studies

HEPATOLOGY, VOLUME 62, NUMBER 1 (SUPPL) AASLD ABSTRACTS 683A
The following authors have nothing to disclose: Hannah K. Drescher, Angela
Schippers, Thomas Clahsen, Hacer Sahin, Norbert Wagner, Konrad L. Streetz,
Daniela C. Kroy
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Association between nonalcoholic fatty liver disease
and bone mineral density: a systematic review and
meta-analysis
Sikarin Upala 1,3 , Veeravich Jaruvongvanich 4,5 , Karn Wijarnpreecha
1,2 , Anawin Sanguankeo 1,3 ; 1 Department of Internal Medicine,
Bassett Medical Center and Columbia University College of Physicians
and Surgeons, Cooperstown, NY; 2 Department of Physiology,
Cardiac Electrophysiology Research and Training Center,
Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand;
3 Department of Preventive and Social Medicine, Faculty of
Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand;
4 Department of Internal Medicine, University of Hawaii, Honolulu,
HI; 5 Department of Internal Medicine, Faculty of Medicine, Chulalongkorn
University, Bangkok, Thailand
Purpose: Several major risk factors for osteoporosis have been
identified. One of these risk factors is chronic inflammation.
Several recent studies have supported the association between
low bone mineral density (BMD) and nonalcoholic fatty liver
disease (NAFLD), which comprises a spectrum of disorders
involving liver inflammation. However, conflicting evidence
regarding this association has been obtained thus far. We
therefore conducted a meta-analysis of observational studies
to show the association between NAFLD and BMD. Methods:
The Cochrane Central Register of Controlled Trials, Cochrane
Library, Medline, and Embase were searched from database
inception to November 2014 for all observational studies evaluating
the association between NAFLD or nonalcoholic steatohepatitis
(NASH) and bone mass, BMD, or osteoporosis. All
patients were ≥18 years of age and had no other cause of liver
disease, osteoporosis, or pathological bone disease at baseline.
Risk factors were NAFLD and NASH; control subjects were
individuals without NAFLD. Results: Eleven articles underwent
full-length review. Data were extracted from 5 cross-sectional
studies involving 1,276 participants; 638 had NAFLD. The
main meta-analysis showed no significant difference in BMD
between patients with fatty liver disease and controls. This may
be explained by the confounding effects of body mass index on
BMD in patients with NAFLD. Among all variables analyzed,
body mass index had the strongest and most significant predictive
effect on the difference in BMD. Conclusions: Controversy
exists regarding the effect of BMD on NAFLD. Further studies
are required to fully show this relationship.
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Aliskiren reduces liver and epididymal fat steatosis and
increases skeletal muscle insulin sensitivity in high-fat
diet-fed mice
Kuei-Chuan Lee, Yun-Cheng Hsieh, Ying-Ying Yang, Che-Chang
Chan, Yi-Hsiang Huang, Han-Chieh Lin; Taipei Veterans General
hospital, Taipei, Taiwan
Aliskiren has been found to reduce chronic injury and steatosis
in the liver of methionine-choline-deficient (MCD) diet-fed
mice. This study investigated whether aliskiren has an anti-steatotic
effect in HFD-fed mice, which are more relevant to human
patients with non-alcoholic fatty liver disease than MCD mice.
Mice fed with 4-week normal chow or HFD randomly received
aliskiren (50 mg/kg/day) or vehicle via osmotic minipumps for
further 4 weeks. Aliskiren reduced systemic insulin resistance,
hepatic steatosis, epididymal fat mass and increased gastrocnemius
muscle glucose transporter type 4 levels with lower
tissue angiotensin II levels in the HFD-fed mice. In addition, aliskiren
lowered nuclear peroxisome proliferator-activated receptor
gamma and its down-signaling molecules and increased
cytochrome P450 4A14 and carnitine palmitoyltransferase 1A
(CPT1a) in liver. In epididymal fat, aliskiren inhibited expressions
of lipogenic genes, leading to decrease in fat mass, body
weight, and serum levels of leptin and free fatty acid. Notably,
in the gastrocnemius muscle, aliskiren increased phosphorylation
of insulin receptor substrate 1 and Akt. Based on these
beneficial effects on liver, peripheral fat and skeletal muscle,
aliskiren is a promising therapeutic agent for patients with
NAFLD.
Disclosures:
The following authors have nothing to disclose: Kuei-Chuan Lee, Yun-Cheng
Hsieh, Ying-Ying Yang, Che-Chang Chan, Yi-Hsiang Huang, Han-Chieh Lin
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A DPP-4 inhibitor, sitagliptin, can be preventative
drug for the acceleration of the development in NAFLD
caused by lipopolysaccharides through inhibiting
expression of MyD88 and NFκB.
Keisuke Yokohama 2,1 , Shinya Fukunishi 1 , Sanomura Makoto 2 ,
Akira Asai 1 , Yasuhiro Tsuds 1 , Kazuhide Higuchi 1 ; 1 2nd Department
of internal medicine, Osaka Medical College, Osaka, Japan;
2 Gastroenterology, Hokusetsu general hospital, Osaka, Japan
Disclosures:
The following authors have nothing to disclose: Sikarin Upala, Veeravich Jaruvongvanich,
Karn Wijarnpreecha, Anawin Sanguankeo
Aims: Nonalcoholic fatty liver disease (NAFLD) is a chronic
liver disease, and commonly observed in patients with obesity
or type 2 diabetes mellitus (T2DM). Characterized by metabolic
syndrome, hepatic steatosis, and liver inflammation,
nonalcoholic steatohepatitis(NASH)is believed to be under
the influence of the gut microflora. Some reports showed that