Effect of BM 17.0744, a PPARα ligand, on the metabolism of perfused hearts from control and diabetic mice
Abstract
Peroxisome proliferator-activated receptor-α (PPARα) regulates the expression of fatty acid (FA) oxidation genes in liver and heart. Although PPARα ligands increased FA oxidation in cultured cardiomyocytes, the cardiac effects of chronic PPARα ligand administration in vivo have not been studied. Diabetic db/db mouse hearts exhibit characteristics of a diabetic cardiomyopathy, with altered metabolism and reduced contractile function. A testable hypothesis is that chronic administration of a PPARα agonist to db/db mice will normalize cardiac metabolism and improve contractile function. Therefore, a PPARα ligand (BM 17.0744) was administered orally to control and type 2 diabetic (db/db) mice (37.9 ± 2.5 mg/(kg·d) for 8 weeks), and effects on cardiac metabolism and contractile function were assessed. BM 17.0744 reduced plasma glucose in db/db mice, but no change was observed in control mice. FA oxidation was significantly reduced in BM 17.0744 treated db/db hearts with a corresponding increase in glycolysis and glucose oxidation; glucose and FA oxidation in control hearts was unchanged by BM 17.0744. PPARα treatment did not alter expression of PPARα target genes in either control or diabetic hearts. Therefore, metabolic alterations in hearts from PPARα-treated diabetic mice most likely reflect indirect mechanisms related to improvement in diabetic status in vivo. Despite normalization of cardiac metabolism, PPARα treatment did not improve cardiac function in diabetic hearts.Key words: PPAR, cardiac metabolism and function, diabetes.
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Treatment of db/db mice with PPAR-γ or PPAR-α agonists can improve cardiac metabolism, but do not necessarily restore cardiac function.
“Similar studies in db/db mice revealed that treatment of these mice with PPAR-γ or PPAR-α agonists can improve cardiac metabolism, but do not necessarily restore cardiac function (1, 2, 36).”
From Cardiac remodeling in obesity (2008) · cites this paper as [2]
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- Authors
- Aasum, E., Cooper, M., Severson, D. L., & Larsen, T. S.
- Affiliations
- UiT The Arctic University of Norway (NO)
- Venue
- Canadian Journal of Physiology and Pharmacology
- Publisher
- Canadian Science Publishing
- Published
- 2005-02-01
- Volume
- 83
- Issue
- 2
- Pages
- 183-190
- ISSN
- 0008-4212 (ISSN-L)
- 1205-7541
- OpenAlex
- W1966076812
- Cited by
- 37
- References
- 44
- Citations by year
- 2018: 2 · 2016: 2 · 2015: 1 · 2013: 2 · 2012: 6
- FWCI
- 1.63
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Canadian Journal of Physiology and Pharmacology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Paraoxonase enzyme and polymorphisms
- Keywords
- PPARα agonist, diabetic cardiomyopathy, db/db mice, type 2 diabetes, myocardial metabolism, fatty acid oxidation, glycolysis, glucose oxidation, cardiac contractile function, plasma glucose
- MeSH terms
- Animals, Carnitine O-Palmitoyltransferase, Cells, Cultured, Diabetes Mellitus, Type 2, Fatty Acids, Glucose, Glycolysis, Lauric Acids, Myocardial Contraction, Myocardium, Oxidation-Reduction, Perfusion, Protein Kinases, RNA, Messenger, Myocytes, Cardiac, Acyl-CoA Oxidase, PPAR alpha, Mice, In Vitro Techniques
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