北京体育大学学报
北京體育大學學報
북경체육대학학보
Journal of Beijing University of Physical Education
2011年
3期
67~70
,共null页
高脂饮食 肥胖 肥胖抵抗 瘦素 AMPK活性
高脂飲食 肥胖 肥胖牴抗 瘦素 AMPK活性
고지음식 비반 비반저항 수소 AMPK활성
High fat diet; obese; obese resistance; leptin; activity of AMPK
目的：旨在发现肥胖和肥胖抵抗大鼠体脂、细胞形态、瘦素、AMPK发生的变化,研究肥胖抵抗发生的机制,为预防人类肥胖,调整不合理的饮食结构,降低疾病的发生提供一定的理论依据。方法：选取3-4周龄离乳SD雄性大鼠90只,适应性喂养1周后,随机分为2组,正常对照组（NS）9只、高脂饮食诱导组（HS）81只,通过13周的高脂饮食诱导催肥,选出肥胖大鼠8只,肥胖抵抗大鼠8只,进行体重,体脂,细胞形态学、瘦素与AMPK活性测试。结果：1）高脂饮食喂养导致大鼠肥胖、体脂增加,同时出现肥胖和肥胖抵抗两种现象;2）肥胖抵抗大鼠体脂百分比显著低于肥胖组大鼠,与正常对照组大鼠相比有升高趋势;3）在相同面积视野下,肥胖组与肥胖抵抗组大鼠肠系膜脂肪细胞数量显著低于正常对照组,而脂肪厚度显著增加;同时肥胖抵抗组大鼠肠系膜脂肪细胞数量较肥胖组稍高,而脂肪厚度较肥胖组大鼠下降;4）肥胖组与肥胖抵抗组大鼠瘦素水平在喂养过程中出现增加趋势且显著高于正常对照组;5）肥胖组大鼠AMPK活性在喂养过程中出现下降趋势,肥胖抵抗组大鼠出现升高趋势且显著高于肥胖组大鼠。结论：经高脂喂养的大鼠出现肥胖抵抗现象可能与其瘦素水平提高,从而促进AMPK活性提高有关。
目的：旨在髮現肥胖和肥胖牴抗大鼠體脂、細胞形態、瘦素、AMPK髮生的變化,研究肥胖牴抗髮生的機製,為預防人類肥胖,調整不閤理的飲食結構,降低疾病的髮生提供一定的理論依據。方法：選取3-4週齡離乳SD雄性大鼠90隻,適應性餵養1週後,隨機分為2組,正常對照組（NS）9隻、高脂飲食誘導組（HS）81隻,通過13週的高脂飲食誘導催肥,選齣肥胖大鼠8隻,肥胖牴抗大鼠8隻,進行體重,體脂,細胞形態學、瘦素與AMPK活性測試。結果：1）高脂飲食餵養導緻大鼠肥胖、體脂增加,同時齣現肥胖和肥胖牴抗兩種現象;2）肥胖牴抗大鼠體脂百分比顯著低于肥胖組大鼠,與正常對照組大鼠相比有升高趨勢;3）在相同麵積視野下,肥胖組與肥胖牴抗組大鼠腸繫膜脂肪細胞數量顯著低于正常對照組,而脂肪厚度顯著增加;同時肥胖牴抗組大鼠腸繫膜脂肪細胞數量較肥胖組稍高,而脂肪厚度較肥胖組大鼠下降;4）肥胖組與肥胖牴抗組大鼠瘦素水平在餵養過程中齣現增加趨勢且顯著高于正常對照組;5）肥胖組大鼠AMPK活性在餵養過程中齣現下降趨勢,肥胖牴抗組大鼠齣現升高趨勢且顯著高于肥胖組大鼠。結論：經高脂餵養的大鼠齣現肥胖牴抗現象可能與其瘦素水平提高,從而促進AMPK活性提高有關。
목적：지재발현비반화비반저항대서체지、세포형태、수소、AMPK발생적변화,연구비반저항발생적궤제,위예방인류비반,조정불합리적음식결구,강저질병적발생제공일정적이론의거。방법：선취3-4주령리유SD웅성대서90지,괄응성위양1주후,수궤분위2조,정상대조조（NS）9지、고지음식유도조（HS）81지,통과13주적고지음식유도최비,선출비반대서8지,비반저항대서8지,진행체중,체지,세포형태학、수소여AMPK활성측시。결과：1）고지음식위양도치대서비반、체지증가,동시출현비반화비반저항량충현상;2）비반저항대서체지백분비현저저우비반조대서,여정상대조조대서상비유승고추세;3）재상동면적시야하,비반조여비반저항조대서장계막지방세포수량현저저우정상대조조,이지방후도현저증가;동시비반저항조대서장계막지방세포수량교비반조초고,이지방후도교비반조대서하강;4）비반조여비반저항조대서수소수평재위양과정중출현증가추세차현저고우정상대조조;5）비반조대서AMPK활성재위양과정중출현하강추세,비반저항조대서출현승고추세차현저고우비반조대서。결론：경고지위양적대서출현비반저항현상가능여기수소수평제고,종이촉진AMPK활성제고유관。
Objective：This article＇s aim was to discover the variance of body weight,body fat,tissue morphology,leptin and activity of AMPK between obesity and obesity-resistant rats and research the mechanism of DIO-R,provide some theoretical basis for prevention of human obesity,the readjustment of irrational diet,reduce the incidence of disease.Methods： 90 male weanling SD rats aged 3-4 week,adaptive feeding for one week were randomly divided into two groups,9 in normal control group（NS）,81 in high-fat diet-induced group（HS）,through the 13-week high-fat diet-induced fatten to elect eight obese rats and eight obesity-resistant rats to measure body weight,body fat,cell morphology test,test leptin in blood and activity of AMPK.Results：1）Rats which fed by high-fat diet result in weight increased and occurred obesity and obesity-resistance.2）The obesity-resistant rats＇ weight were notably lower than obese rats and normal rats,the percentage of body fat content was also significantly lower than obese rats in obesity-resistant rats,also showed increasing trend comparing with the normal rats.3）In the same proportion,the mesenteric fat cells in obesity-resistance and obese ones were notably lower than in normal ones,the fat thickness increased significantly.The obesity-resistance rats had lower mesenteric fat cells and fat thickness than obese ones,but had no notable changes.4）The leptin values of obesity-resistance and obese rats appeared to have an increasing trend,the values also significantly higher than normal ones.5）The decreasing trend of activity of AMPK appeared in obese rats,in contrast,the increasing trend appeared in obesity-resistance rats and significantly higher than obese ones.Conclusions：The result of obesity-resistance was leaded by increasing of activity of AMPK by leptin increasing.
