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李燕, 侯孟君, 唐志红, 凌文华. 不同脂肪酸负荷膳食对小鼠胆固醇代谢的影响[J]. 中国公共卫生, 2004, 20(11): 1299-1301.
引用本文: 李燕, 侯孟君, 唐志红, 凌文华. 不同脂肪酸负荷膳食对小鼠胆固醇代谢的影响[J]. 中国公共卫生, 2004, 20(11): 1299-1301.
LI Yan, HOU Meng-jun, TANG Zhi-hong, . Effects of dietary fats on chlesterol homestasis in mice[J]. Chinese Journal of Public Health, 2004, 20(11): 1299-1301.
Citation: LI Yan, HOU Meng-jun, TANG Zhi-hong, . Effects of dietary fats on chlesterol homestasis in mice[J]. Chinese Journal of Public Health, 2004, 20(11): 1299-1301.

不同脂肪酸负荷膳食对小鼠胆固醇代谢的影响

Effects of dietary fats on chlesterol homestasis in mice

  • 摘要:
      目的   为研究脂肪酸对胆固醇代谢可能的分子机制。
      方法   C57小鼠75只, 随机分为5组, 各组饲以相应配方饲料6周。
      结果   与胆固醇膳食(Chol)相比, 胆固醇+多不饱和脂肪酸膳食(Chol+PUFA)可增加血清总胆固醇、机体总胆汁酸(P<0.05), 降低肝脏胆固醇(P<0.05);胆固醇+单不饱和脂肪酸膳食(Chol+MUFA)动物血清总胆固醇不变, 机体总胆汁酸明显增加(P<0.05), 肝脏胆固醇降低(P<0.05);胆固醇+饱和脂肪酸(Chol+SFA)膳食可明显增加(P<0.05)血清总胆固醇和肝脏胆固醇, 降低(P<0.05)机体总胆汁酸。此外, PUFA、MUFA和SFA均明显降低肝脏胆固醇7α-羟化酶(CYP7a1)mRNA和蛋白的表达.
      结论   膳食脂肪酸可通过CYP7a1调节机体胆固醇内稳态, 多不饱和脂肪酸和单不饱和脂肪酸可诱导胆固醇转化为胆汁酸进而维持机体胆固醇在较低水平, 而此过程中产生的大量胆汁酸又可反馈抑制CYP7a1的表达; 相反, 饱和脂肪酸可能通过直接抑制或不改变CYP7a1的表达, 导致膳食胆固醇在体积的堆积。

     

    Abstract:
      Objective   To investigate the molecular mechanism of the effect of fatty acid on cholesterol homeostasis.
      Methods   C57BL/6J mice(n=75)were randomly divided into five groups and respectively received formula mash for 6 weeks.
      Results   Compared with the results observed in mice fed Chol diet, the mice fed Chol+PUFA diet had signiacant higher(P<0.05)serum total cholesterol and bile acid pool, lower(P<0.05)liver cholesterol; Chol+MUFA diet resulted the same serum total cholesterol, higher(P<0.05)bile acid pool, lower(P<0.05)liver cholesterol level; Chol+SFA diet resulted higher(P<0.05)serum total cholesterol and liver cholesterol, lower(P<0.05)bile acid pool. In addition, PUFA, MUFA and SFA all decreased mRAN and protein expression of C YP7a1 in liver.
      Conclusion   The effect of fatty acid on cholesterol level was related to C YP7a1 and the type of dietary fat important in elaborating the regulatory potential on it. PU FA and MUFA may maintain body cholesterol homeostasis by increasing the conversion of cholesterol to bile acid, and the lowered C YP7a1 gene expression likely resulted from the rising feedback inhibition of total bile acid returning to the liver rather than direct inhibition. Hypercholesterolemia SFA may be mediated through its inhibitory effect or no effect on cyp7a1 in the liver directly.

     

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