studies

1300A AASLD ABSTRACTS HEPATOLOGY, October, 2015
Disclosures:
Kenji Ikeda - Speaking and Teaching: Eisai company, Dainippon Sumitomo
Pharmaceutical company
Norio Akuta - Patent Held/Filed: SRL. Inc.; Speaking and Teaching: Mitsubishi
Tanabe Pharma, Janssen Pharmaceutical K.K., Bristol-Myers Squibb
Fumitaka Suzuki - Speaking and Teaching: BMS
Yoshiyuki Suzuki - Speaking and Teaching: Bristol-Myers Squibb
Satoshi Mochida - Grant/Research Support: Chugai, MSD, Tioray Medical,
BMS; Speaking and Teaching: MSD, Toray Medical, BMS, Tanabe Mitsubishi
Hiromitsu Kumada - Patent Held/Filed: SRL; Speaking and Teaching: Bristol-Myers
Squibb,Pharma International, MSD, Janssen Pharma., Glaxosmithkline
The following authors have nothing to disclose: Yusuke Kawamura, Yasuji
Arase, Yushi Sorin, Hideo Kunimoto, Hitomi Sezaki, Tetsuya Hosaka, Masahiro
Kobayashi, Satoshi Saitoh, Mie Inao
2242
WITHDRAWN
2243
Differences of lifestyle behaviors between non-obese
and obese non-alcoholic fatty liver disease; beyond visceral
obesity and metabolic syndrome
Joo Hee Kwak 1 , Dae Won Jun 1 , Seung Min Lee 2 , Yong Kyun
Cho 3 , Eun Chul Jang 4 ; 1 Department of Internal Medicine, Hanyang
University College of Medicine, Seoul, Korea (the Republic of);
2 Department of Food and Nutrition, Sungshin Women’s University,
Seoul, Korea (the Republic of); 3 Department of Internal Medicine,
Kangbuk Samsung Hospital, Sungkyunkwan University, School of
Medicine, Seoul, Korea (the Republic of); 4 Department of Occupational
and Environmental Medicine, Soonchunhyang University
Cheonan Hospital, Cheonan, Korea (the Republic of)
Background and Aims: Best way to treat non-alcoholic fatty
liver disease (NAFLD) is weight reduction. bu However, strategy
of lifestyle modification in non-obese NAFLD patient is
unclear. The aim of study was to investigate differences of
lifestyle behaviors between non-obese and obese non-alcoholic
fatty liver disease. Methods: This study has been performed
with 209 patients who wanted to participate in nutrition education
program because of their abnormal liver enzyme or
fatty liver. All participants undertook computed tomography.
NAFLD was diagnosed when liver/spleen Hounsfield Unit (HU)
was less than 1.1. Five day food record and physical activity
was measured by two dietitians. Results: Prevalence of NAFLD
was significantly higher as 66.1% in obese subjects (BMI >25)
than 42.4% in normal weight (BMI≤25) (p=0.001). Non-obese
NAFLD group showed higher visceral fat area, aminotransferase
activity, and fasting glucose compare to normal liver/
spleen HU subjects. In univariate analysis, non-obese NAFLD
group showed higher carbohydrate intake (281 g/day vs. 246
g/day), and did lower moderate level exercise compare to
control group (p=0.013). But total calorie intake (1,955 Kcal
vs. 1,837 Kcal) and walking time/week were not difference.
In multivariate analysis, the amount of carbohydrate (p=0.018)
and more than 2 hours of exercise a week (p=0.010) were
risk factors for NAFLD independent with visceral fat area and
total calorie intake. Meanwhile fasting glucose (p25). Conclusions: The moderate level exercise of 2 hours a
week and the amount of carbohydrate intake were independent
risk factor in non-obese NAFLD patients.
Disclosures:
The following authors have nothing to disclose: Joo Hee Kwak, Dae Won Jun,
Seung Min Lee, Yong Kyun Cho, Eun Chul Jang
2244
Subtyping nonalcoholic steatohepatitis for the development
of effective treatments
Ibon Martinez-Arranz 1 , Cristina Alonso 1 , David Fernández 2 ,
Rebeca Mayo 1 , Marta Varela 2 , Mazen Noureddin 3 , Maria L. Martinez-Chantar
2 , Shelly C. Lu 3 , Azucena Castro 1 , Jose M. Mato 2 ;
1 OWL, Derio, Spain; 2 CIC bioGUNE, Ciberehd, Derio, Spain;
3 Division of Gastroenterology, Cedars-Sinai Medical Center, Los
Angeles, CA
NASH (nonalcoholic steatohepatitis) is a histopathological
definition that groups together defects in diverse biochemical
processes that cause hepatic fat accumulation, inflammation
and necrosis as it were a single disease. The identification
of the types of mechanisms leading to NASH, together with
the development of noninvasive biomarkers of these different
NASH subtypes, is central for the development of precision
treatments, since the pathways that should be targeted will
depend upon the specific subtype of NASH. For tissues whose
primary physiological role is metabolic, such as the liver,
metabolites are unquestionably the best indicators of organ
function. Therefore, the detailed analysis of serum metabolome
may reveal metabolic profiles that may be used as disease
biomarkers. We previously found that hepatic methionine adenosyltransferase
(MAT, the enzyme that synthesizes S-adenosylmethionine
or SAMe) deletion (Mat1a KO) in mice led to the
spontaneous development of NASH and liver cancer. NASH
patients often show reduced expression of MAT1A, indicating
that the Mat1a KO mouse model is relevant to study human
NASH. Here we have analyzed the serum lipidome (over 400
different molecular species) in 10-11 month old Mat1a KO
with histological diagnose of NASH and wild type mice with
normal liver (twelve animals per group), and selected the top
fifty serum lipids that more significantly differentiated between
both genotypes. Then, we observed that this serum biomarker
panel robustly classified a cohort of 387 patients with biopsy
proven NAFLD into two well-defined clusters, based on optimum
average silhouette width, with around 66% of the patients
showing a MAT1A metabolic subtype (M-subtype). Since there
is considerable interest in the utility of SAMe to ameliorate
NAFLD, these results suggest that NAFLD patients with a serum
M-subtype are best suited to be selected to study the efficacy
of SAMe treatment.
Disclosures:
The following authors have nothing to disclose: Ibon Martinez-Arranz, Cristina
Alonso, David Fernández, Rebeca Mayo, Marta Varela, Mazen Noureddin,
Maria L. Martinez-Chantar, Shelly C. Lu, Azucena Castro, Jose M. Mato