中华老年医学杂志
中華老年醫學雜誌
중화노년의학잡지
Chinese Journal of Geriatrics
2011年
8期
684-686
,共3页
赵玉岩%王露%马东杰%田蕾%郑德禄
趙玉巖%王露%馬東傑%田蕾%鄭德祿
조옥암%왕로%마동걸%전뢰%정덕록
肥胖症%基因表达
肥胖癥%基因錶達
비반증%기인표체
Obesity%Gene expression
目的 探讨营养性肥胖大鼠下丘脑组织中增食欲素A(Orexin A)的表达及其与高瘦素、高胰岛素和高脂血症的关系.方法 高脂膳食诱导建立营养性肥胖Wistar大鼠模型;采用放射免疫法和生化酶法检测肥胖大鼠血清瘦素、血清胰岛素及C肽、三酰甘油和总胆固醇;应用实时定量PCR分析法检测肥胖大鼠下丘脑组织中增食欲素A的表达.结果 喂养8周时,肥胖组大鼠体质量、Lee's指数、血糖、三酰甘油及总胆固醇水平较对照组均明显增加(P＜0.01);肥胖组大鼠血清瘦素(1.74±0.36)/μg/L、胰岛素(35±5)MIU/L和C肽含量(0.21±0.04)μg/L,均高于对照组(1.27±0.11)μg/L、(23±4)MIU/L和(0.14±0.03)μg/L,差异均有统计学意义(P＜0.01);肥胖组大鼠下丘脑组织中增食欲素A mRNA水平较对照组降低,分别为6.8±2.3和14.5±3.6(t=-8.06,P＜0.01);增食欲素A mRNA水平与血清瘦素(r=-0.726)、胰岛素(r=-0.506)及C肽含量(r=-0.664)显著负相关(均P＜0.01).结论 高脂饮食可诱导Wistar大鼠体内瘦素抵抗和营养性肥胖的发生,营养性肥胖大鼠下丘脑神经元增食欲素A基因的异常表达与瘦素水平及胰岛素抵抗的发生密切相关.
目的 探討營養性肥胖大鼠下丘腦組織中增食欲素A(Orexin A)的錶達及其與高瘦素、高胰島素和高脂血癥的關繫.方法 高脂膳食誘導建立營養性肥胖Wistar大鼠模型;採用放射免疫法和生化酶法檢測肥胖大鼠血清瘦素、血清胰島素及C肽、三酰甘油和總膽固醇;應用實時定量PCR分析法檢測肥胖大鼠下丘腦組織中增食欲素A的錶達.結果 餵養8週時,肥胖組大鼠體質量、Lee's指數、血糖、三酰甘油及總膽固醇水平較對照組均明顯增加(P＜0.01);肥胖組大鼠血清瘦素(1.74±0.36)/μg/L、胰島素(35±5)MIU/L和C肽含量(0.21±0.04)μg/L,均高于對照組(1.27±0.11)μg/L、(23±4)MIU/L和(0.14±0.03)μg/L,差異均有統計學意義(P＜0.01);肥胖組大鼠下丘腦組織中增食欲素A mRNA水平較對照組降低,分彆為6.8±2.3和14.5±3.6(t=-8.06,P＜0.01);增食欲素A mRNA水平與血清瘦素(r=-0.726)、胰島素(r=-0.506)及C肽含量(r=-0.664)顯著負相關(均P＜0.01).結論 高脂飲食可誘導Wistar大鼠體內瘦素牴抗和營養性肥胖的髮生,營養性肥胖大鼠下丘腦神經元增食欲素A基因的異常錶達與瘦素水平及胰島素牴抗的髮生密切相關.
목적 탐토영양성비반대서하구뇌조직중증식욕소A(Orexin A)적표체급기여고수소、고이도소화고지혈증적관계.방법 고지선식유도건립영양성비반Wistar대서모형;채용방사면역법화생화매법검측비반대서혈청수소、혈청이도소급C태、삼선감유화총담고순;응용실시정량PCR분석법검측비반대서하구뇌조직중증식욕소A적표체.결과 위양8주시,비반조대서체질량、Lee's지수、혈당、삼선감유급총담고순수평교대조조균명현증가(P＜0.01);비반조대서혈청수소(1.74±0.36)/μg/L、이도소(35±5)MIU/L화C태함량(0.21±0.04)μg/L,균고우대조조(1.27±0.11)μg/L、(23±4)MIU/L화(0.14±0.03)μg/L,차이균유통계학의의(P＜0.01);비반조대서하구뇌조직중증식욕소A mRNA수평교대조조강저,분별위6.8±2.3화14.5±3.6(t=-8.06,P＜0.01);증식욕소A mRNA수평여혈청수소(r=-0.726)、이도소(r=-0.506)급C태함량(r=-0.664)현저부상관(균P＜0.01).결론 고지음식가유도Wistar대서체내수소저항화영양성비반적발생,영양성비반대서하구뇌신경원증식욕소A기인적이상표체여수소수평급이도소저항적발생밀절상관.
Objective To evaluate the relationships of the expression of orexin A in hypothalamus with hyperleptinemia, hyperinsulinism, and hyperlipidemia in alimentary obesity rats.Methods The alimentary obesity rat model was induced by high-fat diet in Wistar rats. The levels of leptin, insulin, C-peptide, total cholesterol (TC) and triglyeride (TG) were detected by luminescent immunoassay and biochemistry enzymic method. The gene expression of orexin A in rat hypothalamus was detected by real-time PCR. The correlation between orexin A and leptin was analyzed. Results After 8 weeks of high-fat diet feeding, the body weight, Lee's index, blood glucose, TG and TC significantly increased in obesity rat group (P＜0. 01). The levels of serum leptin, insulin and C-peptide were significantly higher in obesity rats than in controls [( 1.74±0. 36)μg/Lvs. (1.27±0.11) μg/L, (35±5) MIU/L vs. (23±4) MIU/L, (0.21±0.04) μg/L vs.(0. 14±0. 03) μg/L respectively, P＜0.01]. However, the level of orexin A mRNA was lower in obesity rats than in controls (6.8±2.3 vs. 14.5±3.6, t=-8.06, P＜0.01). The correlation coefficient (r) of orexin A mRNA with serum leptin, insulin, and C-peptide in alimentary obesity rat were -0. 726 (P＜0.01), -0. 506 (P＜0.01) and -0. 664 (P＜0.01), respectively. Conclusions High-fat diet can induce leptin-resistance and alimentary obesity in Wistar rat. The down-regulation of orexin A in rat hypothalamus would be correlated closely to the leptin and insulin resistance in alimentary obesity.
