Response to Comment on: Jeon et al. Helicobacter pylori Infection Is Associated With an Increased Rate of Diabetes. Diabetes Care 2012;35:520–525

We thank Schattner for highlighting the association between hepatitis C virus (HCV) infection and diabetes (1), which further attests to the role of infections in diabetes. Indeed, multiple studies, including those conducted in HIV-infected individuals (2) and in the general population (3), have shown that HCV infection is associated with prevalent and incident diabetes. As Schattner described, tumor necrosis factor (TNF)-α may mediate the association between HCV and diabetes. We also examined the inflammatory pathway as a potential mechanism linking Helicobacter pylori (H. pylori) and diabetes, but our data did not substantiate the hypothesis, since interleukin-6 and C-reactive protein levels were not different between H. pylori–infected and noninfected individuals at baseline. We additionally examined TNF-α levels, which also did not differ by H. pylori infection.

Systemic inflammation may not be the only mediating pathway between infections, such as H. pylori and HCV, and diabetes. H. pylori is a pathogen that specifically targets the digestive tract, which plays a major role in absorption of glucose and lipids. In fact, there is active research underway regarding the role of gut microbiota in insulin resistance through altered energy harvesting and lipid metabolism (4). In parallel, HCV may have a unique local effect that is intimately linked to insulin resistance, since HCV has been detected in the pancreas where it may have a direct cytopathic effect on pancreatic islets, leading to reduced release of insulin (5).

We absolutely agree on the need for further studies on the potential causative role of H. pylori and HCV on diabetes that could be used to inform effective prevention strategies for diabetes.