Glucolipid Metabolic Disorders and Helicobacter pylori Infection

糖脂代谢紊乱与幽门螺杆菌感染

阅读:1

Abstract

Due to its high incidence and severe consequences, glucolipid metabolic disorders (GLMD) remain a significant challenge for the global medical community. Helicobacter pylori (H. pylori), a Gram-negative bacterium that colonizes the gastric mucosa, has a high infection rate worldwide, exceeding 50% in the global population. Although numerous studies have explored the associations between H. pylori and individual metabolic diseases, a systematic review framework that integrates these findings to provide a comprehensive perspective on GLMD is still lacking. Recent studies have indicated that H. pylori infection can lead to disturbances in lipid and glucose metabolism; however, this area of research is fraught with controversy, even yielding completely opposing conclusions. Based on this, we systematically reviewed the research on the association between H. pylori and type 2 diabetes (T2DM), metabolic dysfunction-associated steatotic liver disease (MASLD), and atherosclerosis (AS). We conducted an in-depth analysis of how H. pylori infection influences the onset and progression of GLMD through multiple mechanisms, including the induction of inflammatory responses, exacerbation of oxidative stress, and impairment of insulin sensitivity. Simultaneously, we highlighted the roles of bacterial virulence factors and the exosomes they regulate in metabolism. In conclusion, we have determined that H. pylori infection may induce inflammatory responses, exacerbate oxidative stress, and impair insulin sensitivity by regulating the levels of inflammatory cytokines, adiponectin (ADPN), leptin, vitamin D, homocysteine, and exosomes, thereby collectively influencing the occurrence and progression of the aforementioned diseases. Therefore, effective control and treatment of H. pylori infection should not be neglected in the management of GLMD.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。