Huang C T, Woodward W E, Hornick R B, Rodriguez J T, Nichols B L
Am J Clin Nutr. 1976 Sep;29(9):949-55. doi: 10.1093/ajcn/29.9.949.
Fecal bile acid and neutral sterol patterns of five healthy adult male volunteers, who were challenged by a virulent Shigella flexneri 2a (M42-43) strain and developed dysentery were studied. It was observed that cholic acid was increased from 1.9 +/- 0.4% of total bile acid in the feces before infection to 14.5 +/- 2.1% during diarrhea (P less than 0.001). Chenodeoxycholic acid also was increased from 3.2 +/- 0.7 to 8.7 +/- 3.2% in diarrhea but the difference was not significant statistically. Deoxycholic and lithocholic acids constituted 34.1 +/- 4.1 and 40.5 +/- 2.8%, respectively, of total bile acid in the normal controls as compared to 13.9 +/- 2.5 and 24.8 +/- 2.5% for the same subjects during diarrhea (P less than 0.005). Total excretion of bile acids, expressed as mg/kg of body weight per day, were higher in diarrhea (5.4 +/- 1.0) than that in controls (4,2 +/- 1.0) but the difference was not statistically significant. In the neutral sterol fraction, unmodified cholesterol was increased during diarrhea (86.2 +/- 8.7 versus 25.0 +/- 4.8% of total cholesterol metabolites in controls, P less than 0.001). Coprostanol was decreased in shigellosis (12.2 +/- 8.2 versus 65.8 +/- 4.7% in controls, P less than 0.001). Epicoprostanol, coprostanone, and unidentified cholesterol metabolites also were reduced in shigellosis. The effect of diarrhea on the plant sterols was not as consistent. However, unidentified plant sterols were reduced significantly in shigellosis stools. Total excretion of cholesterol metabolites and plant sterols, when expressed as mg/kg of body weight per day, were 6.8 +/- 1.7 and 0.6 +/- 0.2), respectively, in Shigellosis. These values were not significantly different from the corresponding values for controls (10.3 +/- 3.0 and 0.8 +/- 0.2). One subject's stool samples were studied during infection for the sequence of bile acid alteration. A progressive reduction of bacterial activity upon fecal steroids was evident following the initial diarrheal episode. The production of coprostanol was correlated with 7 alpha-dehydroxylation of cholic acid (r = 0.937, P less than 0.001) and chenodeoxycholic acid (r = 0.755, P less than 0.01).
对5名健康成年男性志愿者进行了研究，他们受到强毒力福氏志贺菌2a（M42 - 43）菌株攻击并患上痢疾。观察到胆酸在感染前粪便中占总胆汁酸的1.9±0.4%，腹泻期间增至14.5±2.1%（P＜0.001）。鹅去氧胆酸在腹泻时也从3.2±0.7%增至8.7±3.2%，但差异无统计学意义。脱氧胆酸和石胆酸在正常对照组中分别占总胆汁酸的34.1±4.1%和40.5±2.8%，而同一受试者腹泻时分别为13.9±2.5%和24.8±2.5%（P＜0.005）。以每天毫克/千克体重表示的胆汁酸总排泄量在腹泻时（5.4±1.0）高于对照组（4.2±1.0），但差异无统计学意义。在中性固醇部分，未修饰的胆固醇在腹泻时增加（腹泻时占总胆固醇代谢产物的86.2±8.7%，对照组为25.0±4.8%，P＜0.001）。粪甾烷醇在志贺菌病时减少（志贺菌病时为12.2±8.2%，对照组为65.8±4.7%，P＜0.001）。表胆甾烷醇、粪甾烷酮和未鉴定的胆固醇代谢产物在志贺菌病时也减少。腹泻对植物甾醇的影响不太一致。然而，未鉴定的植物甾醇在志贺菌病粪便中显著减少。以每天毫克/千克体重表示的胆固醇代谢产物和植物甾醇总排泄量在志贺菌病时分别为6.8±1.7和0.6±0.2），与对照组相应值（10.3±3.0和0.8±0.2）无显著差异。对一名受试者感染期间的粪便样本进行了胆汁酸变化序列研究。初次腹泻发作后，粪便类固醇上的细菌活性逐渐降低。粪甾烷醇的产生与胆酸（r = 0.937，P＜0.001）和鹅去氧胆酸（r = 0.755，P＜0.01）的7α-脱羟基作用相关。
