Helicobacter pylori infection and diabetes: is it a myth or fact?

Abstract

Helicobacter pylori (H. pylori) is one of the most common human bacterial pathogens, and infection causes a wide array of gastric disorders, including simple gastritis, peptic ulcers and gastric malignancies. Gastrointestinal inflammation caused by H. pylori can influence the absorption of glucose and lipids, which are also abnormal in diabetes mellitus. Type 2 diabetes mellitus (T2DM), formerly known as non-insulin-dependent diabetes mellitus or adult-onset diabetes, is a metabolic disorder that is characterized by high levels of blood glucose resulting from insulin resistance and relative insulin deficiency. It is an emerging pandemic and is rapidly becoming a serious threat to public health. Emerging data now indicate a strong relationship between H. pylori infection and the incidence of T2DM. The mechanisms underlying the pathogenesis of diabetes are complex, involving insulin resistance, chronic inflammation, insulin secretion deficiency as a result of pancreas β-cell dysfunction, glucotoxicity, and lipotoxicity. H. pylori infection is known to be involved in the pathogenesis of insulin resistance, and the growing awareness of its role in diabetes is important for the early detection of glucose dysregulation and prevention of T2DM in high-risk communities. This review probes the possible relationship between H. pylori and diabetes according to epidemiological surveys and discusses putative mechanisms underlying this correlation.

Keywords: Cytokines; Helicobacter pylori; Inflammation; Insulin resistance; Type 2 diabetes.

Figures

Figure 1

Potential mechanisms for contribution of Helicobacter pylori to type 2 diabetes mellitus. Insulin resistance and abnormal insulin secretion are central to the development of type 2 diabetes mellitus (T2DM). On the one hand, Helicobacter pylori (H. pylori) infection brings about chronic low-grade inflammation with upregulation of several cytokines such as C-reactive protein (CRP), tumor necrosis factor (TNF) and interleukin (IL)-1β, which may influence insulin action and pancreatic β cell secretion. On the other hand, H. pylori-induced gastritis can potentially affect the secretion of gastric hormones, including leptin, ghrelin, gastrin, and somatostatin, which could affect insulin sensitivity and glucose homeostasis. In addition, other mechanisms and mediators may be involved in the possible causative relationship between H. pylori infection and T2DM.