Data from: The role of morbidly obesity in the promotion of metabolic disruptions and non-alcoholic steatohepatitis by Helicobacter Pylori

Helicobacter pylori (HP) infection has been associated to an increased
rate of type 2 diabetes (T2D) and liver disease through its effect on
insulin resistance and systemic inflammation. However, results are
inconstant and no studies exist in morbidly obese patients, in which both
insulin resistance and inflammation coexist. Material and Methods:
Cross-sectional study to evaluate the relationship between HP infection
and alterations in carbohydrate metabolism, lipid profile, inflammation
markers, and liver disease in patients awaiting for bariatric surgery. HP
infection was histologically assessed in gastric antrum biopsy from 416
subjects. Liver biopsy was also available in 93 subjects. Results: Both
impaired fasting glucose and T2D were similar when comparing subjects with
and without HP infection (24.2% vs. 22%, p=0.290 and 29.4% vs. 29.1%,
p=0.916, respectively), with no differences between groups in the HOMA-IR,
lipid profile neither inflammatory parameters. However, HP infection was
higher among subjects with a BMI ? 40.0 kg/m2 in comparison with lower
degrees of obesity (71.7% vs. 60.0%, p=0.041). In addition, subjects
without HP infection showed higher degrees of steatosis (44.1±26.4% vs.
32.0±20.7%, p=0.038), as well as a lower prevalence of non-alcoholic
steatohepatitis (9.3% vs. 30.7%, p=0.023). Conclusions: In patients with
morbid obesity, HP infection does not seem to be associated with abnormal
carbohydrate metabolism. In addition, less advanced degrees of
non-alcoholic fatty disease were observed. We suggest that low-grade
inflammation that accompanies obesity mitigates the diabetogenic effect of
HP, so the presence of obesity should be considered in studies that
evaluate the HP metabolic effects.