Yoon Jin Choi1, Nayoung Kim2,3, Hyuk Yoon1, Cheol Min Shin1, Young Soo Park1, Ji Hyun Park4, Ryoung Hee Nam1, Dong Ho Lee1,4, Hyun Chae Jung4. 1. Department of Internal Medicine, Seoul National University Bundang Hospital, 173-82, Gumi-ro, Bundang-gu, Seongnam, Gyeonggi-do, 463-707, South Korea. 2. Department of Internal Medicine, Seoul National University Bundang Hospital, 173-82, Gumi-ro, Bundang-gu, Seongnam, Gyeonggi-do, 463-707, South Korea. nayoungkim49@empas.com. 3. Department of Internal Medicine and Liver Research Institute, Seoul National University College of Medicine, Seoul, South Korea. nayoungkim49@empas.com. 4. Department of Internal Medicine and Liver Research Institute, Seoul National University College of Medicine, Seoul, South Korea.
Abstract
BACKGROUND: Ghrelin has been indicated as one of the etiological factors in functional dyspepsia (FD). METHODS: We analyzed 179 patients with FD (based on the Rome III criteria) and 103 asymptomatic healthy individuals (controls) who had undergone endoscopy at Seoul National University Bundang Hospital from February 2011 to June 2014. FD patients were classified into three groups by means of a self-reported questionnaire: patients with postprandial distress syndrome (PDS; n = 49), patients with epigastric pain syndrome (EPS; n = 45), and patients with a combination of these two types (mixed group; n = 85). The fasting blood levels of acyl ghrelin and desacyl ghrelin and messenger RNA (mRNA) expression of preproghrelin in the fundic mucosa were measured by ELISAs and reverse transcription quantitative real-time PCR, respectively. One year after participant enrollment, they were measured again in 79 participants and the changes in the values were compared according to Helicobacter pylori eradication or symptom response. RESULTS: Plasma acyl ghrelin level was lower in the PDS group than in the control and EPS groups (control group 14.1 fmol/mL, PDS group 8.9 fmol/mL, EPS group 13.8 fmol/mL, mixed group 11.3 fmol/mL; P = 0.003 and P = 0.012, respectively). One year after the eradication of H. pylori, plasma acyl ghrelin level was increased and gastric preproghrelin mRNA expression was upregulated (P = 0.004 and P < 0.001, respectively). Patients with abatement of symptoms demonstrated an increase in plasma acyl ghrelin level (from 11.51 to 21.00 fmol/L, P = 0.040). CONCLUSIONS: Our results suggest that plasma acyl ghrelin plays a role in the development of PDS. H. pylori eradication upregulates preproghrelin mRNA expression and increases plasma acyl ghrelin level, contributing to the abatement of PDS symptoms.
BACKGROUND:Ghrelin has been indicated as one of the etiological factors in functional dyspepsia (FD). METHODS: We analyzed 179 patients with FD (based on the Rome III criteria) and 103 asymptomatic healthy individuals (controls) who had undergone endoscopy at Seoul National University Bundang Hospital from February 2011 to June 2014. FDpatients were classified into three groups by means of a self-reported questionnaire: patients with postprandial distress syndrome (PDS; n = 49), patients with epigastric pain syndrome (EPS; n = 45), and patients with a combination of these two types (mixed group; n = 85). The fasting blood levels of acyl ghrelin and desacyl ghrelin and messenger RNA (mRNA) expression of preproghrelin in the fundic mucosa were measured by ELISAs and reverse transcription quantitative real-time PCR, respectively. One year after participant enrollment, they were measured again in 79 participants and the changes in the values were compared according to Helicobacter pylori eradication or symptom response. RESULTS: Plasma acyl ghrelin level was lower in the PDS group than in the control and EPS groups (control group 14.1 fmol/mL, PDS group 8.9 fmol/mL, EPS group 13.8 fmol/mL, mixed group 11.3 fmol/mL; P = 0.003 and P = 0.012, respectively). One year after the eradication of H. pylori, plasma acyl ghrelin level was increased and gastric preproghrelin mRNA expression was upregulated (P = 0.004 and P < 0.001, respectively). Patients with abatement of symptoms demonstrated an increase in plasma acyl ghrelin level (from 11.51 to 21.00 fmol/L, P = 0.040). CONCLUSIONS: Our results suggest that plasma acyl ghrelin plays a role in the development of PDS. H. pylori eradication upregulates preproghrelin mRNA expression and increases plasma acyl ghrelin level, contributing to the abatement of PDS symptoms.
Authors: M A Bednarek; S D Feighner; S S Pong; K K McKee; D L Hreniuk; M V Silva; V A Warren; A D Howard; L H Van Der Ploeg; J V Heck Journal: J Med Chem Date: 2000-11-16 Impact factor: 7.446
Authors: H Miwa; S Hirai; A Nagahara; T Murai; T Nishira; S Kikuchi; Y Takei; S Watanabe; N Sato Journal: Aliment Pharmacol Ther Date: 2000-03 Impact factor: 8.171
Authors: Jatin Roper; Fritz Francois; Peter L Shue; Michelle S Mourad; Zhiheng Pei; Asalia Z Olivares de Perez; Guillermo I Perez-Perez; Chi-Hong Tseng; Martin J Blaser Journal: J Clin Endocrinol Metab Date: 2008-04-08 Impact factor: 5.958
Authors: Yoon Jin Choi; Young Soo Park; Nayoung Kim; Yong Sung Kim; Sun Min Lee; Dong Ho Lee; Hyun Chae Jung Journal: World J Gastroenterol Date: 2017-12-07 Impact factor: 5.742
Authors: Won Seok Kim; Yonghoon Choi; Nayoung Kim; Seon Hee Lim; Gitark Noh; Ki Wook Kim; Jaehyung Park; Hyeongho Jo; Hyuk Yoon; Cheol Min Shin; Young Soo Park; Dong Ho Lee Journal: Korean J Intern Med Date: 2022-01-07 Impact factor: 3.165
Authors: Ju Yup Lee; Nayoung Kim; Yoon Jin Choi; Ji Hyun Park; Hassan Ashktorab; Duane T Smoot; Dong Ho Lee Journal: J Neurogastroenterol Motil Date: 2020-04-30 Impact factor: 4.924