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Journal of Zhejiang University SCIENCE B 2006 Vol.7 No.8 P.627~633

10.1631/jzus.2006.B0627


Research on the protection effect of pioglitazone for non-alcoholic fatty liver disease (NAFLD) in rats


Author(s):  XU Ping, ZHANG Xing-guo, LI You-ming, YU Chao-hui, XU Lei, XU Gen-yun

Affiliation(s):  Department of Gastroenterology, the First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310003, China; more

Corresponding email(s):   zlym@zju.edu.cn

Key Words:  Fatty liver, Insulin resistance, Pioglitazone


XU Ping, ZHANG Xing-guo, LI You-ming, YU Chao-hui, XU Lei, XU Gen-yun. Research on the protection effect of pioglitazone for non-alcoholic fatty liver disease (NAFLD) in rats[J]. Journal of Zhejiang University Science B, 2006, 7(8): 627~633.

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author="XU Ping, ZHANG Xing-guo, LI You-ming, YU Chao-hui, XU Lei, XU Gen-yun",
journal="Journal of Zhejiang University Science B",
volume="7",
number="8",
pages="627~633",
year="2006",
publisher="Zhejiang University Press & Springer",
doi="10.1631/jzus.2006.B0627"
}

%0 Journal Article
%T Research on the protection effect of pioglitazone for non-alcoholic fatty liver disease (NAFLD) in rats
%A XU Ping
%A ZHANG Xing-guo
%A LI You-ming
%A YU Chao-hui
%A XU Lei
%A XU Gen-yun
%J Journal of Zhejiang University SCIENCE B
%V 7
%N 8
%P 627~633
%@ 1673-1581
%D 2006
%I Zhejiang University Press & Springer
%DOI 10.1631/jzus.2006.B0627

TY - JOUR
T1 - Research on the protection effect of pioglitazone for non-alcoholic fatty liver disease (NAFLD) in rats
A1 - XU Ping
A1 - ZHANG Xing-guo
A1 - LI You-ming
A1 - YU Chao-hui
A1 - XU Lei
A1 - XU Gen-yun
J0 - Journal of Zhejiang University Science B
VL - 7
IS - 8
SP - 627
EP - 633
%@ 1673-1581
Y1 - 2006
PB - Zhejiang University Press & Springer
ER -
DOI - 10.1631/jzus.2006.B0627


Abstract: 
Objective: The prevalence of non-alcoholic fatty liver disease (NAFLD) has markedly increased. insulin resistance has been implicated in the pathogenesis of NAFLD. This study was aimed at observing the relationship between insulin resistance and NAFLD, and evaluating the role of pioglitazone (PGZ) acting as insulin-sensitizing agents in the prevention and treatment of rat fatty liver induced by high fat feeding. Methods: The rats were separated randomly into 6 groups: model group I were fed high fat diet for 8 weeks, PGZ prevention group were given PGZ 4 mg/(kg∙d) simultaneously, while control group I were fed normal food for 8 weeks; model group II were fed high fat diet for 16 weeks, PGZ treatment group were given PGZ 4 mg/(kg∙d) orally simultaneous with high fat diet for 8 weeks after high fat feeding for 8 weeks, control group II were fed normal food for 16 weeks. The rats were sacrificed after 8 weeks and 16 weeks respectively. Liver weight, body weight, serum activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), tumor necrosis factor alpha (TNF-α), fasting blood glucose (FBG), fasting plasma insulin (FINS), HOMA (homeostasis model assessment) insulin resistance index (HOMA-IR), and the liver histology of rats of all groups were assayed. Results: After 8 weeks, the liver in model group I showed typical steatosis, accompanied with mild to moderate lobular inflammatory cell infiltration, liver indexes and serum levels of ALT, AST, ALP, TNF-α were significantly increased (P<0.05) compared with control group I. Whereas, the degree of hepatic injury was attenuated in PGZ prevention group, liver indexes and serum levels of ALT, ALP were significantly decreased (P<0.05) compared with model group I. After 16 weeks, notable steatosis, and lobular inflammation were observed in model group II rat liver, while the degree of hepatic injury was attenuated in the PGZ treatment group. Liver index, serum levels of ALT, AST, ALP, FINS and HOMA-IR were significantly increased (P<0.05) in model group II compared with control group II. Whereas, in PGZ treatment group, serum levels of AST and FINS showed decreasing tendency, liver indexes, serum levels of ALT, ALP, TNF-α and HOMA-IR were significantly decreased compared with model group II. Conclusion: insulin resistance plays a role in the pathogenesis of NAFLD in rats. pioglitazone can attenuate insulin resistance and biochemical and histological injury in high fat-induced fatty liver in rats.

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