益生菌和酸奶对乳糖不耐受者的作用研究

EFFECTS OF PROBIOTICS AND YOGHURT ON LACTOSE INTOLERANCE

目的:研究益生菌和酸奶对乳糖不耐症(lactoseintolerance,LI)者的作用及其机制。方法:以经乳糖负荷试验筛选的乳糖不耐受者11名为对象,持续摄入益生菌(含B.longum)和酸奶(含L.bulgaricus,S.thermophilus,B.animalis)14d进行补充研究。试验分3个阶段,第1阶段为基值阶段1w,第2阶段为补充阶段2w,第3阶段为补充后阶段1w。在第2阶段前后1d分别进行双标稳定同位素13C-lactose/2H-glucose负荷试验,分析受试者摄入底物后6h呼气H2浓度值,以及血浆13C-glucose和2H-glucose浓度,并计算乳糖消化指数(lactosedigestionindex,LDI),乳糖消化量和口—结肠转运时间(orocecaltransittime,OCTT)。整个实验期间共收集5次粪便样本,分析β-半乳糖苷酶活性。结果:在第2阶段补充结束后个体LI症状评分显著低于补充前(7.09±5.50vs16.09±10.03,P<0.05);LDI、乳糖消化量、OCTT和各时间点呼气H2浓度在补充前后无显著性改变;粪便β-半乳糖苷酶活性在补充第1w即开始升高,补充第2w显著高于基值(147.6±165.8IUvs77.3±77.2IU,P<0.05)。结论:持续摄入益生菌和酸奶具有明显改善乳糖不耐受症状的作用,其原因可能与结肠β-半乳糖苷酶活性的增加有关。

Objective： To Study the effect of probiotics and yoghurt on lactose intolerance （LI） and its mechanism. Method- Eleven volunteers with LI were recruited and given supplementation with Bifina capsule （with B. longum） and yoghurt （with L. bulgaricus, S. thermophilus, B. animalis） for 14 d. The study was divided into 3 phases- 1 w basal period, 2 w supplementation period and 1 w post-supplementation period. Two ^13C-lactose/^ 2H-glucose tests were performed 1 d before and after supplementation period, respectively. The LI symptoms were recorded with questionnaire, and 6h hydrogen excretion, the concentration of plasma ^13C-glucose and ^2H-glucose were measured. The degree of lactose digestion index （LDI）, lactose digestion amount, and the orocecal transit time （OCTT） were calculated and compared before and after supplementation.Five fecal samples were collected during the three periods and the β-galactosidase activity was analyzed. Results： LI symptoms were alleviated significantly after supplementation （7.09 ± 5.50 vs 16.09±10.03, P〈0.05）, while there were no changes in LDI, lactose digestion amount, breath H2 excretion and OCTT. The colonic β-galactosidase activity was significantly higher at the end of supplementation than basal period （147.6±165.8IU vs 77.3-±77.2IU, P〈0.05）. Conclusion： The probiotics and yoghurt had significant improving effect on LI, which was not caused probably by colonic metabolic factors.