Eun Jeong Jang

The influence of the eradication of Helicobacter pylori on gastric ghrelin, appetite, and body mass index in patients with peptic ulcer disease

Background and Aim:  Helicobacter pylori (H. pylori) infection has been known to influence the gastric leptin and ghrelin secretion, for which the exact pathogenic role has not been documented yet. This study was designed to investigate the influence of H. pylori eradication on plasma or gastric levels of ghrelin, body mass index (BMI), and resultant levels of appetite in patients with peptic ulcer disease.

Eradication of Helicobacter pylori Increases Ghrelin mRNA Expression in the Gastric Mucosa

It has been suggested that Helicobacter pylori eradication may influence production of some peptides in the stomach, which can affect appetite. This hypothesis is controversial. To verify the hypothesis, we conducted this randomized controlled trial using H. pylori infected subjects without any gastrointestinal symptoms. The treatment group received triple H. pylori eradication therapy for 7 days and the control group received no medication. We measured ghrelin, obestatin and the tumor necrosis factor-α (TNF-α) mRNA levels in endoscopic biopsy specimens and the changes from baseline to follow-up. The plasma active n-octanoyl ghrelin and obestatin levels were measured in both groups. The ghrelin/obestatin ratios in plasma and gastric mRNA expression were calculated at baseline and follow-up. Ghrelin mRNA expression in the fundic mucosa after H. pylori eradication increased significantly compared to the control group (4.47±2.14 vs. 1.79±0.96, P=0.009), independent of inflammatory changes. However, obestatin mRNA expression decreased in the antral mucosa (-0.57±1.06 vs. 0.41±0.72, P=0.028). The treatment group showed a marginal increase (P=0.060) in plasma ghrelin/obestatin ratio. The TNF-α mRNA expression also decreased significantly with treatment. This randomized controlled trial demonstrates that H. pylori eradication increases ghrelin mRNA expression, independent of inflammatory cell changes.

Measurement of antioxidant capacity using the biological antioxidant potential test and its role as a predictive marker of metabolic syndrome

Background/Aims Oxidative stress increases the risk of cardiovascular complications of metabolic syndrome (MetS). This study was conducted to examine the difference in antioxidant capacity according to the presence of MetS, and to characterize the association between antioxidant capacity and MetS-related factors. Methods We used the biological antioxidant potential (BAP) test to estimate antioxidant capacity. The BAP test has recently been used as an indicator of antioxidant capacity. We measured BAP levels in 45 patients with MetS (mean age, 44.6 ± 1.1 years) and 47 age- and sex-matched controls (mean age, 42.7 ± 1.1 years). To evaluate the association between antioxidant capacity and MetS, adiponectin, high-sensitivity C-reactive protein (hs-CRP), interleukin-6, tumor necrosis factor-α, and homeostatic model assessment for insulin resistance (HOMA-IR), linear regression and logistic analyses were performed. Results The mean BAP of the MetS group (1,937.3 ± 36.5 µmol/L) was significantly lower than that of the non-MetS group (2,101.7 ± 29.5 µmol/L). Also, the mean BAP was low in persons having low high density lipoprotein and high triglyceride. Reduced antioxidant capacity was significantly associated with adiponectin, HOMA-IR and hs-CRP after adjusting for age and sex. The odds ratios for MetS with BAP, log adiponectin, log HOMA-IR, and log hs-CRP were 0.63 (95% confidence interval [CI], 0.49 to 0.82), 0.22 (0.10 to 0.51), 14.24 (4.35 to 46.58), and 1.93 (1.36 to 2.75), respectively. Conclusions Persons with MetS showed reduced antioxidant capacity. We identified relationships between antioxidant capacity measured by BAP test and MetS, as well as MetS-related factors, such as insulin resistance, hs-CRP, and adiponectin.

Novel single nucleotide polymorphism of the VEGF gene as a risk predictor for gastroduodenal ulcers.

Background and Aim:  The gastroduodenal ulcer (GDU) mostly develops on the lesser curvature side of stomach and the anterior wall of duodenal bulb, irrespective of the etiologies including Helicobacter pylori infection, non‐steroidal anti‐inflammatory drugs, alcohol, etc. However, a clear explanation as to why ulcers are prevalent in these areas has still not been given. The current study was designed to evaluate whether the vascular endothelial growth factor (VEGF) polymorphism could predict susceptibility to GDU through deranged angiogenic activities.