医学综述
醫學綜述
의학종술
MEDICAL RECAPITULATE
2014年
23期
4382-4384
,共3页
李弘磊%周玲%杨涛%范红旗
李弘磊%週玲%楊濤%範紅旂
리홍뢰%주령%양도%범홍기
肥胖%胰岛素抵抗%代谢综合征%非酯化脂肪酸
肥胖%胰島素牴抗%代謝綜閤徵%非酯化脂肪痠
비반%이도소저항%대사종합정%비지화지방산
Obesity%Insulin resistance%Metabolic syndrome%Non-esterified fatty acids
目的:研究肥胖对糖脂代谢及血压的影响,并探讨其病理生理学机制。方法选取2009年4月至2012年3月在南京市大厂医院体检中心进行健康体检的肥胖患者31例作为肥胖组,33例超重患者为超重组,37例健康人作为对照组。分别测定三组研究对象的空腹血糖( FPG)、空腹胰岛素(FINS)、总胆固醇(TC)、三酰甘油(TG)、高密度脂蛋白胆固醇(HDL-C)、尿酸(UA)、收缩压(SBP)、舒张压(DBP)、身高及体质量,计算胰岛素抵抗指数(HOMA-IR)、β细胞分泌功能指数(HO-MA-β)和体质量指数( BMI),对各组数据进行比较。结果三组研究对象的 FPG、FINS、HOMA-IR、UA、TC、TG、HDL-C及SBP、DBP比较,差异有统计学意义(P<0.05),HOMA-β比较差异无统计学意义(P>0.05);肥胖组与超重组的FINS、HOMA-IR、TG、UA均显著高于对照组(P<0.01),HDL-C 则显著低于对照组(P<0.01);肥胖组FPG、TC、SBP、DBP 显著高于对照组(P <0.05),而超重组的与对照组比较无统计学意义(P>0.05);肥胖组FINS、HOMA-IR、TG、UA 显著高于超重组(P<0.05或P<0.01),HDL-C则显著低于超重组(P<0.01),两组 FPG、TC、SBP、DBP 比较无统计学意义(P >0.05)。结论肥胖可导致胰岛素抵抗,其病理生理机制促进了代谢综合征其他组分,如血糖、血脂及血压的进展。
目的:研究肥胖對糖脂代謝及血壓的影響,併探討其病理生理學機製。方法選取2009年4月至2012年3月在南京市大廠醫院體檢中心進行健康體檢的肥胖患者31例作為肥胖組,33例超重患者為超重組,37例健康人作為對照組。分彆測定三組研究對象的空腹血糖( FPG)、空腹胰島素(FINS)、總膽固醇(TC)、三酰甘油(TG)、高密度脂蛋白膽固醇(HDL-C)、尿痠(UA)、收縮壓(SBP)、舒張壓(DBP)、身高及體質量,計算胰島素牴抗指數(HOMA-IR)、β細胞分泌功能指數(HO-MA-β)和體質量指數( BMI),對各組數據進行比較。結果三組研究對象的 FPG、FINS、HOMA-IR、UA、TC、TG、HDL-C及SBP、DBP比較,差異有統計學意義(P<0.05),HOMA-β比較差異無統計學意義(P>0.05);肥胖組與超重組的FINS、HOMA-IR、TG、UA均顯著高于對照組(P<0.01),HDL-C 則顯著低于對照組(P<0.01);肥胖組FPG、TC、SBP、DBP 顯著高于對照組(P <0.05),而超重組的與對照組比較無統計學意義(P>0.05);肥胖組FINS、HOMA-IR、TG、UA 顯著高于超重組(P<0.05或P<0.01),HDL-C則顯著低于超重組(P<0.01),兩組 FPG、TC、SBP、DBP 比較無統計學意義(P >0.05)。結論肥胖可導緻胰島素牴抗,其病理生理機製促進瞭代謝綜閤徵其他組分,如血糖、血脂及血壓的進展。
목적:연구비반대당지대사급혈압적영향,병탐토기병리생이학궤제。방법선취2009년4월지2012년3월재남경시대엄의원체검중심진행건강체검적비반환자31례작위비반조,33례초중환자위초중조,37례건강인작위대조조。분별측정삼조연구대상적공복혈당( FPG)、공복이도소(FINS)、총담고순(TC)、삼선감유(TG)、고밀도지단백담고순(HDL-C)、뇨산(UA)、수축압(SBP)、서장압(DBP)、신고급체질량,계산이도소저항지수(HOMA-IR)、β세포분비공능지수(HO-MA-β)화체질량지수( BMI),대각조수거진행비교。결과삼조연구대상적 FPG、FINS、HOMA-IR、UA、TC、TG、HDL-C급SBP、DBP비교,차이유통계학의의(P<0.05),HOMA-β비교차이무통계학의의(P>0.05);비반조여초중조적FINS、HOMA-IR、TG、UA균현저고우대조조(P<0.01),HDL-C 칙현저저우대조조(P<0.01);비반조FPG、TC、SBP、DBP 현저고우대조조(P <0.05),이초중조적여대조조비교무통계학의의(P>0.05);비반조FINS、HOMA-IR、TG、UA 현저고우초중조(P<0.05혹P<0.01),HDL-C칙현저저우초중조(P<0.01),량조 FPG、TC、SBP、DBP 비교무통계학의의(P >0.05)。결론비반가도치이도소저항,기병리생리궤제촉진료대사종합정기타조분,여혈당、혈지급혈압적진전。
Objective To investigate the effect of obesity on glucolipid metabolism and blood pressure , as well as its underlying mechanism .Methods A total of 101 cases of patients underwent physical examina-tion in the healthcare center of Nanjing Dachang Hospital from Apr .2009 to Mar.2012 were randomly select-ed,including 31 obese patients as the obesity group,33 over-weight patients as the over-weight group,and 37 health people as the control group.Fasting plasma glucose(FPG),fasting insulin(FINS),total cholesterol (TC),triglyceride(TG),high density lipoprotein cholesterol(HDL-C),uric acid(UA),systolic blood pres-sure(SBP),diastolic blood pressure(DBP),body height and weight of the three groups were measured,and insulin resistance index( HOMA-IR) ,the function index of islet beta-cell( HOMA-β) and body mass index (BMI) were calculated.ANOVA was applied for the interclass comparison.Results FPG,FINS,HOMA-IR,UA,TC,TG,HDL-C,SBP and DBP differed significantly among the three groups,the differences were statistically significant(P<0.05),but HOMA-βhad no statistically significant difference(P>0.05).Com-pared with the control group,FINS,HOMA-IR,TG and UA of the obesity group and over-weight group were significantly higher(P<0.01),whereas HDL-C was significantly lower than the control group(P<0.01). FPG,TC,SBP and DBP of the obesity group were significantly higher than those of the control group ( P <0.05), while there were no statistically significant differences in those indexes between the over-weight group and the control group.Compared with the over-weight group,FINS,HOMA-IR,TG and UA of the obe-sity group were significantly higher(P<0.05 or P<0.01),and HDL-C was significantly lower(P<0.01), while there were no statistically significant differences of FPG,TC,SBP and DBP between the two groups (P>0.05).Conclusion Obesity can cause insulin resistance,its pathophysiological mechanism plays an important role in the development of metabolic syndrome .