Abstract
Helicobacter pylori (H. pylori) which colonizes the stomach can cause a wide array of gastric disorders, including chronic gastritis, peptic ulcer, and gastric cancer. Recently, accumulating evidence has implicated H. pylori infection in extragastrointestinal diseases such as cardiovascular diseases, neurological disorders, and metabolic diseases. At the same time, many scholars have noted the relationship between H. pylori infection and non-alcoholic fatty liver disease (NAFLD). Despite the positive association between H. pylori and NAFLD reported in some researches, there are opposite perspectives denying their relationship. Due to high prevalence, unclear etiology and difficult treatment of NAFLD, confirming the pathogenicity of H. pylori infection in NAFLD will undoubtedly provide insights for novel treatment strategies for NAFLD. This paper will review the relationship between H. pylori infection and NAFLD and the possible pathogenic mechanisms.
Highlights
Helicobacter pylori (H. pylori) is a gram-negative microaerophilic bacterium that colonizes the stomach of humans
A prospective, open-label, single-center study which consisted of 159 non-alcoholic fatty liver disease (NAFLD) patients, revealed that the HOMA-insulin resistance (IR), TC, TG, LDL-C, and C-reactive protein (CRP) levels were significantly higher and HDL-C levels were significantly lower in patients with H. pylori infection (P < 0.05), while homeostatic model assessment of insulin resistance (HOMA-IR), TC, TG, LDL-C, and CRP levels in patients with successful eradication were significantly decreased compared to the pretreatment levels (P < 0.05)
The results indicated that ongoing crosstalk occurs between H. pylori and the normal gut microbiota, which is associated with metabolism and gut inflammation
Summary
Helicobacter pylori (H. pylori) is a gram-negative microaerophilic bacterium that colonizes the stomach of humans. Many studies have reported that H. pylori infection is closely related to the development of NAFLD (Polyzos et al, 2013a; Sumida et al, 2015).
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
