PPARβ/δ null mice show defective myelination of the corpus callosum, reduced adipose tissue and altered inflammatory response in the epidermis [89]. In B12 oligodendrocyte-like cells ethanol was shown to selectively reduce PPARβ/δ expression by increased mRNA degradation without affecting PPARα and PPARγ [90]. These observations could possibly undercover a mechanism underling the ethanol-induced myelination defects and neurological impairment in the foetus [91]. In a recent study by Venkata et al. PPARα and β/δ were shown to be differentially affected by acetaldehyde and ethanol, respectively. The authors show that in MCF-7 breast cancer cell line acetaldehyde inhibits PPARα but not PPARβ/δ, while the latter is inhibited directly by ethanol [92]. A growing body of evidence suggests an association between ethanol consumption and increased cancer risk in different tissues, including breast [93, 94]. More studies are needed to elucidate the effects of ethanol metabolism on PPARβ/δ and the underling mechanisms, but it is intriguing to speculate that some effects of ethanol on peripheral tissues could be mediated by this poorly understood PPAR isoform.
