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endoscopy, between August 2006 and December 2011. Sarcopenia was defined as an appen-
dicular skeletal muscle mass (ASM) /body weight value beyond two standard deviations
below the mean for healthy young adults. The ASM was estimated using bioelectrical
impedance analysis. Results: Participants were categorized into four groups according to
their obesity and sarcopenic status: normal, obese, sarcopenic, and sarcopenic obese. In a
multivariable model adjusted for age, sex, smoking status, alcohol intake, regular exercise,
and metabolic variables, the risk of erosive esophagitis was higher in obese [adjusted odds
ratio(aOR), 1.38; 95% confidence interval (CI), 1.26-1.52], sarcopenic (aOR, 2.20; 95% CI,
1.48-3.29), and sarcopenic obese participants (aOR, 1.68; 95% CI, 1.39-2.03) than in normal
participants. Comparing sarcopenic and sarcopenic obese participants to obese participants,
the ORs for erosive esophagitis were 1.59 (95% CI, 1.06-2.38) and 1.22 (95% CI, 1.02-1.47),
respectively. In dose-response analyses, increasing sarcopenia severity showed a positive
and graded relationship with overall, LA-B or higher grade, and LA-C erosive esophagitis.
Conclusions: Our findings suggest that sarcopenia, regardless of obesity status, is strongly
and progressively associated with the risk of erosive esophagitis.
The risk of erosive esophagitis according to sarcopenic obesity groups
Model 1 adjusted for age and sex. Model 2 adjusted for age, sex, smoking status, alcohol
intake, and regular exercise. Model 3 adjusted for systolic blood pressure, triglycerides,
HDL-cholesterol, and fasting glucose in addition to the factors included in model 2. OR,
odds ratio; CI, confidence intervals.
The risk of erosive esophagitis by LA classification according to sarcopenia status
Multivariable model was adjusted for age, sex, waist circumference, smoking status, alcohol
intake, and regular exercise. Participants with class I sarcopenia were those with weight-
adjusted skeletal muscle mass index between one and two standard deviations below the
sex-specific values measured in young healthy adults Participants with class II sarcopenia
were those with weight-adjusted skeletal muscle mass index more than two standard devia-
tions below the sex-specific values measured in young healthy adults LA, Los Angeles; OR,
odds ratio; CI, confidence intervals; ASM, appendicular skeletal muscle mass.
Sa1102
BARRETT'S EPITHELIUM DISPLAYS INCREASED EXPRESSION OF ST6GAL-
I, A GLYCOSYLTRANSFERASE STRONGLY ASSOCIATED WITH MUCOSAL
CARCINOGENESIS
Katie L. Alexander, Lesley E. Smythies, Asmi Chakraborty, Lois Musgrove, Susan Bellis,
Phillip D. Smith, Shajan Peter
Backgrounds/Aims: Barret t's esophagus (BE) is characterized by the transformation of
squamous epithelium in the distal esophagus into columnar epithelium with goblet cells.
This transformation occurs in patients with long-term gastroesophageal reflux disease
(GERD), driving dysplasia and increased risk for esophageal cancer. Glycosyltransferase
ST6Gal-I adds a2,6-linked sialic acids to the N-glycans of the death receptors TNFR1 and
CD95, thereby blocking homeostatic apoptosis. Because ST6Gal-I is strongly associated with
colonic, gastric, and pancreatic adenocarcinoma, we sought to determine the potential
involvement of ST6Gal-I in the epithelial changes associated with BE. Methods: We assessed
ST6Gal-I expression in biopsies from patients with differing grades of BE and in epithelial
stem cell organoids generated from columnar epithelium in the distal esophagus and normal
columnar epithelium from matched gastroesophageal junction (GEJ). Results: Study partici-
pants included 8 patients (5 males; mean age 64 ± 10 yrs) with BE, maximum length 8.25
± 2 cm, with intestinal metaplasia (n=2) and dysplasia (n=6). ST6Gal-I mRNA expression was
sharply increased in Barrett's esophageal tissue compared with ST6Gal-I mRNA expression
in the normal distal esophagus (NE) (p=0.02). In addition, epithelial stem cell organoids
derived from Barrett's epithelium expressed significantly higher levels of ST6-Gal-I mRNA
(p=0.01) compared with epithelial stem cell organoids derived from the columnar epithelium
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GEJ (n=4). Increased ST6Gal-I protein expression in the epithelial stem cell organoids was
confirmed at the protein level using immunofluorescence staining. Further, preliminary
studies indicate that elevated ST6Gal-I expression correlates with increasing grades of prema-
lignant changes during the progression of BE to esophageal cancer. Conclusion: These novel
findings implicate a potential role for ST6Gal-I-mediated inhibition of homeostatic apoptosis
in Barrett's epithelium and possibly esophageal adenocarcinoma.
