AIM: To assess the effect of Helicobacter pylori(H. pylori) infection on metabolic parameters in Mongolian gerbils.METHODS: A total of 40 male, 5- to 8-wk-old, specific-pathogen-free Mongolian gerbils(30-50 g) were randomly allocated into two groups: a control group(n = 20) and an H. pylori group(n = 20). After a two-week acclimation period, the control group was administered Brucella broth and the H. pylori group was challenged intra-gastrically five times every other day with approximately 109/CFU H. pylori ATCC43504(Cag A+, Vac A+). Each group was then divided into two subgroups, which were sacrificed at either 6 or 12 mo. The control and H. pylori subgroups each contained 10 Mongolian gerbils. Body weight, abdominal circumference, and body length were measured, and body mass index(BMI) and Lee’s index were calculated. Biochemical assays were used to detect serum indexes, including glucose, glycated hemoglobin(GHb), glycated hemoglobin A1c(Hb A1c), triacylglycerol, and total cholesterol, using an automatic biochemistry analyzer. Inflammatory cytokines, including interleukin(IL)-1β, IL-2, IL-4,IL-10, IL-12, tumor necrosis factor-α(TNF-α) and interferon(IFN)-g, were assayed using ELISA. The expression of insulin and insulin-like growth factor 1(IGF-1) was detected by immunohistochemistry, and islet apoptosis was measured using the terminal deoxynucleotidyl transferase-mediated d UTP nick end labeling(TUNEL) assay.RESULTS: At each time point, body weight, abdominal circumference, BMI, and Lee’s index were increased after H. pylori infection. However, these differences were not significant. H. pylori infection significantly increased the GHb(5.45 ± 0.53 vs 4.98 ± 0.22, P < 0.05) and Hb A1c(4.91 ± 0.61 vs 4.61 ± 0.15, P < 0.05) levels at 12 mo. We observed no significant differences in serum biochemical indexes, including fasting blood glucose, triacylglycerol and total cholesterol, at 6 or 12 mo after infection. H. pylori infection significantly increased the expression of IGF-1(P < 0.05). Insulin levels from the pancreas and the apoptotic rate of islet β-cells remained unchanged. Also, we observed no significant differences among cytokines levels, including IL-1β, IL-2, IL-4, IL-10, IL-12, TNF-α and IFN-g. IL-4 was the only exception, which increased at 6(44.36 ± 25.17 vs 17.38 ± 3.47, P < 0.05) and 12 mo(33.41 ± 10.00 vs 18.91 ± 5.31, P < 0.05) after H. pylori infection.CONCLUSION: Long-term H. pylori infection is significantly associated with high levels of Hb A1 c in Mongolian gerbils, indicating a potential role of H. pylori infection in glucose dysregulation. AIM: To assess the effect of Helicobacter pylori (H. pylori) infection on metabolic parameters in Mongolian gerbils. METHODS: A total of 40 male, 5- to 8-wk-old, After a two-week acclimation period, the control group was administered Brucella broth and the H. pylori group (n = 20) and an H. pylori group was challenged intra-gastrically five times every other day with approximately 109 / CFU H. pylori ATCC 43504 (Cag A +, Vac A +). Each group was then divided into two subgroups, which were sacrificed at either 6 or 12 mo. The control and H Body weight, abdominal circumference, and body length were measured, and body mass index (BMI) and Lee’s index were calculated. Biochemical assays were used to detect serum indicators, including glucose, glycated hemoglobin ), glycated hemoglobin A1c (Hb A1c), triacylglycerol, and total cholest Inflammatory cytokines, including interleukin (IL) -1β, IL-2, IL-4, IL-10, IL-12, tumor necrosis factor-α (TNF- -g, were assayed using ELISA. The expression of insulin and insulin-like growth factor 1 (IGF-1) was detected by immunohistochemistry, and islet apoptosis was measured using the terminal deoxynucleotidyl transferase-mediated d UTP nick end labeling (TUNEL) assay .Results: At each time point, body weight, abdominal circumference, BMI, and Lee’s index were increased after H. pylori infection. However, these differences were not significant. H. pylori infection significantly increased the GHb (5.45 ± 0.53 vs 4.98 ± 0.22, P <0.05) and Hb A1c (4.91 ± 0.61 vs. 4.61 ± 0.15, P <0.05) levels at 12 mo. We observed no significant differences in serum biochemical indexes, including fasting blood glucose, triacylglycerol and total cholesterol, at 6 or 12 mo after infection. H. pylori infection significantly increased the expression of IGF-1 (P <0.05). Insulin levels from the pancreas and the apoptotic rate of islet β-cells were unchanged unchanged. Also, we observed no significant differences among cytokines levels, including IL-1β, IL- IL-4 was the only exception, which increased at 6 (44.36 ± 25.17 vs 17.38 ± 3.47, P <0.05) and 12 mo (33.41 ± 10.00 vs 18.91 ± 5.31, P <0.05) after H. pylori infection. CONCLUSION: Long-term H. pylori infection was significantly associated with high levels of Hb A1 c in Mongolian gerbils, indicating a potential role of H. pylori infection in glucose dysregulation .