Jeon et al. (1) have convincingly demonstrated that individuals seropositive for Helicobactor pylori (H. pylori) at enrollment were significantly more likely to develop diabetes. The mechanism remains unclear.
Chronic hepatitis C is another infectious disease found to be associated with an increased incidence of diabetes, independent of the development of liver cirrhosis (2). Hepatitis C virus–mediated induction of inflammatory cytokines, in particular tumor necrosis factor (TNF)-α, may be the pathogenetic link between hepatitis C virus and diabetes. TNF-α is increased in the liver and serum of patients with chronic hepatitis C, correlates with the severity of inflammation, and induces insulin resistance by several intriguing mechanisms (3,4).
TNF-α may also underlie the recent observation by Jeon et al. of the increased risk of H. pylori–infected patients to develop diabetes. The host immune response to H. pylori infection is complex and involves upregulation of several proinflammatory cytokines. A T helper type 1 response is induced, and high levels of several cytokines including TNF-α, interleukin-6, and interferon-γ have been identified both locally in the chronically inflamed antral mucosa and in the plasma (5). Increased insulin resistance and incident diabetes may be secondary to the effect of H. pylori–induced cytokines, particularly in patients who are already at risk for developing diabetes because of other common concurrent factors.
Further exploration of these associations is warranted and may possibly change the current attitude toward the eradication of H. pylori in colonized asymptomatic adults.
Acknowledgments
No potential conflicts of interest relevant to this article were reported.
