| First Author | Carley AN | Year | 2005 |
| Journal | Biochim Biophys Acta | Volume | 1734 |
| Issue | 2 | Pages | 112-26 |
| PubMed ID | 15904868 | Mgi Jnum | J:99066 |
| Mgi Id | MGI:3581074 | Doi | 10.1016/j.bbalip.2005.03.005 |
| Citation | Carley AN, et al. (2005) Fatty acid metabolism is enhanced in type 2 diabetic hearts. Biochim Biophys Acta 1734(2):112-26 |
| abstractText | The metabolic phenotype of hearts has been investigated using rodent models of type 2 diabetes which exhibit obesity and insulin resistance: db/db and ob/ob mice, and Zucker fatty and ZDF rats. In general, cardiac fatty acid (FA) utilization is enhanced in type 2 diabetic hearts, with increased rates of FA oxidation (db/db, ob/ob and ZDF models) and increased FA esterification into cellular triacylglycerols (db/db hearts). Hearts from db/db and ob/ob mice and ZDF rat hearts all have elevated levels of myocardial triacylglycerols, consistent with enhanced FA utilization. A number of mechanisms may be responsible for enhanced FA utilization in type 2 diabetic hearts: (i) increased FA uptake into cardiac myocytes and into mitochondria; (ii) altered mitochondrial function, with up-regulation of uncoupling proteins; and (iii) stimulation of peroxisome proliferator-activated receptor-alpha. Enhanced cardiac FA utilization in rodent type 2 diabetic models is associated with reduced cardiac contractile function, perhaps as a consequence of lipotoxicity and/or reduced cardiac efficiency. Similar results have been obtained with human type 2 diabetic hearts, suggesting that pharmacological interventions that can reduce cardiac FA utilization may have beneficial effects on contractile function. |
