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研究生:張美玲
研究生(外文):Mei-Ling Chang
論文名稱:信義鄉鄉民肥胖症之共病症及PPARγ2基因型的探討
論文名稱(外文):The study of co-morbidity and peroxisome proliferator activated receptor γ2 (PPARγ2) genotype of obesity in Hsin-Yi country
指導教授:吳芳鴦
指導教授(外文):Fang-Yang Wu
學位類別:碩士
校院名稱:中國醫藥學院
系所名稱:環境醫學研究所
學門:醫藥衛生學門
學類:公共衛生學類
論文種類:學術論文
論文出版年:2003
畢業學年度:91
語文別:中文
論文頁數:85
中文關鍵詞:PPARγ2BMI值肥胖症共病症原住民
外文關鍵詞:PPARγ2BMI valueobesityco-morbidityaborigine
相關次數:
  • 被引用被引用:9
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  • 下載下載:88
  • 收藏至我的研究室書目清單書目收藏:4
本研究的目的是在探討(1)原住民與非原住民之肥胖與其共病症有無差異;(2)不同種族之PPARγ2基因對肥胖及高血脂的影響;(3)PPARγ2基因(P12和P115)與肥胖程度有無相關。研究對象是從2002年接受南投縣信義鄉成人健檢之民眾中,按肥胖分層後,隨機選取肥胖組(BMI≧27者)333人,及非肥胖組(BMI<27者)438人。
生理生化值之比較分析顯示BMI值、三酸甘油酯、尿酸、GOT、GPT值,不論男女性原住民均比非原住民高。其中,男女性原住民之BMI值各為26.8±3.7與26.8±4.4 kg/m2,接近肥胖。三酸甘油酯、GOT、GPT值只有男性原住民超過正常值,而尿酸則不論是男女性原住民均超過正常值。以有無肥胖分組比較生理生化值,顯示BMI值、三酸甘油酯、收縮壓、舒張壓與尿酸都具有統計上的顯著差異。
以P12基因型分析,全體研究對象之P12P野生型與P12A變異型之頻率分布各為93.4%與6.6%;而Pro與Ala對偶基因頻率則各為0.936與0.064。若將全體研究對象分為非肥胖與肥胖,或以種族分為原住民與非原住民,其基因型與對偶基因頻率分布均類似於全體研究對象之頻率。以上以χ2-檢定及適合度檢定,都無統計上的顯著差異。另外,在P115基因型,全體均為P115P野生型,未發現P115G變異型。
以肥胖症有無分組之邏輯斯回歸分析顯示年齡越大者肥胖比例有漸減之趨勢;有肥胖症且天天吸菸者的OR值為沒有者的0.6倍;有高血脂症、糖尿病、高血壓及高尿酸血症且有肥胖症的OR值各為正常者的1.45、1.6、1.45及1.72倍,經多變項邏輯斯回歸分析後,與肥胖症有關的因子有
年齡、抽煙習慣、糖尿病、高血壓與高尿酸血症。若將非肥胖組改為瘦子組(BMI<24),以邏輯斯回歸分析與肥胖症相關因子,除了上述的相關因子外,尚多了高血脂變項,且以上均具有統計意義。
結論:本研究顯示肥胖症之共病症有高尿酸血症、痛風、高膽固醇血症及肝功能異常,且具有明顯的種族差異。而PPARγ2之P12基因型與對偶基因頻率的分布,不論是在原住民或非原住民並沒有發現差異,與肥胖症也不具有相關。此外,肥胖組雖然具有較高的三酸甘油酯且其值接近異常值邊緣,但P12基因對於血清膽固醇與三酸甘油酯的濃度並沒有產生影響。
The purpose of this study were to explore:(1) If obesity and co morbidity had difference between aborigines and non- aborigines. (2) If the influence of PPARγ2 to obesity and hyperlipemia differed from race to race. (3) If there was difference between PPARγ2(P12 and P115) and the level of obesity. The subjects of this study were aimed at the grown-ups that had their checkups in Hisn-Yi Country, Nan-tou County in 2002. A number of 333 people were randomly selected for the obesity group (BMI ≥ 27) and a number of 438 people were chosen for the non-obesity group (BMI < 27).
For the comparison and analysis of biochemical values, aborigines of both genders had higher values of BMI, triglyceride, uric acid, GOT and GPT than non-aborigines. BMI values of male and female aborigines were 26.8±3.7 and 26.8±4.4 kg/m2 respectively, which were close to obesity. Only male aborigines had higher triglyceride, GOT and GPT values than normal; however, uric acid was beyond normal for both genders of aborigines. If biochemical values were compared for obesity and non-obesity groups, BMI, triglyceride, systolic pressure, diastolic pressure and uric acid values varied significantly and statistically.
For P12 genotype analysis, the frequency distribution of P12F wild type and P12A variant type was 93.4% and 6.6% respectively and allele frequency for Pro and Ala was 0.936 and 0.064. When subjects of this study were divided into obesity and non-obesity groups or aborigines and non-aborigines, distribution of genotype and allele frequency were similar to the frequency of the subjects of this study as a whole. X2 test and Goodness of fit test were conducted for the above values and there was no statistical significant difference. Besides, for P115 genotype, all of them belonged to P115P wild type homogeneous zygotes,no P115G variant type heterogeneous zygotes were found.
