Szilagyi Andrew, Shrier Ian, Heilpern Debra, Je Jung, Park Sunghoon, Chong George, Lalonde Catherine, Cote Louis-Francois, Lee Byong
Division of Gastroenterology, Department of Medicine, McGill School of Medicine, Montreal, Quebec.
Can J Gastroenterol. 2010 Jun;24(6):373-9. doi: 10.1155/2010/649312.
The ability to digest lactose divides the world's population into two phenotypes that may be risk variability markers for several diseases. Prebiotic effects likely favour lactose maldigesters who experience lactose spilling into their colon.
To evaluate the effects of fixed-dose lactose solutions on fecal bifidobacteria and lactobacilli in digesters and maldigesters, and to determine whether the concept of a difference in ability to digest lactose is supported.
A four-week study was performed in 23 lactose maldigesters and 18 digesters. Following two weeks of dairy food withdrawal, subjects ingested 25 g of lactose twice a day for two weeks. Stool bifidobacteria and lactobacilli counts pre- and postintervention were measured as the primary outcome. For secondary outcomes, total anaerobes, Enterobacteriaceae, beta-galactosidase and N-acetyl-beta-D-glucosaminidase activity in stool, as well as breath hydrogen and symptoms following lactose challenge tests, were measured.
Lactose maldigesters had a mean change difference (0.72 log10 colony forming unitsg stool; P=0.04) in bifidobacteria counts compared with lactose digesters. Lactobacilli counts were increased, but not significantly. Nevertheless, reduced breath hydrogen after lactose ingestion correlated with lactobacilli (r=-0.5; P<0.001). Reduced total breath hydrogen and symptom scorestogether, with a rise in fecal enzymes after intervention, were appropriate, but not significant.
Despite failure to achieve full colonic adaptation, the present study provided evidence for a differential impact of lactose on microflora depending on genetic lactase status. A prebiotic effect was evident in lactose maldigesters but not in lactose digesters. This may play a role in modifying the mechanisms of certain disease risks related to dairy food consumption between the two phenotypes.
消化乳糖的能力将世界人口分为两种表型,这两种表型可能是多种疾病风险变异性的标志物。益生元效应可能有利于乳糖消化不良者,这些人会出现乳糖溢入结肠的情况。
评估固定剂量乳糖溶液对乳糖消化者和乳糖消化不良者粪便中双歧杆菌和乳酸杆菌的影响,并确定乳糖消化能力差异这一概念是否得到支持。
对23名乳糖消化不良者和18名乳糖消化者进行了为期四周的研究。在停止食用乳制品两周后,受试者每天两次摄入25克乳糖,持续两周。干预前后的粪便双歧杆菌和乳酸杆菌计数作为主要结果进行测量。作为次要结果,测量了粪便中的总厌氧菌、肠杆菌科、β-半乳糖苷酶和N-乙酰-β-D-氨基葡萄糖苷酶活性,以及乳糖激发试验后的呼出气氢气和症状。
与乳糖消化者相比,乳糖消化不良者的双歧杆菌计数平均变化差异为(0.72 log10菌落形成单位/克粪便;P = 0.04)。乳酸杆菌计数有所增加,但不显著。然而,摄入乳糖后呼出气氢气的减少与乳酸杆菌有关(r = -0.5;P < 0.001)。干预后呼出气氢气总量和症状评分的降低,以及粪便酶的升高是合理的,但不显著。
尽管未能实现完全的结肠适应,但本研究提供了证据,表明乳糖对微生物群的影响因遗传乳糖酶状态而异。益生元效应在乳糖消化不良者中明显,但在乳糖消化者中不明显。这可能在改变两种表型之间与食用乳制品相关的某些疾病风险机制中发挥作用。