摘要
为建立由高脂饲料诱导的肥胖易感(obesity-susceptible,OS)和肥胖抵抗(obesity-resistant,OR)大鼠模型,并探讨在高脂饲料中添加丁酸钠对二者的作用,给予SD(Sprague-Dawley)大鼠高脂饲料饲喂3周后依据其体质量增加量排序并再分组,上1/3作为OS组,下1/3作为OR组,继续给予高脂饲料喂养12周,OS大鼠体质量增加明显,体质指数、皮下脂肪、内脏脂肪和体脂肪含量以及血清总胆固醇、甘油三酯、低密度脂蛋白、瘦素与对照组比较显著增高,差异有统计学意义(P<0.05),OR组各项指标与对照组比较在统计学上无显著差异(P>0.05).按照此造模方法从饲喂高脂饲料第4周起,丁酸钠干预(obesity intervention with sodium butyrate,OI)组增加8 mmol/L丁酸钠生理盐水(0.9%氯化钠)溶液1 m L灌胃,1次/日;肥胖对照(obesity control,OC)组则用1 m L 0.9%氯化钠溶液灌胃,1次/日,共干预16周.结果表明:添加丁酸钠后,OI组大鼠体质量增加、体质指数、皮下脂肪、内脏脂肪和体脂肪含量以及血清总胆固醇、甘油三酯、低密度脂蛋白、瘦素与OC组比较均显著改善,差异有统计学意义(P<0.05).说明SD大鼠对于高脂饲料具有不同的应答能力,可获得肥胖敏感及肥胖抵抗模型;对于高脂饮食敏感的SD大鼠,在其高脂饲料中添加丁酸盐能够改善其体质量增加与体质指数,减少体脂肪含量,降低血脂与血清瘦素水平.
Summary Obesity has been reported as an increasingly prevalent and highly heritable health problem leading to increased risks for several common diseases . Human obesity can be induced by genetic factors such as loss‐of‐function mutations in individual genes . The products of these genes are essential for normal body mass regulation in both laboratory animals and humans . Nevertheless , the role of gene‐environment interactions in the etiology of obesity cannot be ignored . Diet is a major factor of our current obesogenic environment , and the interests have been aroused in rodent models of diet‐induced obesity (DIO) . The SD (Sprague‐Dawley) rat model of DIO was&amp;nbsp;been reported to exhibit a clear segregation into susceptible and resistant subpopulations shortly after being transferred to a high energy diet .
出处
《浙江大学学报(农业与生命科学版)》
CAS
CSCD
北大核心
2015年第2期195-200,共6页
Journal of Zhejiang University:Agriculture and Life Sciences
基金
中央高校基本科研业务费专项资金(2011QC073)
湖北省自然科学基金(2013CFB197)
关键词
丁酸钠
高脂饲料
肥胖
sodium butyrate
high-fat diet
obesity