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• W2336692571 startingPage "367" @default.
• W2336692571 abstract "Phenobarbital (PB) antagonized insulin to inactivate the insulin receptor and attenuated the insulin receptor downstream protein kinase B (AKT)–forkhead box protein O1 and extracellular signal-regulated kinase 1/2 signals in mouse primary hepatocytes and HepG2 cells. Hepatic AKT began dephosphorylation in an early stage of PB treatment, and blood glucose levels transiently increased in both wild-type and constitutive androstane receptor (CAR) knockout (KO) mice. On the other hand, blood glucose levels increased in wild-type mice, but not KO mice, in later stages of PB treatment. As a result, PB, acting as an insulin receptor antagonist, elicited CAR-independent increases and CAR-dependent decreases of blood glucose levels at these different stages of treatment, respectively. Reciprocally, insulin activation of the insulin receptor repressed CAR activation and induction of its target <i>CYP2B6</i> gene in HepG2 cells. Thus, PB and insulin cross-talk through the insulin receptor to regulate glucose and drug metabolism reciprocally." @default.
• W2336692571 created "2016-06-24" @default.
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• W2336692571 date "2016-03-18" @default.
• W2336692571 modified "2023-09-24" @default.
• W2336692571 title "Phenobarbital and Insulin Reciprocate Activation of the Nuclear Receptor Constitutive Androstane Receptor through the Insulin Receptor" @default.
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• W2336692571 doi "https://doi.org/10.1124/jpet.116.232140" @default.
• W2336692571 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4851327" @default.
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• W2336692571 hasPublicationYear "2016" @default.
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