Association of low serum adiponectin levels with erosive esophagitis in men: An analysis of 2405 subjects undergoing physical check-ups

Department of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan.
Journal of Gastroenterology (Impact Factor: 4.52). 08/2011; 46(12):1361-7. DOI: 10.1007/s00535-011-0453-3
Source: PubMed


Obesity is a risk factor for gastro-esophageal reflux disease (GERD). It is generally considered that intra-abdominal pressure in obese subjects is involved in the pathogenesis of GERD through acid exposure to the esophagus. Recently, visceral fat has been recognized as an endocrine organ that secretes various adipocytokines including adiponectin. The aim of this study was to elucidate the relation between adiponectin and erosive esophagitis.
This was a cross-sectional retrospective observational study: 2405 consecutive subjects who underwent screening esophago-gastro-duodenoscopy with serum adiponectin measurement as part of their physical check-up programs were analyzed. Clinical factors were compared between subjects with and without erosive esophagitis. The association between adiponectin and erosive esophagitis was assessed using a bootstrapping re-sampling method after adjustment for factors that tended to be different in univariate analysis.
Serum adiponectin levels were significantly lower in those with erosive esophagitis (8.17 μg/ml) than in those without (10.1). The erosive esophagitis group had a greater body mass index (BMI) and waist circumference (WC) and a higher prevalence of hiatal hernia. Using the bootstrap method, with a lower adiponectin cut-off value of 3-7 μg/ml, the lower limit of the 95% confidence interval of the adjusted odds ratio consistently exceeded 1 after adjustment for BMI and hiatal hernia in men. When adjusting for WC instead of BMI, the effect of adiponectin was reduced but remained significant at a lower cut-off value (3-3.5 μg/ml).
Low serum adiponectin levels may be associated with an increased risk for erosive esophagitis in men.

