.2. Biochemistry detection(1)Biochemistry detection To observe the improve effects ofβ-glucan to obesity,blood lipid disorder,hyperglycaemia hepatic function,renal function of metabolic syndrome rats.We checked serum TG,TC,LDL-C,HDL-C,FBS,ALT,AST,Cr,UA etc. with automated biochemistry analysator (7600-020,HITACHI,Japan).(2) Determination of ant-oxidase serum SOD,MDA(3) Determination of cytokines serum TNF-α,IL-6(ELSIA)(4) mRNA expression detection The regulation effect ofβ-glucan to TNF-αmRNA ,PPAR-γmRNA and Leptin mRNA expression of viscero-fat of metabolic syndrome rats was determined with real-time fluorogenetic quantitative PCR.3. Statistical analysisAll statistical analysis was performed by using the programme statistical package for social science (SPSS) for windows version 11.5. The descriptive statistics of mean±SD and the proportion (%) of numeric values were calculated. Results1. Animal experiments(1) We successfully replicated the rat metabolic syndrome model with high fat and high sugar animal feeds.(2)β-glucan can ameliorate obesity,blood lipid disorder and hyperglycemia of metabolic syndrome rats better than those of positive control group.2. Experiments on mechanism ofβ-glucan against metabolic syndrome(1)β-glucan can inhibit serum IL-6 and TNF-αexpression.(2) The expression level of TNF-αmRNA ofβ-glucan group was significantly lower than that of post-model group.(3) The expression level of PPAR-γmRNA and Leptin mRNA ofβ-glucan group do not change comporising with that of post-model group.Conclusions1. We successfully replicated the rat metabolic syndrome model with high fat and high sugar animal feeds.2.β-glucan can treat metabolic syndrome.3. The possible mechanism ofβ-glucan to reverse metabolic syndrome maybe via ways of down regulation TNF-αmRNA expression ,inhibiting inflammation factor IL-6 and TNF-αexpression ,ameliorating the function of pancreatic island.4. Oatsβ-glucan can not regulation PPAR-γmRNA and Leptin mRNA expression.
Keywords/Search Tags:β-glucan, metabolic syndrome, TNF-αmRNA, PPAR-γmRNA, Real-time fluorogenetic quantitative PCR, insulin
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