高天舒,王宗保,姚峰,许金华,余坚,尹卫东.NO-1886抑制糖尿病兔肝糖原分解和肝脏脂肪病变的实验研究.[J].中南医学科学杂志.,2003,(1):19-21,37.
NO-1886抑制糖尿病兔肝糖原分解和肝脏脂肪病变的实验研究
Liver Glycogenolysis and Fat Pathological Changes Suppressed By NO- 1886 in Diabetic Rabbits
  
DOI:
中文关键词:  NO-1886 糖尿病 兔 肝脏脂肪病变 糖尿病 血清 葡萄糖 肝糖原
英文关键词:NO - 1886,glucose,triglyceride,diabetes,New Zealand white rabbits,liver
基金项目:日本大冡制药厂新药研究基金,湖南省科技厅资助(NO:OOJZN 2032).
高天舒  王宗保  姚峰  许金华  余坚  尹卫东
[1]南华大学外总教研室,湖南衡阳421001 [2]南华大学实验动物部 [3]南华大学病理教研室 [4]南华大学心研所
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中文摘要:
      目的:探讨合成化合物N0—1886是否降低高糖高脂饲料诱发的糖尿病新西兰兔的血清葡萄糖浓度和肝脏病变。方法:体重2kg左右的雄性新西兰兔60只,随机选取20只饲以基础饲料为A组(正常对照组);20只饲以高糖高脂饲料为B纽(糖尿病对照组);20只饲以高糖高脂饲料加1.0%N0—1886为C组(糖尿病治疗组)。分别在0,4,8,12,16,20,24,28周时从禁食过夜的兔子静脉抽取血样测定葡萄糖、甘油三酯水平。第32周末,处死动物,取肝脏一小块,10%福尔马林液固定,常规石蜡包埋切片,分别作H.E和肝糖原染色,光学显微镜下观察。结果:糖尿病对照组1个月后即出现高血糖、高甘油三酯,并随着喂养时间延长而逐渐升高。正常对照组血糖、甘油三酯未见明显升高,两组对比差异具有显著性意义(P<0.05),与糖尿病对照组比较,糖尿病治疗组血糖、甘油三酯有所降低。从肝脏病理切片观察所见,糖尿病对照组肝脏脂肪变性明显,具大量脂肪空泡,并有局灶溶解性坏死,肝糖原极少或消失。而糖尿病治疗组肝脏未见明显脂肪空泡变性,组织结构基本正常,肝糖原丰富。结论:N0—1886不仅可改善脂质代谢紊乱,而义可降低血清葡萄糖,减少肝糖原分解和减轻肝脏脂肪病变。可开发为治疗糖尿病糖代谢紊乱和脂质紊乱的药物。
英文摘要:
      Objective To question whether NO - 1886 ,a synthetic compound, decreases serumal glucose or improves pathological changes in diabetic New Zealand White Rabbits induced by high sucrose and fat feed. Methods 60 rabbits about 2 kg weigh were randomly divided into 3 groups of normal control, diabetes, diabetes treatment, which were fed by basal diet, high sucros and fat feed or with 1.0% NO - 1886 respectively. The concentration of serumal glucose and triglyceride of rabbits, which were inhibited food over night, were analyzed in the 0,4, 8, 12, 16, 20, 24, 28th week respectively. These rabbits were put to death in the 32nd weekend. Liver pathologic changs were observed under microscope after the small lumps of liver were fixed and stained. Results The high se-rumal glucose and triglyceride observed one month late gradually increased in the diabetes group but not in normal control ( P < 0.05) . The seruma glucose and triglyceride of diabetes treatment group were lower than diabetes control. The liver normal structuse and abundant glycogen were observed in the treatment group. There were obvious liver fatty degeneration, many fat bubbles, local solubble necrosis and little or no glycogen in diabetes control. Conclusion NO - 1886 improved lipid metabolic disorder and decreased plasma glucose or liver glycogenolysis and improved liver fat pathological changes. NO - 1886 may be developed as anagent to treat glucose metabolic disorder or lipid disorder in diabetes.
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