Download full-text


Available from: Yoshihiro Kamada,
31 Reads
  • Source
    • "The first of these includes the direct mechanical effects of abdominal obesity, resulting in an elevation of the intragastric and gastroesophageal pressure gradient [10], [24], an increase in acid reflux episodes with longer duration [25], and in transient lower esophageal sphincter (LES) relaxation [26], leading to esophageal mucosal local injury. The second process, from mediator-driven view, is based on inflammatory signals that originate from the visceral adipose tissue, including an increase in proinflammatory cytokines, such as interleukin-6 and tumor necrosis factor-α [27], [28] and a decrease in potentially anti-inflammatory adiponectin [29], [30]. Furthermore, one study showed that adipokines, such as leptin, are positively correlated with WC in overweight subjects, while adiponectin is negatively correlated with it [31]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: To investigate the relationship between overweight and erosive esophagitis (EE) in a non-obese Taiwanese population. A total of 7,352 subjects (non-obese, 5,826; obese, 1,526) from a health examination center at National Cheng Kung University Hospital were enrolled. Central obesity was defined by a waist circumference (WC) ≥90 cm in male and 80 cm in female. Overweight was defined as body mass index (BMI) of 24-26.9 kg/m(2), and general obesity as BMI ≥27 kg/m(2). The Los Angeles classification was adopted to determine the presence of EE. There were significant differences in the prevalence of central obesity and different BMI status between subjects with and without EE in total and non-obese population. In total population, multivariate analyses revealed central obesity (OR, 1.17, 95% CI, 1.02-1.34, p = 0.021) and being obese (OR, 1.28, 95% CI, 1.07-1.52, p = 0.007)/overweight (OR, 1.25, 95% CI, 1.08-1.45, p = 0.003) had positive associations with EE in different model, respectively. When considering the joint effect of central obesity and BMI status, overweight (OR, 1.22; 95% CI, 1.04-1.44; p = 0.016) remained as an independent associated factor of EE but central obesity (OR, 1.06; 95% CI, 0.89-1.26; p = 0.549)/being obese (OR, 1.22; 95% CI, 0.98-1.53; p = 0.082) did not. As for non-obese group, separate model showed central obesity (OR, 1.19, 95% CI, 1.00-1.40, p = 0.046) and overweight (OR, 1.24; 95% CI, 1.07-1.44, p = 0.005) was positively associated with EE, respectively. However, being overweight (OR, 1.20; 95% CI, 1.02-1.42, p = 0.030) but not central obesity (OR, 1.08; 95% CI, 0.90-1.31; p = 0.398) was positively related to EE with considering the effect of overweight and central obesity simultaneously. Overweight effect on EE was more detrimental than central obesity in non-obese subjects. In addition, male gender, hiatus hernia and alcohol use were also associated with increased risk of EE.
    PLoS ONE 11/2013; 8(11):e77932. DOI:10.1371/journal.pone.0077932 · 3.23 Impact Factor
  • Source
    • "Observational studies from Asia have reported a consistent association between WC or VAT and RE [32,33]. Two studies of RE in a Japanese population showed that abdominal obesity may be an important risk factor for RE in males, but not in females [34,35], but another report did not show this association [36], which has led to some controversy about the association between obesity and RE. The present study clearly demonstrated that RE was an independent risk factor for ESBE, while obesity was not a risk factor for RE. "
    [Show abstract] [Hide abstract]
    ABSTRACT: The association between obesity and Barrett's esophagus (BE) in the Japanese population remains unclear. The prevalence of BE and its associated risk factors was examined. A cross-sectional study of 1581 consecutive individuals who underwent upper gastrointestinal endoscopy was conducted. The prevalence of endoscopically suspected BE (ESBE) was evaluated. Obesity was evaluated by body mass index (BMI, >= 25 kg/m2) and waist circumference (WC) (males, >= 85 cm; females, >= 90 cm). Because endoscopic diagnosis of ultra-short ESBE (<1 cm in extent) is difficult and highly unreliable, this type of ESBE was excluded from the study. In proton pump inhibitor (PPI) non-users, the prevalence of ESBE >= 1 cm was 5.6%. In univariate analysis, male sex and reflux esophagitis (RE) were significantly associated with BE, but BMI, WC, and reflux symptoms were not. In multivariate logistic regression analysis, only RE (odds ratio [OR] = 3.48, 95% confidence interval [CI] 1.89-6.41, p < 0.0001) was an independent risk factor for BE; obesity and the other factors were not. In contrast, RE (OR 5.67, p = 0.0004) and large WC (OR 5.09, p = 0.0005) were significant risk factors for ESBE >= 1 cm in PPI users. Only male sex, but not obesity or the other risk factors, was associated with an increased risk of RE in patients not taking PPIs. RE, but not obesity, may have an independent association with the risk of ESBE in the Japanese population. Furthermore, obesity measures were not independent risks for RE. Interestingly, PPI-refractory RE and large WC were risk factors for ESBE >=1 cm in patients taking PPIs.
    BMC Gastroenterology 09/2013; 13(1):143. DOI:10.1186/1471-230X-13-143 · 2.37 Impact Factor
  • Source
    • "Gastro-oesophageal reflux is well established as a risk factor for oesophageal adenocarcinoma and population studies have shown that obesity and gastro-oesophageal reflux together greatly increase the risk of OAC (Lagergren et al., 1999). In keeping with this, cell culture studies have shown that leptin and transient acidexposure are synergistic in inducing leptin-receptor dependent signalling, proliferation and inhibiting apoptosis (Beales and Ogunwobi, 2007), whilst relative adiponectin deficiency has also been reported to be associated with erosive oesophagitis (Kato et al., 2011). The current studies add further weight to the argument that diminished adiponectin levels may contribute to increased risk of OAC in obesity and that further studies examining the anti-cancer effects of adiponectin are warranted. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Obesity is characterized by hyperleptinaemia and hypoadiponectinaemia and these metabolic abnormalities may contribute to the progression of several obesity-associated cancers including oesophageal adenocarcinoma (OAC). We have examined the effects of leptin and adiponectin on OE33 OAC cells. Leptin stimulated proliferation, invasion and migration and inhibited apoptosis in a STAT3-dependant manner. Leptin-stimulated MMP-2 secretion in a partly STAT3-dependent manner and MMP-9 secretion via a STAT3-independent pathway. Adiponectin inhibited leptin-induced proliferation, migration, invasion, MMP secretion and reduced the anti-apoptotic effects: these effects of adiponectin were ameliorated by both a non-specific tyrosine phosphatase inhibitor and a specific PTP1B inhibitor. Adiponectin reduced leptin-stimulated JAK2 activation and STAT3 transcriptional activity in a PTP1B-sensitive manner and adiponectin increased both PTP1B protein and activity. We conclude that adiponectin restrains leptin-induced signalling and pro-carcinogenic behaviour by inhibiting the early events in leptin-induced signal transduction by activating PTP1B. Relative adiponectin deficiency in obesity may contribute to the promotion of OAC.
    Molecular and Cellular Endocrinology 08/2013; 382(1). DOI:10.1016/j.mce.2013.08.013 · 4.41 Impact Factor
Show more