Aims/Introduction Helicobacter pylori infection is associated with insulin resistance and glycemia in non‐diabetes. However, the relationship between H. pylori infection and glycemia in diabetes remains inconclusive. Therefore, we explored the effect of H. pylori infection status and its eradication on glycemic control and antidiabetic therapy in type 2 diabetes patients. Materials and Methods A total of 549 diabetes patients were recruited for sequential two‐step approach (immunoglobulin G [IgG] serology followed by 13 C‐urea breath test [UBT] ) to discriminate “active” (IgG+ and UBT +) from “non‐active” ( UBT − or IgG−) H. pylori infection, and “past” (IgG+ but UBT −) from “never/remote” (IgG−) infection. The differences in hemoglobin A1c (A1C) and antidiabetic regimens between groups were compared. In the “active” infection group, the differences in A1C changes between participants with and without 10‐day eradication therapy were compared after 3 months. Results Despite no between‐group difference in A1C, the “active” infection group ( n = 208) had significantly more prescriptions of oral antidiabetic drug classes (2.1 ± 1.1 vs 1.8 ± 1.1, P = 0.004) and higher percentages of sulfonylurea use (67.3% vs 50.4%, P < 0.001) than the “non‐active” infection group ( n = 341). There were no differences in A1C and oral antidiabetic drug classes between “past” ( n = 111) and “never/remote” infection groups ( n = 230). Compared with the non‐eradication group ( n = 99), the eradication group ( n = 98) had significant within‐group (−0.17 ± 0.80%, P = 0.036) and between‐group (−0.23 ± 0.10%, P = 0.024) improvements in A1C. Conclusions Diabetes patients with active H. pylori infection need higher glycemic treatment intensity to achieve comparable glycemia. Furthermore, H. pylori eradication decreases A1C, and thus improves glycemic control.
Hepassocin (HPS) is a hepatokine that regulates hepatocyte proliferation. It is known that HPS plays an important role in the development of nonalcoholic fatty liver diseases (NAFLD). Fatty acids, such as oleic acid (OLA), exhibit the ability to activate the signal transducer and activator of transcription‐3 (STAT3), and the binding site of STAT3 is found in the promoter region of HPS. However, the regulation of HPS by fatty acids is still obscure. To clarify the regulation of HPS, we detected the expression of HPS by western blots. In addition, a hepatic steatosis cell culture model was established by treatment of different fatty acids, including linoleic acid (LNA), oleic acid, palmitic acid, and stearic acid. The intracellular lipid accumulation was confirmed by oil red O staining. Blocking of STAT3 activity was achieved by the pretreatment of the STAT3 inhibitor, stattic. We found that activation of STAT3 by interleukin‐6 (IL‐6) was mediated in the regulation of HPS expression. Treatment of unsaturated fatty acids significantly induced intracellular lipid accumulation in HepG2 cells. Moreover, the expressions of HPS were increased in unsaturated fatty acid‐treated HepG2 cells, as compared with saturated fatty acid‐treated groups. Also, the expression of HPS induced by OLA was blocked by the inhibition of STAT3 activity. Furthermore, we found that deletion of HPS by small interfering ribonucleic acid transfection decreased the protective effect of OLA on cell viability. Taken together, we provided evidence that STAT3 plays an important role in the regulation of OLA‐induced HPS expression and the increased HPS may further participate in the development of NAFLD. In addition, the increase of HPS might be involved in the protective effect of OLA on cell viability.
Obesity is a public health problem that has raised concerns worldwide and is often associated with hepatic steatosis. Hepassocin is a novel hepatokine that causes hepatic steatosis and induces insulin resistance (IR). However, the role of hepassocin in obesity remains obscure. Thus, the aim of this study was to investigate the relationship between hepassocin levels and obesity. In total, 371 subjects who had a normal weight (NW), were overweight, or were obese were enrolled. We found that hepassocin levels in subjects who were overweight (6,705 ± 1,707 pg/ml) or obese (7,335 ± 2,077 pg/ml) were significantly higher than those of subjects with a NW (5,767 ± 1,500 pg/ml) (p < .001, test for trend). A multiple linear regression analysis showed that the body-mass index, waist circumference, nonalcoholic fatty liver disease, and homeostatic model assessment of IR were independently associated with hepassocin after adjusting for age, sex, highsensitivity C-reactive protein, systolic blood pressure, high-density lipoprotein-cholesterol, log triglycerides, alanine transaminase, and the estimated glomerular filtration rate. This study provides evidence that subjects who were overweight or obese had significantly higher hepassocin levels than those with a NW. Hepassocin may be a useful biomarker in managing obesity and its related metabolic dysregulation.
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