The Possible Role of Helicobacter pylori Infection in Non-alcoholic Fatty Liver Disease

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.

Functional Interactions between Gut Microbiota Transplantation, Quercetin, and High‐Fat Diet Determine Non‐Alcoholic Fatty Liver Disease Development in Germ‐Free Mice

“…Interestingly, a higher detection of Helicobacter genus was observed in the dHFD+ in comparison to the dHFD− . The increased relative abundance of this genus in the HFD‐responder donor supports its possible involvement in the pathogenesis of NAFLD, as previously suggested . Other genera, such as Oscillospira , Lactobacillus , and Alkaliphilus revealed an opposite pattern, showing a higher detection in dHFD− .…”

“…Moreover, Helicobacter pylori seems to contribute to the progression of NAFLD in a mechanism that could involve dysbiosis‐induced endotoxemia and inflammatory response activation . In HFD‐fed dC ‐receiver supplementation with quercetin reduced the increased Helicobacter genus detection, supporting the results described in the A model .…”

Association between Helicobacter pylori infection and nonalcoholic fatty liver disease: A systematic review and meta‐analysis of observational studies

“…Secondly, the hormonal link between H. pylori infection and NAFLD has also been assumed, with particular attention to adiponectin, leptin, and fetuin‐A. These cytokines have been regarded as crucial factors contributing to IR . Adiponectin, an adipocyte‐derived hormone, reduces lipid storage in the liver and protects against inflammation and fibrosis .…”

“…Leptin, the first described adipokine, plays a key role in regulation of energy homeostasis, glucose, and lipid metabolism . H. pylori may dampen the release of leptin from white adipose tissue, and then promote liver stearoyl CoA desaturase, thereby accelerating very‐low‐density lipoprotein cholesterol (VLDL‐C) and liver fat deposition . Similarly, the fetuin‐A, a liver‐derived glycoprotein, is regarded as a crucial pro‐inflammatory mediator that plays a key role in inflammatory and immune diseases .…”

“…H. pylori infection may increase mucosal permeability of the intestine and lead to gut flora dysbiota, and then promote bacterial endotoxins passage to the liver through portal vein circulation. These endotoxins in turn can promote inflammation by increasing pro‐inflammatory cytokines, IR, and increased lipid accumulation in the liver . However, this hypothesis needs to be further verified in well‐designed human studies, taking fully into account the complex interactions with confounding factors, such as environmental and genetic susceptibility factors.…”