According to the Logisitic regression analysis conducted for obesity and non-obesity groups, older people had a decreasing tendency of obesity. Daily smokers with obesity had a higher OR value than non-smokers by 0.6 time. Obese people had higher OR values of hyperlipemia, diabetes, high blood pressure and hyperuricemia than normal people by 1.45, 1.6, 1.45 and 1.72 times. After conducting multivariate regressive analysis, it was found that factors related to obesity included age, smoking habit, diabetes, high blood pressure and hyperuricemia. If we changed the non-obesity group to the slender group (BMI < 24) and conducted Logisitic regression analysis, two more factors related to obesity were added, which were drinking habit and hyperlipemia,and they were statistically significant.
Conclusion: This study showed the co-morbidity of obesity were hyperuricemia, gout, hypercholesterolemia and liver dysfunction. All of them were significant different from race to race. However, there was no difference of PPARγ2 and allele frequency distribution between aborigines and non-aborigines, and it was not associated with obesity, either. Furthermore, though triglyceride value of the obesity group was higher and closer to abnormality, PPARγ2 gene did not impose any impact upon serum cholesterol and the consistency of triglyceride.
•中文摘要…………………………………………………………………I
•英文摘要…………………………………………………………………III
•目錄………………………………………………………………………Ⅵ
•表、圖 目 錄……………………………………………………………IX
•第壹章、前言
•第一節、研究動機………………………………………………………1
•第二節、研究目的………………………………………………………3
•第貳章、文獻探討
•第一節、肥胖……………………………………………………………4
•一、脂肪細胞的簡介……………………………………………………4
•二、肥胖的分期…………………………………………………………5
•三、肥胖的盛行率………………………………………………………8
•四、肥胖對健康的危害…………………………………………………9
•五、造成肥胖的後天因素………………………………………………12
•第二節、造成肥胖的先天基因…………………………………………14
•一、肥胖的遺傳研究……………………………………………………14
•二、與肥胖有關的單基因突變…………………………………………15
•三、決定脂肪細胞分化的轉錄因子……………………………………17
•四、過氧化體增殖劑活化接受器(Peroxisome Proliferator-activated Receptors ,PPARs )………………………………………17
•第三節、過氧化體增生劑活化受體γ(peroxisome proliferator-activated receptorγ,PPARγ)…………………………………………20
•一、PPARγ的簡介……………………………………………………….20
•二、PPARγ的在生物學上的研究……………………………………….21
•三、PPARγ的三種亞型………………………………………………….22
•四、PPARγ2的簡介………………………………………………………23
•五、數種已被鑑定的PPARγ2變異………………………………………24
•第四節、Pro12Ala及P115Gln變異…………………………………….26
•一、Pro12Ala在各種族的發生率………………………………………26
•二、Pro12Ala變異與BMI及血脂的關係……………………………….26
•三、Pro12Ala變異與糖尿病II型,胰島素敏感度的關係……………27
•四、P115Gln變異的發生率及功能…………………………………….28
•第參章、材料與方法
•第一節、研究對象………………………………………………………29
•第二節、研究方法………………………………………………………29
•一、問卷…………………………………………………………………29
•二、血液檢查……………………………………………………………29
•三、PPARγ2 多型性基因之測定……………………………………….30
•第三節、變項分類及名詞定義…………………………………………36
•第四節、統計方法………………………………………………………37
•第五節、使用材料及儀器………………………………………………38
•第肆章、結果……………………………………………………………41
•第伍章、討論……………………………………………………………46
•第陸章、結論……………………………………………………………53
•重要專門詞彙集…………………………………………………………54
•參考文獻…………………………………………………………………55
•圖表………………………………………………………………………68
附錄一、PPARγ基因位置圖………………………………………………77
附錄二、PPARγ2-P12基因型哈溫平衡定律之檢定…………………….78
附錄三、原住民PPARγ2-P12基因型哈溫平衡定律之檢定…………….78
附錄四、非原住民PPARγ2-P12基因型哈溫平衡定律之檢定………….78
附錄五、肥胖與相關因子之單變項與多變項邏輯斯迴歸分析……….79
附錄六、信義鄉原住民與非原住民之基本特徵、生活習慣
及慢性病………………………………………………………………….80
附錄七、信義鄉成人健康檢查問卷調查表…………………………….81
表 目 錄
表一、研究對象與89年底信義鄉居民及89年成人健檢之人口學特徵比較………………………………………………………………………….68
表二、研究對象之基本特徵…………………………………………….69
表三、研究對象之疾病特徵…………………………………………….70
表四、研究對象之生理、生化值之比較……………………………….71
表五、肥胖症患者與非肥胖症患者之生理、生化值比較…………….71
表六、PPARγ2-P12基因型與對偶基因頻率分佈……………………….72
表七、肥胖症與相關因子之單變項與多變項邏輯斯回歸分析……….73
表八、瘦子組及肥胖組與相關因子之單變項與多變項邏輯斯回歸
分析……………………………………………………………………….74
表九、PPARγ2 - P12基因型與生理生化值及疾病之比較…………….75
圖 目 錄
圖一、肥胖症與其併發症之關連圖…………………………………….76
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