Weaver G A, Tangel C T, Krause J A, Parfitt M M, Jenkins P L, Rader J M, Lewis B A, Miller T L, Wolin M J
Department of Medicine, The Mary Imogene Bassett Hospital, Cooperstown, NY 13326, USA.
J Nutr. 1997 May;127(5):717-23. doi: 10.1093/jn/127.5.717.
Earlier studies suggest that butyrate has colonic differentiating and nutritional effects and that acarbose increases butyrate production. To determine the effects of acarbose on colonic fermentation, subjects were given 50-200 mg acarbose or placebo (cornstarch), three times per day, with meals in a double-blind crossover study. Fecal concentrations of starch and starch-fermenting bacteria were measured and fecal fermentation products determined after incubation of fecal suspensions with and without added substrate for 6 and 24 h. Substrate additions were cornstarch, cornstarch plus acarbose and potato starch. Dietary starch consumption was similar during acarbose and placebo treatment periods, but fecal starch concentrations were found to be significantly greater with acarbose treatment. Ratios of starch-fermenting to total anaerobic bacteria were also significantly greater with acarbose treatment. Butyrate in feces, measured either as concentration or as percentage of total short-chain fatty acids, was significantly greater with acarbose treatment than with placebo treatment. Butyrate ranged from 22.3 to 27.5 mol/100 mol for the 50-200 mg, three times per day doses of acarbose compared with 18.3-19.3 mol/100 mol for the comparable placebo periods. The propionate in fecal total short-chain fatty acids was significantly less with acarbose treatment (10.7-12.1 mol/100 mol) than with placebo treatment (13.7-14.2 mol/100 mol). Butyrate production was significantly greater in fermentations in samples collected during acarbose treatment, whereas production of acetate and propionate was significantly less. Fermentation decreased when acarbose was added directly to cornstarch fermentations. Acarbose effectively augmented colonic butyrate production by several mechanisms; it reduced starch absorption, expanded concentrations of starch-fermenting and butyrate-producing bacteria and inhibited starch use by acetate- and propionate-producing bacteria.
早期研究表明,丁酸盐具有结肠分化和营养作用,且阿卡波糖可增加丁酸盐的产生。为确定阿卡波糖对结肠发酵的影响,在一项双盲交叉研究中,让受试者每天随餐服用50 - 200毫克阿卡波糖或安慰剂(玉米淀粉),每日三次。测量粪便中淀粉及淀粉发酵细菌的浓度,并在添加和不添加底物的粪便悬液孵育6小时和24小时后测定粪便发酵产物。添加的底物有玉米淀粉、玉米淀粉加阿卡波糖和马铃薯淀粉。在阿卡波糖和安慰剂治疗期间,膳食淀粉摄入量相似,但发现阿卡波糖治疗时粪便淀粉浓度显著更高。阿卡波糖治疗时,淀粉发酵菌与总厌氧菌的比例也显著更高。以浓度或占总短链脂肪酸的百分比来衡量,阿卡波糖治疗时粪便中的丁酸盐显著高于安慰剂治疗时。对于每天三次、剂量为50 - 200毫克的阿卡波糖,丁酸盐含量在22.3至27.5摩尔/100摩尔之间,而在相应的安慰剂治疗期为18.3 - 19.3摩尔/100摩尔。阿卡波糖治疗时,粪便总短链脂肪酸中的丙酸盐(10.7 - 12.1摩尔/100摩尔)显著低于安慰剂治疗时(13.7 - 14.2摩尔/100摩尔)。在阿卡波糖治疗期间采集的样本发酵过程中,丁酸盐的产生显著增加,而乙酸盐和丙酸盐的产生显著减少。当直接向玉米淀粉发酵中添加阿卡波糖时,发酵作用减弱。阿卡波糖通过多种机制有效增加结肠丁酸盐的产生;它减少淀粉吸收,扩大淀粉发酵菌和丁酸盐产生菌的浓度,并抑制乙酸盐和丙酸盐产生菌利用淀粉。