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乳糖酶基因c/c 13910基因型儿童肥胖症中乳糖酶缺乏症的治疗。

Treatment of lactase deficiency in children's obesity with genotype c/c 13910 of lactase gene.

作者信息

Abaturov Alexandr Ye, Stepanov Yuri M, Nikulina Anna A

机构信息

State Institution "Dnepropetrovsk Medical Academy of the Ministry of Health of Ukraine", Dnipro, Ukraine.

出版信息

Wiad Lek. 2019;72(1):17-21.

PMID:30796855
Abstract

OBJECTIVE

Introduction: Excess lactose in the diet of modern man causes the development of not only lactase deficiency, but it can be a factor that contributes to obesity. The aim: To study associations between obesity and genotype C/C 13910 of lactase gene (LCT) in children, to investigate the effectiveness of treatment using drug exogenous lactase and a low-lactose diet.

PATIENTS AND METHODS

Materials and methods: genotyping of lactase gene by real-time polymerase chain reaction, determining the level of lactose maldigestion by hydrogen breath test (HBT), estimating the insulin resistance with the HOMA-IR index in 70 obese children and 40 healthy children 6 - 18 years. Obese children with genotype C/C 13910 and lactose maldigestion (n=40) were randomized in two groups: children from group I (n=20) received an exogenous lactase preparation, and children from group II (n=20) - low-lactose diet.

RESULTS

Results: in obese children, the genotype C/C 13910 is 2 times more often than in healthy children. Obese children with genotype C/C 13910 have a significantly higher value of HBT (32.8-39.8 ppm) compared to healthy children (p<0.05), and an increased value of the HOMA-IR index. After treatment, there was a significant decrease in HBT and the HOMA-IR index in the two comparison groups.

CONCLUSION

Conclusions: signs of insulin resistance are observed in children with obesity, genotype C/C 13910 and lactose maldigestion. The use of exogenous lactase in the therapy or the administration of a low-lactose diet cause approximately the same decrease in the HOMA-IR index.

摘要

目的

引言:现代人类饮食中过量的乳糖不仅会导致乳糖酶缺乏,还可能是导致肥胖的一个因素。目的:研究儿童肥胖与乳糖酶基因(LCT)C/C 13910基因型之间的关联,探讨使用药物外源性乳糖酶和低乳糖饮食治疗的有效性。

患者与方法

材料与方法:采用实时聚合酶链反应对乳糖酶基因进行基因分型,通过氢呼气试验(HBT)测定乳糖消化不良水平,用HOMA-IR指数评估70名肥胖儿童和40名6至18岁健康儿童的胰岛素抵抗。将基因型为C/C 13910且乳糖消化不良的肥胖儿童(n = 40)随机分为两组:第一组(n = 20)儿童接受外源性乳糖酶制剂,第二组(n = 20)儿童接受低乳糖饮食。

结果

结果:肥胖儿童中,C/C 13910基因型的出现频率是健康儿童的2倍。与健康儿童相比,基因型为C/C 13910的肥胖儿童HBT值显著更高(32.8 - 39.8 ppm)(p<0.05),且HOMA-IR指数升高。治疗后,两个比较组的HBT和HOMA-IR指数均显著下降。

结论

结论:肥胖、基因型为C/C 13910且乳糖消化不良的儿童存在胰岛素抵抗迹象。在治疗中使用外源性乳糖酶或给予低乳糖饮食可使HOMA-IR指数下降幅度大致相同。

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