Diabetes Research and Clinical Practice - Volume 120 - Supplement 1 - October 2016

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abnormalities were significantly reversed by pioglitazone. The
protein expressions reflecting the macroautophagy process,
involving vesicle elongation (Atg7), phagolysosome fusion
(LC3) and lipophagy-specific lysososmal lipolysis (LAL) were
significantly and consistently enhanced well by pioglitazone.
Hepatic expressions of the ATGL and HSL were significantly
stimulated, which mainly distributed over hepatocytes rather
than Kupffer cells. The SiRNA assay of the AML12 liver cells
demonstrated the lipolysis was bothmodulated both by PPARα
and γ activation. However, the autophagy-lipolysis was
dominantly dependent to PPAR α activation.
Conclusion: Our study suggests that pioglitazone did alleviate
hepatic steatosis via enhancing lipophagy and cytosolic
lipolysis of hepatocytes.
PI-35
Adipocyte fatty acid binding protein (A-FABP) is a potential
mediator of heart dysfunction and failure related to obesity
Ruby Lai-chong HOO 1,2,3*, Mi ZHOU1,2, Yong PAN1,2 ,
Lingling SHU 1,2, Cecilia YJ SUNG1,2, Dan ZHONG1,2,
Zhengyuan XIA 1,3,4, Karen Siu-ling LAM1,2,3, Aimin XU1,2,3,5.
1 State Key Laboratory of Pharmaceutical Biotechnology, LKS Faculty
of Medicine, The University of Hong Kong, 2Department of Medicine,
LKS Faculty of Medicine, The University of Hong Kong, 3Research
Centre of Heart, Brain, Hormones and Healthy Ageing, LKS Faculty of
Medicine, The University of Hong Kong, 4Department of
Anaesthesiology, LKS Faculty of Medicine, The University of Hong
Kong, 5Department of Pharmacy and Pharmacology, LKS Faculty of
Medicine, The University of Hong Kong, Hongkong
Obesity predisposes to the development of diabetes, hyper-
tension and dyslipidemia, which are the risk factors for the
development of cardiac artery disease and ischemic cardio-
myopathy. It is also an independent risk factor for the
development of heart failure. Adipocyte fatty acid binding
protein (A-FABP) is an adipokine that mainly expressed in
adipocytes and macrophages and can be released into the
circulation. Emerging clinical evidence suggest that A-FABP is
a key link between obesity and cardiac dysfunction as
elevated circulating A-FABP levels are positively associated
with cardiac contractile dysfunction of obese subjects as well
as left ventricular mass and myocardial performance index in
patients with obstructive sleep apnea syndrome. Circulating
A-FABP is also significantly increased in Chinese subjects
with heart failure and is independently associated with the
deterioration of heart function. Here we investigate the
pathological role of A-FABP in cardiomyopathy associated
with obesity using A-FABP knockout (KO) mice and their
wildtype (WT) littermates.
A-FABP KO mice and their WT littermates were fed with
standard chow (STC) or high fat high cholesterol diet (HFHC)
for 24 weeks with or without treatment of selective A-FABP
inhibitor BMS309403 (BMS). The circulating level and cardiac
expression of A-FABP were markedly elevated in WT mice
after prolonged HFHC diet feeding. A-FABP deficiency pro-
tected against HFHC diet induced- hypertension and -impair-
ment of systolic and diastolic function in mice. Compared
to WT mice, diet-induced cardiomyocyte hypertrophy,
cardiac lipid accumulation and fibrosis were ameliorated in
A-FABP KO mice. These protective actions of A-FABP defi-
ciency were accompanied by reduced cardiac inflammation
and endoplasmic reticulum (ER) stress. Consistently, HFHC
diet-induced cardiomyocyte hypertrophy and cardiac collagen
deposition were significantly diminished in WT mice treated
with BMS.
In conclusion, A-FABP deficiency protects mice against cardio-
myopathy and heart dysfunction associated with obesity.
A-FABP may be the therapeutic target for the treatment of
obesity-related cardiomyopathy.
