PPARα was shown to activate PEPCK promoter activity in Hepa1c1c7 cells [46], and in isolated rat hepatocytes, PEPCK and G6Pase expression increased in response to palmitate [47]. The PEPCK promoter contains 2 intermediate-affinity PPREs [48]. These PPREs were responsible for the upregulation of PEPCK by PPARγ in adipocytes [49], but direct interaction with PPARα was not studied. ChIP experiments showed that upon palmitate treatment, PPARα was recruited to the G6Pase promoter together with HNF4α and several other transcription factors [47]. Sites of interaction with the G6Pase promoter region or functional studies, however, were not reported. No PPRE has been identified in the promoter of LDH or PC [4].
