Why the study?
Does chronic in vivo PPAR stimulation induce myocardial subcellular redistribution of FAT/CD36 and FABPpm?
Does chronic in vivo PPAR stimulation induce myocardial subcellular redistribution of FAT/CD36 and FABPpm?
PPARalpha and PPARbeta activation specifically regulate the plasmalemmal content of fatty acid transporters and subsequent fatty acid metabolism in the myocardium.
No immediate clinical implications from this animal study; leaves open chronic in vivo effects on human myocardial fatty acid transport.
This study reveals that the activation of either PPARalpha (WY 14643) or PPARbeta (GW0742) each induce the translocation of FAT/CD36 from an intracellular pool(s) to the plasma membrane, while PPARbeta also induces the subcellular redistribution of FABPpm(Got2) to the plasma membrane. In contrast, activation of PPARgamma failed to induce the subcellular redistribution of FAT/CD36 and FABPpm. These PPARalpha-, and PPARbeta-induced changes in the plasmalemmal content of these fatty acid transporters were associated with the concurrent upregulation of fatty acid triacylglycerol esterification (PPARbeta) and oxidation (PPARalpha and PPARbeta). Observed effects of chronic PPAR stimulation were not related to either AMPK or ERK1/2 activation.
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Kalinowska et al. (2009) studied this question.
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