It is not clear whether Helicobacter pylori (Hp) infection affects insulin levels and insulin sensitivity. We aimed to determine insulin sensitivity and beta cell function, and to evaluate serum lipids in subjects with and without Hp infection. Eighty non-obese young adult males, 40 of whom were Hp positive and 40 were negative, were included in the study. Two endoscopic biopsy specimens were obtained from each subject. Height, weight and waist-hip circumference were measured, and body mass index (BMI) was calculated. Serum glucose, total, HDL, LDL and VLDL-cholesterol and triglyceride levels were determined. Body fat mass and percentage were determined by bioelectric impedance. Serum insulin levels were measured by the RIA method. HOMA was used as an index of pancreatic beta cell function and insulin sensitivity. The independent-t test was used in the comparison of results. Age, BMI, waist and hip circumferences, and fat percentages did not exhibit any statistical differences. Mean HOMA-B [111.7, in Hp(+) and 112.0 in Hp(-) subjects] and HOMA-S [67.7 in Hp(+) and 60.7 Hp(-) subjects] did not differ amoung the groups. The lipid and aminotransferase levels of the 2 groups were also similar. Conclusion: Hp infection is not associated with impairment of insulin sensitivity and deterioration of the glucose metabolism. It seems to be metabolically neutral in terms of serum lipids and aminotransferase levels.

It is not clear whether Helicobacter pylori (Hp) infection affects insulin levels and insulin sensitivity. We aimed to determine insulin sensitivity and beta cell function, and to evaluate serum lipids in subjects with and without Hp infection. Eighty non-obese young adult males, 40 of whom were Hp positive and 40 were negative, were included in the study. Two endoscopic biopsy specimens were obtained from each subject. Height, weight and waist-hip circumference were measured, and body mass index (BMI) was calculated. Serum glucose, total, HDL, LDL and VLDL-cholesterol and triglyceride levels were determined. Body fat mass and percentage were determined by bioelectric impedance. Serum insulin levels were measured by the RIA method. HOMA was used as an index of pancreatic beta cell function and insulin sensitivity. The independent-t test was used in the comparison of results. Age, BMI, waist and hip circumferences, and fat percentages did not exhibit any statistical differences. Mean HOMA-B [111.7, in Hp(+) and 112.0 in Hp(-) subjects] and HOMA-S [67.7 in Hp(+) and 60.7 Hp(-) subjects] did not differ amoung the groups. The lipid and aminotransferase levels of the 2 groups were also similar. Conclusion: Hp infection is not associated with impairment of insulin sensitivity and deterioration of the glucose metabolism. It seems to be metabolically neutral in terms of serum lipids and aminotransferase levels.