Gut Microbiota: The Missing Link Between Helicobacter pylori Infection and Metabolic Disorders?

Abstract

Helicobacter pylori (H. pylori) is a gram-negative bacterium that infects approximately 4.4 billion individuals worldwide. Although the majority of infected individuals remain asymptomatic, this bacterium colonizes the gastric mucosa causing the development of various clinical conditions as peptic ulcers, chronic gastritis and gastric adenocarcinomas and mucosa-associated lymphoid tissue lymphomas, but complications are not limited to gastric ones. Extradigestive pathologies, including metabolic disturbances such as diabetes, obesity and nonalcoholic fatty liver disease, have also been associated with H. pylori infection. However, the underlying mechanisms connecting H. pylori with extragastric metabolic diseases needs to be clarified. Notably, the latest studies on the topic have confirmed that H. pylori infection modulates gut microbiota in humans. Damage in the gut bacterial community (dysbiosis) has been widely related to metabolic dysregulation by affecting adiposity, host energy balance, carbohydrate metabolism, and hormonal modulation, among others. Taking into account that Type 2 diabetic patients are more prone to be H. pylori positive, gut microbiota emerges as putative key factor responsible for this interaction. In this regard, the therapy of choice for H. pylori eradication, based on proton pump inhibitor combined with two or more antibiotics, also alters gut microbiota composition, but consequences on metabolic health of the patients has been scarcely explored. Recent studies from our group showed that, despite decreasing gut bacterial diversity, conventional H. pylori eradication therapy is related to positive changes in glucose and lipid profiles. The mechanistic insights explaining these effects should also be addressed in future research. This review will deal with the role of gut microbiota as the linking factor between H. pylori infection and metabolic diseases, and discussed the impact that gut bacterial modulation by H. pylori eradication treatment can also have in host’s metabolism. For this purpose, new evidence from the latest human studies published in more recent years will be analyzed.

Helicobacter pylori infection and the progression of atherosclerosis: A systematic review and meta‑analysis

“…This in turn promotes the oxidation of low‐density lipoproteins, which is a key event in AS 55 . Diabetes can accelerate the progression of AS, 56 and H. pylori infection can promote the development of diabetes, as well as worse blood sugar control and insulin response, and partly due to increased inflammation 57 . In short, the internal mechanism of H. pylori leading to AS may be mainly due to the increase in human inflammatory stress, abnormal blood lipids, and abnormal glucose metabolism caused by H. pylori .…”

Gut Commensal Parabacteroides goldsteinii MTS01 Alters Gut Microbiota Composition and Reduces Cholesterol to Mitigate Helicobacter pylori-Induced Pathogenesis

“…Gut or fecal microbiota containing both intestinal and gastric microbiota may affect the pathology of H. pylori infection ( 21 , 22 ), and we analyzed their composition. Microbiota DNA in mouse stool was extracted using the QIAamp PowerFecal Pro DNA Kit (Qiagen) and applied to the amplification of 16S rRNA V3–V4 region using PCR, as described previously ( 23 , 24 ).…”

Gastrointestinal microbiome and Helicobacter pylori: Eradicate, leave it as it is, or take a personalized benefit–risk approach?

“…Suggested mechanisms of this effect range from an improvement in the symptoms of postprandial dyspepsia[ 16 ] to changes in the regulation of leptin and ghrelin[ 17 ] mediated by antibiotic-associated changes in the microbiota (especially by the imbalance between bacterial producers of lactate and acetate)[ 18 ]. In general, however, the data in various studies are contradictory and indicate weight gain, weight loss, or the absence of an effect of H. pylori eradication on body weight; this may be due to differences in the characteristics of the studied populations, such as age, nosology, and composition of the GI microbiota[ 19 ]. Further in-depth study of the microbiome-mediated effects of H. pylori and eradication therapy on human host metabolism, including nutrient uptake, energy homeostasis, bodyweight, hormone secretion, lipid profile, and glucose homeostasis/glycemic control, will provide clinically important findings for the management of H. pylori infection.…”