MedWire News: Study results show that Helicobacter pylori infection increases insulin resistance through elevation of fetuin A, which could indicate a link with diabetes.
"Among the various factors capable of inducing insulin resistance, the upregulation of α2-Heremans Schmid glycoprotein, also known as human fetuin A, has been linked with impaired insulin sensitivity, glucose metabolism and, subsequently, the onset of diabetes mellitus," explain Spyros Potamianos (University of Thessaly, Larissa, Greece) and colleagues.
Certain pathogens have been observed to increase levels of fetuin A. To investigate whether H. pylori is such an infection, the researchers measured levels of fetuin A and fasting insulin and glucose in 105 non-diabetic individuals who were undergoing esophagogastroduodenoscopy due to dyspeptic complaints.
As reported in the journal Diabetologia, 72 participants were found to be infected with H. pylori and 33 were not. In multivariate analysis (adjusted for age, gender, body mass index, lipids, and C-reactive protein), H. pylori-positive individuals had significantly higher levels of fetuin A (0.74 vs 0.57 g/l) and homeostasis model assessment of insulin resistance (2.6-2.8 vs 1.9-2.0) than those who were not infected.
Potamianos and team say that the "data from the present study are consistent with the notion that H. pylori infection may induce insulin resistance."
However, they caution that "the present model cannot be regarded as final, since it was shaped based upon the findings of a study of a more or less observational nature."
They conclude: "Further research is therefore required, preferably using a more 'mechanistic' approach so that the conclusions presented above may be verified, and perhaps expanded by the inclusion of other constituents, eg, adipokines, gastrin or somatostatin, before a widely accepted mechanism is completely established."
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