RGD Reference Report - Diabetic cardiomyopathy: effects of fenofibrate and metformin in an experimental model--the Zucker diabetic rat. - Rat Genome Database

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Diabetic cardiomyopathy: effects of fenofibrate and metformin in an experimental model--the Zucker diabetic rat.

Authors: Forcheron, F  Basset, A  Abdallah, P  Del Carmine, P  Gadot, N  Beylot, M 
Citation: Forcheron F, etal., Cardiovasc Diabetol. 2009 Mar 24;8:16.
RGD ID: 5509944
Pubmed: PMID:19317897   (View Abstract at PubMed)
PMCID: PMC2664796   (View Article at PubMed Central)
DOI: DOI:10.1186/1475-2840-8-16   (Journal Full-text)

BACKGROUND: Diabetic cardiomyopathy (DCM) contributes to cardiac failure in diabetic patients. It is characterized by excessive lipids accumulation, with increased triacylglycerol (TAG) stores, and fibrosis in left ventricle (LV). The mechanisms responsible are incompletely known and no specific treatment is presently defined. We evaluated the possible usefulness of two molecules promoting lipid oxidation, fenofibrate and metformin, in an experimental model of DCM, the Zucker diabetic rat (ZDF). METHODS: ZDF and controls (C) rats were studied at 7, 14 and 21 weeks. After an initial study at 7 weeks, ZDF rats received no treatment, metformin or fenofibrate until final studies (at 14 or 21 weeks). C rats received no treatment. Each study comprised measurements of metabolic parameters (plasma glucose, TAG, insulin levels) and sampling of heart for histology and measurements of TAG content and relevant mRNA concentration. RESULTS: ZDF rats were insulin-resistant at 7 weeks, type 2 diabetic at 14 weeks and diabetic with insulin deficiency at 21 weeks. Their plasma TAG levels were increased. ZDF rats had at 7 weeks an increased LV TAG content with some fibrosis. LV TAG content increased in untreated ZDF rats at 14 and 21 weeks and was always higher than in C. Fibrosis increased also moderately in untreated ZDF rats. Metformin and fenofibrate decreased plasma TAG concentrations. LV TAG content was decreased by metformin (14 and 21 weeks) and by fenofibrate (14 weeks). Fibrosis was reduced by fenofibrate only and was increased by metformin. Among the mRNA measured, fenofibrate increased Acyl-CoA Oxidase mRNA level, metformin decreased Acyl-CoA Synthase and increased AdipoR1 and pro-inflammatory mRNA levels. CONCLUSION: Fenofibrate had favourable actions on DCM. Metformin had beneficial effect on TAG content but not on fibrosis. PPARalpha agonists could be useful for the prevention and treatment of DCM.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Diabetic Cardiomyopathies  ISOPpara (Rattus norvegicus)5509944; 5509944 RGD 
Diabetic Cardiomyopathies  IDA 5509944Strain: ZDFRGD 

Objects Annotated

Genes (Rattus norvegicus)
Ppara  (peroxisome proliferator activated receptor alpha)

Genes (Mus musculus)
Ppara  (peroxisome proliferator activated receptor alpha)

Genes (Homo sapiens)
PPARA  (peroxisome proliferator activated receptor alpha)


Additional Information