Metabolic characterization of volume overload heart failure due to aorto-caval fistula in rats
Language English Country Netherlands Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
- MeSH
- Aorta surgery MeSH
- Arteriovenous Fistula MeSH
- Arteriovenous Shunt, Surgical MeSH
- Biomarkers metabolism MeSH
- Epididymis metabolism pathology MeSH
- Glucose Tolerance Test MeSH
- Glutathione metabolism MeSH
- Hemodynamics MeSH
- Insulin blood MeSH
- Liver pathology MeSH
- Myocytes, Cardiac metabolism pathology MeSH
- Rats MeSH
- Fatty Acids, Nonesterified blood MeSH
- Thiobarbituric Acid Reactive Substances metabolism MeSH
- Kidney pathology MeSH
- Lipid Metabolism MeSH
- Myocardium metabolism pathology MeSH
- Oxidative Stress MeSH
- Lung pathology MeSH
- Rats, Wistar MeSH
- Ventricular Remodeling MeSH
- Heart physiopathology MeSH
- Heart Failure metabolism pathology physiopathology MeSH
- Gene Expression Profiling MeSH
- Superoxide Dismutase metabolism MeSH
- Adipose Tissue metabolism pathology MeSH
- Organ Size MeSH
- Venae Cavae surgery MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Biomarkers MeSH
- Glutathione MeSH
- Insulin MeSH
- Fatty Acids, Nonesterified MeSH
- Thiobarbituric Acid Reactive Substances MeSH
- Superoxide Dismutase MeSH
Metabolic interactions between adipose tissue and the heart may play an active role in progression of heart failure (HF). The aim of the study was to examine changes in myocardial and adipose tissue metabolism and gene expression in a rat HF model induced by chronic volume overload. HF was induced by volume overload from aorto-caval fistula (ACF) in 3-month-old male Wistar rats and animals were studied in the phase of decompensated HF (22nd week). HF rats showed marked eccentric cardiac hypertrophy, pulmonary congestion, increased LV end-diastolic pressure, and intraabdominal fat depletion. HF rats had preserved glucose tolerance, but increased circulating free fatty acids (FFA) and attenuated insulin response during oral glucose challenge. Isolated organ studies showed preserved responsiveness of adipose tissue lipolysis and lipogenesis to epinephrine and insulin in ACF. The heart of HF animals had markedly reduced triglyceride content (almost to half of controls), attenuated anti-oxidative reserve (GSH/GSSG), upregulated HF markers (ANP, periostin, thrombospondin-4), specific signaling pathways (Wnt, TGF-β), and downregulated enzymes of mitochondrial fatty acid oxidation, citric acid cycle, and respiratory chain. Adipose tissue transcription profiling showed upregulated receptor for gastric inhibitory polypeptide. In conclusion, ACF-induced HF model displays several deregulations of systemic metabolism. Despite elevation of systemic FFAs, myocardial triglycerides are low and insulin levels are attenuated, arguing against a role of lipotoxicity or insulin resistance in this model. Attenuated postprandial insulin response and relative lack of its antilipolytic effects may facilitate intraabdominal fat depletion observed in ACF-HF animals.
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