Possible association between Helicobacter pylori infection and nonalcoholic fatty liver disease

被引:41
作者
Chen, Chang-Xi [1 ,2 ]
Mao, Yu-Shan [3 ]
Foster, Parker [4 ]
Zhu, Zhong-Wei [2 ]
Du, Juan [2 ]
Guo, Chuan-Yong [5 ]
机构
[1] Soochow Univ, Affiliated Hosp 1, Dept Gastroenterol, Suzhou 215006, Peoples R China
[2] Zhenhai Lianhua Hosp, Dept Gastroenterol, Ningbo 315207, Zhejiang, Peoples R China
[3] Ningbo Univ, Coll Med, Affiliated Hosp, Dept Endocrinol, Ningbo 315020, Zhejiang, Peoples R China
[4] NIH, Dept Radiol & Imaging Sci, Bethesda, MD 20852 USA
[5] Tongji Univ, Sch Med, Shanghai Peoples Hosp 10, Dept Gastroenterol, Shanghai 200072, Peoples R China
关键词
nonalcoholic fatty liver disease; Helicobacter pylori infection; ResNet Database; pathway enrichment analysis; network connectivity analysis; GASTRIC EPITHELIAL-CELLS; INSULIN-RESISTANCE; MANAGEMENT; EPIDEMIOLOGY; GASTROENTEROLOGY; INFLAMMATION; PROGRESSION; POPULATION; PREVALENCE; HYPOTHESIS;
D O I
10.1139/apnm-2016-0499
中图分类号
R15 [营养卫生、食品卫生]; TS201 [基础科学];
学科分类号
100403 ;
摘要
Possible association between Helicobacter pylori infection (HPI) and nonalcoholic fatty liver disease (NAFLD) has been proposed by several studies with inconsistent conclusions. Here, we studied the association between HPI and NAFLD at 3 levels: (i) genetic level; (ii) small molecular level; and (iii) clinical level. Relation data between diseases, genes, and small molecules were acquired from Pathway Studio ResNet Mammalian database. Clinical data were acquired from 2263 elderly South Chinese subjects, including 603 NAFLD patients and 1660 subjects without NAFLD. Results showed that HPI and NAFLD present significantly shared genetic bases (95 genes, p value = 2.5E-72), demonstrating multiple common genetic pathways (enrichment p value <= 4.38E-20 for the top 10 pathways). Genetic network analysis suggested that mutual regulation may exist between HPI and NAFLD through 21 out of 95 genes. Furthermore, 85 out of the 95 genes manifested strong interaction with 12 small molecules/drugs that demonstrate effectiveness in treating both diseases. Clinical results showed that HPI rate in the NAFLD group was significantly higher than that in the group without NAFLD (51.9% vs. 43.6%; p value = 4.9E-4). Multivariate logistic regression results supported the observations and suggested that HPI served as a risk factor for NAFLD in the experiment data studied (odds ratio: 1.387, p value = 0.018). Results from this study support the hypothesis that complex biological association may exist between HPI and NAFLD, which partially explains the significant clinical co-incidence in the elderly population of south China.
引用
收藏
页码:295 / 301
页数:7
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