Sa1103
NON-OBESE NON-ALCOHOLIC FATTY LIVER DISEASE IS ASSOCITED
WITH EROSIVE ESOPHAGITIS
Ki Bae Bang, Jeong Eun Shin, Hyun Deok Shin, Kwang Woo Nam, Yong Kyun Cho
Background/Aims: Obesity has been registered as a risk factor for GERD. Although non-
alcoholic fatty liver disease(NAFLD) shares common features such as insulin resistance or
metabolic syndrome with obesity, data regarding the association between the NAFLD and
GERD is scarce. This study aimed to investigate the relationship between the NAFLD and
erosive esophagitis in non-obese, non-diabetic Korean adults Methods: A cross-section study
was performed to assess the association between the erosive esophagitis and NAFLD in non-
obese, non-diabetic participants. A total of 17445 subjects who underwent health check-
up and upper endoscopy were enrolled. Fatty liver disease was diagnosed using ultrasonogra-
phy. The presence and odds ratio (OR) of erosive esophagitis was accessed in patients with
NAFLD Results: Participants with erosive esophagitis were associated with NAFLD. The
prevalence of erosive esophagitis was higher in subjects with NAFLD than those without
NAFLD (6.7% vs. 3.6%, p< 0.001). The risk of erosive esophagitis was significantly high
in subjects with NAFLD (OR 1.93, 95% confidence interval[CI] 1.62-2.30). After adjustment
with multiple variables including metabolic component, abdominal obesity and smoking,
the association between the erosive esophagitis and NAFLD remained significance (OR 1.44,
95% CI 1.18-1.75, p< 0.001). Conclusions: Erosive esophagitis is highly prevalent in
non-obese, non-diabetic NAFLD patients. NAFLD is independently associated with erosive
esophagitis regardless of obesity. Our result might represent another putative cause of erosive
esophagitis such as hormonal factors besides obesity.
Sa1104
P-AKT/AKT PATHWAYS IN THE CRURAL DIAPHRAGM ARE INVOLVED IN
THE PATHOGENESIS OF REFLUX ESOPHAGITIS IN RATS
Miguel Angelo N. Souza, Jéssica A. Leandro, Mônica C. Andrade, Mônica Belém, Marcia
N. Alves, Armenio Aguiar Santos
Anatomical and functional deficiencies of the CD in reflux esophagitis patients support the
possibility of a skeletal muscle deficiency in GERD (Souza et al. Neurogastroenterol Motil,
2016). The level of AKT phosphorylation (p-Akt) and Muscle RING finger 1 (MuRF-1) are
associated with skeletal muscle atrophy. Preliminary data from our laboratory showed that
rats with reflux esophagitis have increased activity of esophageal myeloperoxidade (MPO)
and enhanced phosphorylation of Akt in the CD but not in the rectus abdominis. Increased
p-Akt/Akt after 5 days of denervation of the diaphragm in rats has been demonstrated
previously (Argadine, 2011). Our aim is to show if these proteins are also detectable and
differently expressed in the CD in an animal model of reflux esophagitis. Methods: We
studied different signaling pathways (Akt, p-Akt and MuRF-1) of CD in a Wistar rats model
of reflux esophagitis and in a sham group. The local Ethical Comittee approved the protocol.
The esophagitis was induced by pyloric stenosis and the gastric fundus tying (Omura, 1999).
After extraction, protein was determined by the BCA method and its expression was done
by Western Blot followed by chemiluminescence detection. We also measured the MPO
activity of the esophagus in the two groups, according to Bradley & Priebat (1982). Data
were compared by the unpaired test t test and represented by mean ± SEM. Results: The
survival rate was lower in the esophagitis (E) group (sham: 11 out of 12 vs E: 11 out of
24) between the 1st and 7th day after surgery (p = 0.022). The animals body weights did
not differ before the surgery. Following 3 and 3 days after surgery, respectively, the esophagitis
group had a lower body weight (sham: 276.7 ± 5.45 vs E: 235.6 ± 7.85, p = 0.0005; sham:
286.5 ± 5.99 vs E 240.9 ± 11.51, p = 0.003; respectively). MPO activity of esophagus was
enhanced in the esophagitis group (sham, n = 6: 0.3 ± 0.10 vs E, n = 7: 0.8 ± 0.11, p <
0.05. The Akt (Akt/Tubulin: sham 1.09 ± 0.09 vs E 1.09 ± 0.18, p > 0.05), p-Akt (p-Akt/
Tubulin: sham 0.38 ± 0.09 vs E 0.73 ± 0.17, p > 0.05), and MuRF-1 (MuRF-1/Tubulin:
sham 1.32 ± 0.25 vs E 0.53 ± 0.23, p > 0.05) expressions were not different between the
two groups (n = 4). However, the active/phosphorylated form of Akt was increased as show
by the increased pAkt-Tubulin/Akt-Tubulin ratio: sham 0.34 ± 0.08 vs E 0.65 ± 0.05, p <
0.05. Conclusions: Our model yielded significant esophageal inflammation as revealed by
the increased MPO activity. In an animal model of reflux esophagitis, the expression of key
proteins of atrophy signaling pathways was detectable, and the phosphorylation of AKT was
increased. Therefore, reflux esophagitis is sufficient to challenge the hypertrophy/atrophy
pathways in the CD. These pathways may be associated with the functional deficiencies of
the CD previously described by our group.
Sa1105
P-AKT/AKT PATHWAYS IN THE CRURAL DIAPHRAGM ARE INVOLVED IN
THE PATHOGENESIS OF REFLUX ESOPHAGITIS IN HUMANS — A
PRELIMINARY REPORT
Mônica C. Andrade, Marcia N. Alves, Jéssica A. Leandro, Marcellus Souza, Armenio
Aguiar Santos, Miguel Angelo N. Souza
Introduction: Anatomical and functional deficiencies of the CD in reflux esophagitis patients
support the possibility of a skeletal muscle deficiency in GERD (Souza MAN et al. Neuro-
gastroenterol Motil 2016). The level of AKT phosphorylation (Phospho-AKT, P-AKT) and
Muscle RING finger 1 (MURF-1) are associated with skeletal muscle atrophy. Preliminary
data from our laboratory showed that rats with reflux esophagitis have increased activity of
esophageal myeloperoxidade and enhanced phosphorylation of AKT in the CD but not in
AGA Abstracts