2011 ADA Posters 1261-2041.indd - Diabetes
2011 ADA Posters 1261-2041.indd - Diabetes
2011 ADA Posters 1261-2041.indd - Diabetes
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were improved by fenofi brate and pioglitazone. High fat diet induced TG<br />
accumulation in skeletal muscle was also decreased 20% by fenofi brate<br />
and 24% by pioglitazone. ATGL protein expression was respectively reduced<br />
40% and 18% in adipose tissue and skeletal muscle of HFD rats and was<br />
increased after pioglitazone treatment in these tissues. ATGL was increased<br />
in skeletal muscle but has no change in adipose tissue by fenofi brate.<br />
Fenofi brate and pioglitazone treatment improved insulin sensitivity and<br />
increased ATGL protein and coincide with decreased TG content in skeletal<br />
muscle. These fi ndings suggest that fenofi brate and pioglitazone ameliorate<br />
insulin resistance through decreased ectopic TG content mediated by<br />
increased ATGL in mainly tissues.<br />
Supported by: National Natural Science Foundation of China Project (30670989)<br />
1831-P<br />
Fenofi brate Involves in CCK-Induced Reduction of Food Intake in<br />
Rats<br />
YING HAN, MI-KYOUNG PARK, SO-YOUNG PARK, SU KYUNG PARK, DUK KYU<br />
KIM, HYE-JEONG LEE, Busan, Republic of Korea<br />
Fenofi brate has been reported to decrease food intake independent of<br />
leptin in rodents. We hypothesized that fenofi brate might decrease food<br />
intake via cholecystokinin (CCK) dependent pathway. Otsuka Long-Evans<br />
Tokushima fatty (OLETF) rats, which genetically lack CCK receptor as a result<br />
of mutation, were divided into OLETF-fenofi brate group (n=5) and OLETFcontrol<br />
group (n=5). OLETF-fenofi brate group was fed with standard rat chow<br />
and fenofi brate (30mg/kg/day) and OLETF-control group was only fed with<br />
standard rat chow for the same period as control. Long-Evans Tokushima<br />
Otsuka (LETO) rats which have normal CCK receptor, as control groups to<br />
OLETF rats, were also divided into LETO-fenofi brate group (30mg/kg/day)<br />
(n=5) and LETO-control group (n=5). After 11 weeks of fenofi brate treatment,<br />
food intakes of the fenofi brate group were signifi cantly decreased than those<br />
of the control group in the LETO rats (P< 0.05), but there was no signifi cant<br />
difference in the OLETF rats. The levels of blood β-ketone, plasma leptin,<br />
and fasting blood sugar (FBS) did not show signifi cant difference between<br />
the fenofi brate and control groups neither in the LETO rats nor in the OLETF<br />
rats. To investigate the expression of CCK by fenofi brate, the protein level<br />
of CCK were analyzed with small intestinal tissue of the rats. Fenofi brate<br />
treatment groups showed that the protein levels of PPARa and CCK were<br />
signifi cantly increased in the small intestine than control groups both in the<br />
LETO and OLETF rats. To examine the expression of CCK by fenofi brate, the<br />
Caco-2 cells, intestinal epithelial cell line, were cultured in the presence of<br />
fenofi brate for 24 hours. Fenofi brate treatment signifi cantly increased the<br />
protein expressions of PPARα and CCK in the Caco-2 cells. In conclusion,<br />
fenofi brate treatment decreased food intake in the LETO rats which have<br />
normal CCK receptor, but not in the OLETF rats which lack CCK receptor. The<br />
possible anorexigenic mechanism by fenofi brate might be up-regulation of<br />
CCK in the small intestine.<br />
1832-P<br />
High Free Fatty Acids Level Related with Microalbuminuria in Obese<br />
Rats<br />
XIAO DONG SUN, YE RONG YU, LI NA HAN, BEN WANG, Chengdu, China<br />
It is known that obesity is associated with microalbuminuria (MAU), which<br />
is not only an early manifestation of kidney damage, but also an independent<br />
risk factor for ischemic cardiovascular disease. High free fatty acids (FFAs)<br />
level is a common feature of obesity and can cause impaired endotheliumdependent<br />
vasodilatation (EDV). We hypothesized that increased release<br />
of FFAs from excessive visceral fat accumulation is related to increased<br />
urine albumin excretion and reduced circulating FFAs level by fenofi brate<br />
has renal protective effects in MAU by improving endothelial dysfunction<br />
in diet-induced obese rats. Male Wistar rats 4 weeks in age were<br />
randomly divided into three groups. The rats in the control group, obesity<br />
group and fenofi brate group were fed with normal diet, high-fat diet, and<br />
high-fat diet plus fenofi brate (100mg/kg/d), respectively. At the end of 24<br />
weeks, body weight increased 32.8% in obese rats compared to control<br />
group. The serum FFAs and TG levels increased signifi cantly in obese rats.<br />
Fenofi brate intervention decreased serum FFAs and TG levels by 43.4% and<br />
48% respectively, accompanied by reduced ratio of perirenal fat to body<br />
weight (PF/BW) and visceral fat to body weight(VF/BW). Urinary albumin/<br />
creatinine ratio (ACR) increased in obese rats (56.09±22.64 VS 19.52±7.30<br />
mg/g, P