Turley S D, West C E
Lipids. 1976 Jul;11(7):571-7. doi: 10.1007/BF02532904.
The effects of feeding diest containing either cholesterol (0.24% w/w) or cholestyramine (2.5% w/w) and of fasting on sterol synthesis in the liver, ileum, and lung of both male and female guinea pigs have been studied by measuring the incorporation by tissue slices of 14C-labeled acetate into total digitoninpredipitable sterols. Cholesterol feeding significantly decreased (P less than 0.05) sterol synthesis in the liver, ileum, and lung of the males and in the ileum of females. Cholestyramine feeding stimulated the rate of hepatic sterol synthesis 13-fold but did not significantly affect sterologenesis in the ileum. Sterol synthesis in the lung was significantly increased (P less than 0.05) but to a much lesser extent than in the liver. Fatty acid synthesis in the liver, ileum, and lung was not significantly affected by either cholesterol or cholestyramine feeding. In guinea pigs fasted for 24 hr, sterol synthesis was inhibited in all three tissues, the most pronounced effect occurring in the liver. Only in the lung was fatty acid synthesis significantly decreased (P less than 0.001) by fasting. Cholesterol feeding resulted in increased concentrations of cholesterol in the plasma and liver. Cholestyramine feeding reduced plasma cholesterol concentration by 81% in females and by 64% in males. However, it did not significantly change the tissue cholesterol concentrations. Fasting resulted in a significant increase (P less than 0.05) in plasma cholesterol concentration but did not effect the concentration of cholesterol in the tissues. It was concluded that in the normal guinea pig, the feedback inhibition produced by both cholesterol and also possibly by bile acids suppresses sterol synthesis in the liver to very low rates compared to those in the small intestine, where sterologenesis is not only less sensitive to the cholesterol negative feedback system than that in the liver, but also is not subject to regulation by the bile acid negative feedback system.
通过测量组织切片将14C标记的乙酸盐掺入总洋地黄皂苷可沉淀固醇中的量，研究了给雄性和雌性豚鼠喂食含胆固醇（0.24% w/w）或消胆胺（2.5% w/w）的饮食以及禁食对肝脏、回肠和肺中固醇合成的影响。喂食胆固醇显著降低了（P<0.05）雄性豚鼠肝脏、回肠和肺以及雌性豚鼠回肠中的固醇合成。喂食消胆胺刺激肝脏固醇合成速率提高了13倍，但对回肠中的固醇生成没有显著影响。肺中的固醇合成显著增加（P<0.05），但程度远低于肝脏。喂食胆固醇或消胆胺对肝脏、回肠和肺中的脂肪酸合成没有显著影响。在禁食24小时的豚鼠中，所有三个组织中的固醇合成均受到抑制，最明显的影响发生在肝脏。只有在肺中，禁食才使脂肪酸合成显著降低（P<0.001）。喂食胆固醇导致血浆和肝脏中胆固醇浓度升高。喂食消胆胺使雌性血浆胆固醇浓度降低81%，使雄性降低64%。然而，它并没有显著改变组织中的胆固醇浓度。禁食导致血浆胆固醇浓度显著升高（P<0.05），但不影响组织中胆固醇的浓度。得出的结论是，在正常豚鼠中，胆固醇以及可能还有胆汁酸产生的反馈抑制将肝脏中的固醇合成抑制到非常低的速率，与小肠中的速率相比，小肠中的固醇生成不仅对胆固醇负反馈系统的敏感性低于肝脏，而且不受胆汁酸负反馈系统的调节。
