[ 摘要 ]

本研究目的探討肥胖症與瘦素 (LEP)、瘦素受體 (LEPR)、胰島素誘導基因 (INSIG2) 之單核?˙霰亄坐峖撗M瘦素濃度、生活型態、共病症之相關性。研究對象為參與2007年信義鄉與中西區衛生所舉辦之成人健檢民眾，共691人，肥胖組 (BMI ≥ 27)有221人 (32%)，非肥胖組 (BMI < 27)有470人 (68%)，同時收集血液與基本人口學資料，其後利用結構式問卷進行訪視，內容包含詳細人口學資料、疾病史與生活型態資料，訪視率為59%。



結果顯示非肥胖組與肥胖組中年齡中位數各為57歲與55歲，非原住民肥胖盛行率為17.7%而原住民肥胖盛行率為58.8%。肥胖組的收縮壓、舒張壓、三酸甘油脂、尿酸及瘦素濃度皆高於非肥胖組，高密度脂蛋白膽固醇在肥胖組中則比非肥胖組低。三個肥胖易感性基因之基因型頻率經適合度檢定後皆符合哈溫定律。利用羅吉斯迴歸調整人口學變項與生化值異常等干擾因子後發現INSIG2 rs7566605單核?˙霰亄坐W帶有GC基因型與CC基因型者其肥胖的勝算相較於GG基因型者分別為0.62倍 (95% CI: 0.40-0.94) 及0.46倍 (95% CI: 0.24-0.82)，而瘦素濃度過高者 (男性 ≥ 7.85 ng/ml，女性 ≥ 21.98 ng/ml) 其肥胖的風險瘦素正常者的4.39倍 (95% CI: 2.76-6.99)，在生活習慣方面調整干擾因子後無規律運動習慣者肥胖風險為有規律運動者的3.14倍 (95% CI: 1.63-6.05)。使用卡方檢定檢定肥胖與共病症的關係發現肥胖組比非肥胖組具有較高罹患高血壓、三酸甘油脂過高、高密度脂蛋白膽固醇過低、糖尿病與高尿酸血症 (含痛風) 的風險，以上敘述均具有統計上顯著意義。



本研究中只有INSIG2 rs7566605單核?˙藻h形性與肥胖症有相關性存在，而肥胖組發生高血壓、三酸甘油脂、糖尿病等共病症的風險較高，且具有較不健康的生活型態。



[ 英文摘要 ]

The aim of our study was to investigate the relationships between the genotypes of LEP G-2548A, LEPR rs1137100 and INSIG2 rs7566605 and serum leptin concentration, lifestyle habits and other comorbidities (such as high blood pressure and diabetes) in the obesity. The residents in Hsin-I township of Nantou County and in the central-western district of Taichung City participating in the National Adult Health Examination Project in Year 2007 were recruited as the study subjects. Among the 691 participants, those with the BMI ≥ 27 (32%) were classified as obese and the remainders (68%) with the from all participants BMI<27 were non-obese. We collected the fasting blood samples and questionnaire for the information of baseline demographic characteristics. We later interviewed structured questionnaires for additional information on demography characteristics, history of diseases and lifestyles, about 59% response.

Our results showed the median ages were 57years in non-obese and 55years in obese, with the prevalence of obesity lower in non-aborigines than in aborigines (17.7% vs. 58.8%). The obese subjects had higher systolic blood pressure, diastolic blood pressure, triglyceride, uric acid and serum leptin than non-obese, but lower HDL, compared with non-obese. The genotypes of the three single nucleotide polymorphisms (SNPs) were confirmed with Hardy-Weinberg equilibrium. After adjustment of confounding factors, results of mutiple logistic regression analyses revealed decreased risks for obesity in INSIG2 rs7566605 CC genotype and CG genotype than GG genotype (OR = 0.62; 95% CI: 0.40-0.94 and OR = 0.46; 95% CI:0.24-0.82), respectively. The odds of obesity was increased among those with high leptin (leptin ≥ 7.85 ng/ml for men, leptin ≥ 21.95 ng/ml for women) (OR = 4.39, 95% CI: 2.76-6.99).As of lifestyles, the risk of obesity was also increased due to no regular exercise (OR = 3.14, 95% CI:1.63-6.15). Using χ2-test, we estimated the association between obesity and comorbidities, and found that the risks for hypertension, hypertriglyceridemia, lower-HDL, diabetes and hyperuricemia (include gout) were significantly higher in the obese than in the non-obese.

This study found that only the INSIG2 polymorphism was significantly associated with obesity in LEP, LEPR and INSIG2. The obese had a higher risk of comobidites (such as hypertension, hypertriglyceridemia, diabetes etc.) and they had unhealthy lifestyles.