Tetradecylthioacetic Acid Increases Fat Metabolism and Improves Cardiac Function in Experimental Heart Failure
Autor: | Christen P. Dahl, Jan Otto Beitnes, Erik Øie, Pavol Bohov, Arne Yndestad, Pål Aukrust, Thor Edvardsen, Thor Ueland, Rolf K. Berge |
---|---|
Jazyk: | angličtina |
Rok vydání: | 2013 |
Předmět: |
Male
medicine.medical_specialty Clinical chemistry Myocardial Infarction Sulfides 030204 cardiovascular system & hematology Biology Biochemistry Antioxidants Fats 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Fatty Acids Omega-6 Internal medicine Fatty Acids Omega-3 medicine Animals Myocardial infarction Rats Wistar 030304 developmental biology Heart Failure 2. Zero hunger chemistry.chemical_classification 0303 health sciences Cholesterol Myocardium Organic Chemistry Hemodynamics Fatty acid Tetradecylthioacetic acid Heart Cell Biology Lipid Metabolism medicine.disease Lipids Rats 3. Good health Endocrinology chemistry Heart failure Myocardial infarction complications lipids (amino acids peptides and proteins) sense organs Oxidation-Reduction Polyunsaturated fatty acid |
Zdroj: | Lipids; Vol 48 |
ISSN: | 0024-4201 |
DOI: | 10.1007/s11745-012-3749-z |
Popis: | Changes in myocardial metabolism, including a shift from fatty acid to glucose utilization and changes in fatty acid availability and composition are characteristics of heart failure development. Tetradecylthioacetic acid (TTA) is a fatty acid analogue lacking the ability to undergo mitochondrial β-oxidation. TTA promotes hepatic proliferation of mitochondria and peroxisomes and also decreases serum triglycerides and cholesterol in animals. We investigated the effect of TTA, in combination with a high-fat or regular diet, in a rat model of post-myocardial infarction heart failure. TTA had a beneficial effect on cardiac function in post-myocardial infarction heart failure without affecting myocardial remodeling. These effects of TTA on myocardial function were accompanied by decreased free fatty acids in plasma, increased myocardial proportion of n-3 polyunsaturated fatty acids (PUFA) and a decreased proportion of n-6 PUFA. Myocardial enzyme gene expression during TTA treatment suggested that the increase in n-3 PUFA could reflect increased n-3 PUFA synthesis and inadequately increased n-3 PUFA β-oxidation. Based on our data, it is unlikely that the changes are secondary to alterations in other tissues as plasma and liver showed an opposite pattern with decreased n-3 PUFA during TTA treatment. The present study suggests that TTA may improve myocardial function in heart failure, potentially involving its ability to decrease the availability of FFA and increase the myocardial proportion of n-3 PUFA. |
Databáze: | OpenAIRE |
Externí odkaz: |