Acknowledgement: This project is supported by RGC HKU
767913.
PI-36
The association between GFR and metabolic syndrome in
Korean population
Nanhee CHO1, Gyeongim YU2, Donghoon SHIN 2, Minji KIM1,
Hana KANG1, Hochan CHO1*. 1Department of Endocrinology,
Internal Medicine, Keimyung University DongSan Medical Center,
2Department of Preventive Medicine, Keimyung University School of
Medicine, Korea
Background: Metabolic syndrome (MS) is a cluster of cardio-
vascular risk factors and chronic kidney disease (CKD) is an
increasingly common and progresses to end-stage renal
disease with combined complications. The aim of our study
was to investigate the relationship between CKD and key
components of MS.
Methods: We recruited 2,403 Korean adults Goryeong region
in KoGES_Multi-Rural (MR) communities cohort study
from February 2006 to March 2009. Metabolic parameters,
clinical characteristics, biochemical markers were obtained in
each subject. The MS was defined by the National Cholesterol
Education Program Adult Treatment Panel III criteria as
three or more of five components where the cut-off point of
waist circumference (WC) was modified for Korean as ≥ 90 cm
in men and ≥80 cm in women according to the recommenda-
tion by WHO West Pacific Region. CKD was defined as an
estimated glomerular filtration rate (GFR) less than 60 mL/min/
1.73 m2.
Results: Among 2,403 subjects (Mean age 61.62 ± 9.97), preva-
lence of MS and CKD were 44.9% (1,078 cases) and 9.2% (222
cases). The presence of CKD according to GFR was significantly
associated with key components of MS including WC, blood
pressure, HDL, triglyceride, and fasting glucose levels (P < 0.01).
The prevalence of CKD was 67.6% in the subjects with MS. The
incidence of CKD was significantly higher in subjects who was
diagnosed as MS compared to subjects without MS (13.9% vs
5.4%, p < 0.05).
Conclusions: This study shows that CKD according to was
significantly associated with the components of the MS,
suggesting metabolic syndrome may be an independent risk
factor for developing CKD.
Acknowledgement: This work was supported by the Research
Program funded by the Korea Centers for Disease Control and
Prevention (2006-E71009-00, 2007-E71002-00, 2008-E71004-00,
2009-E71006-00).
PI-38
N-acetylcytein improves high-fat-induced overweight and fat
accumulation, insulin resistance and glucose intolerance
through reducing mitochondrial ROS in visceral fat
Hung-Yu LIN1, Pei-Wen WANG1*, Shao-Wen WENG1,
Hsiao-Mei KUO1, Chia-Shiang CHANG1, Ching-Yi LIN 1,
Cheng-Feng TSAO1. 1Department of Internal Medicine, Kaohsiung
Chang Gung Memorial Hospital and Chang Gung University College
of Medicine, Kaohsiung, Taiwan
Obesity, especially accumulation of visceral fat (VF), is a
major risk of diabetes and related cardiovascular diseases.
Mitochondrial reactive oxygen species (ROS), a critical source
of intracellular oxidative stress, is associatedwith excessive fat
accumulation in VF. However, whether intervention reducing
mitochondrial ROS is able to reduce obesity and diabetes
progression remain elusive. Here we present that antioxidant
N-acetylcystein (NAC) reduced VF mass, VF oxidative damage,
insulin resistance and glucose intolerance in an obesitymouse
model induced by high fat high sugar (HFHS) diet. C57BL6 mice
fed for six months were divided to three groups: control diet
(CD), HFHS or HFHS combined with NAC (HFHS + NAC). HFHS
diet significantly induced overweight, VF accumulation, VF
oxidative damage, VF mitochondrial ROS and development of
insulin resistance as well as glucose intolerance. Importantly,
HFHS + NAC showed reduction in HFHS-caused overweight, VF
accumulation, VF oxidative damage, VF mitochondrial ROS
Poster Presentations / Diabetes Research and Clinical Practice 120S1 (2016) S65–S211 S192