NDLI: Therapy with Astragalus polysaccharides rescues lipotoxic cardiomyopathy in MHC-PPARα mice

Content Provider	Springer Nature Link
Author	Chen, Wei Chen, Wenjie Xia, Yanping Zhao, Xuelan Wang, Hao Yu, Maohua Li, Yiming Ye, Hongying Zhang, Yu
Copyright Year	2012
Abstract	Obesity-related diabetes mellitus leads to lipotoxic cardiomyopathy resulting in a form of cardiac dysfunction. Mice with heart-specific overexpression of peroxisome proliferator-activated receptor (PPAR) α showed a metabolic and cardiomyopathic phenotype similar to the diabetic heart. To define the role of Astragalus Polysaccharides (APS) treatment for PPARα-mediated lipotoxicity in the pathogenesis of diabetic cardiomyopathy, myosin heavy chain [MHC]-PPARα mice with high-fat diet were administrated with APS or vehicle for 16 weeks. The APS treatment prevented myocardial long-chain triglyceride accumulation, ultrastructure abnormality in cardiac myocytes and cardiac dysfunction in the MHC-PPARα mice, which was associated with reduced free fatty acids (FFA) utilization and increased glucose uptake and oxidation in hearts by APS treatment. Consistent with the metabolic changes, activation of PPARα gene regulatory pathway involved in FFA-oxidation in the MHC-PPARα heart was down-regulated by APS treatment, while suppression of PPARα target genes involved in glucose uptake and oxidation in the MHC-PPARα hearts was normalized by APS administration. We conclude that therapy with APS might lead to the inhibition of PPARα-mediate lipotoxicity in the pathogenesis of diabetic cardiomyopathy.
Starting Page	2449
Ending Page	2459
Page Count	11
File Format	PDF
ISSN	03014851
Journal	Molecular Biology Reports
Volume Number	40
Issue Number	3
e-ISSN	15734978
Language	English
Publisher	Springer Netherlands
Publisher Date	2012-11-30
Publisher Place	Dordrecht
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Cardiomyopathy Diabetes mellitus Fatty acids Lipid metabolism PPARα Animal Anatomy / Morphology / Histology Animal Biochemistry
Content Type	Text
Resource Type	Article
Subject	Genetics Medicine Molecular Biology

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