Illman R J, Topping D L, McIntosh G H, Trimble R P, Storer G B, Taylor M N, Cheng B Q
CSIRO Division of Human Nutrition, Glenthorne Laboratory, O'Halloran Hill, Australia.
Ann Nutr Metab. 1988;32(2):95-107.
In adult male rats fed a non-purified diet supplemented with 5% sodium propionate, plasma cholesterol concentrations were significantly depressed. Although liver cholesterol was increased by feeding propionate, rates of hepatic cholesterol and fatty acid synthesis were unchanged. Tissue concentrations and rates of synthesis of cholesterol were also unaffected by dietary propionate in stomach, small intestine and caecum. Concentrations of propionate in hepatic portal venous plasma were raised by feeding the supplemented diet but the increase was low in comparison to the dietary intake. Examination of the gut contents revealed concentrations of total volatile fatty acids (VFA) of 19 mumol/ml in the stomach contents of control rats and 148 mumol/ml (of which propionate contributed 116 mumol/ml) in those fed the supplemented diet. Duodenal and ileal concentrations of VFA were very low and were only slightly raised in the propionate-fed rats while caecal VFA were the same in both groups with a combined mean of 159 mumol/ml. These data indicate that in the rat, the absorption of dietary propionate appears to occur in the stomach. In pigs fed a standard ration hepatic portal venous VFA remained low for the first 4 h after feeding but then rose with the onset of large bowel fermentation. Feeding the diet supplemented with propionate caused hepatic portal venous plasma concentrations to rise by approximately 0.4 mumol/ml. This increase was apparent 30 min after feeding and was sustained for 3 h but subsequently there was no difference to controls. As in the rat, the absorption of dietary propionate appeared to occur in the upper gastrointestinal tract. The transport of propionate via the porcine hepatic portal vein also appeared insufficient to account for the dietary intake and suggests metabolism of the acid by the upper gastrointestinal tract. Further studies with perfused livers from fed rats indicated that propionate at a concentration of 1 mumol/ml did not alter cholesterol synthesis but that inhibition occurred at 18 mumol of propionate/ml. It appears that a redistribution of cholesterol from the plasma to the liver, rather than inhibition of hepatic and intestinal cholesterol synthesis, is responsible for the hypocholesterolaemic effects of dietary propionate. Because the absorption and transport of dietary propionate appears to follow a time course which differs considerably to that of the acid produced by the large bowel microflora, we conclude also that VFA produced by such fermentation would not seem to be responsible for the hypocholesterolaemic effects of certain water-soluble plant fibres.
在喂食添加5%丙酸钠的非纯化日粮的成年雄性大鼠中，血浆胆固醇浓度显著降低。尽管喂食丙酸盐会使肝脏胆固醇增加，但肝脏胆固醇和脂肪酸合成速率未发生变化。胃、小肠和盲肠中的胆固醇组织浓度和合成速率也不受日粮丙酸盐的影响。喂食添加日粮会使肝门静脉血浆中的丙酸盐浓度升高，但与日粮摄入量相比，升高幅度较小。对肠道内容物的检测显示，对照大鼠胃内容物中总挥发性脂肪酸（VFA）浓度为19 μmol/ml，而喂食添加日粮的大鼠胃内容物中总挥发性脂肪酸浓度为148 μmol/ml（其中丙酸盐占116 μmol/ml）。十二指肠和回肠中的VFA浓度非常低，在喂食丙酸盐的大鼠中仅略有升高，而两组大鼠盲肠中的VFA浓度相同，平均合并浓度为159 μmol/ml。这些数据表明，在大鼠中，日粮丙酸盐的吸收似乎发生在胃中。在喂食标准日粮的猪中，喂食后最初4小时肝门静脉VFA水平仍然较低，但随后随着大肠发酵的开始而升高。喂食添加丙酸盐的日粮会使肝门静脉血浆浓度升高约0.4 μmol/ml。喂食后30分钟这种升高就很明显，并持续3小时，但随后与对照组没有差异。与大鼠一样，日粮丙酸盐的吸收似乎发生在上消化道。丙酸盐通过猪肝门静脉的转运似乎也不足以解释日粮摄入量，并表明该酸在上消化道中发生了代谢。对喂食大鼠的灌注肝脏进行的进一步研究表明，浓度为1 μmol/ml的丙酸盐不会改变胆固醇合成，但当丙酸盐浓度达到18 μmol/ml时会发生抑制。日粮丙酸盐的降胆固醇作用似乎是由于胆固醇从血浆重新分布到肝脏，而不是抑制肝脏和肠道胆固醇合成。由于日粮丙酸盐的吸收和转运似乎遵循与大肠微生物群产生的酸有很大不同的时间进程，我们还得出结论，这种发酵产生的VFA似乎不是某些水溶性植物纤维降胆固醇作用的原因。
