| First Author | He L | Year | 2012 |
| Journal | J Biol Chem | Volume | 287 |
| Issue | 38 | Pages | 32069-77 |
| PubMed ID | 22815486 | Mgi Jnum | J:278697 |
| Mgi Id | MGI:6359618 | Doi | 10.1074/jbc.M112.385864 |
| Citation | He L, et al. (2012) Transcriptional co-activator p300 maintains basal hepatic gluconeogenesis. J Biol Chem 287(38):32069-77 |
| abstractText | A major cause of fasting hyperglycemia in diabetes mellitus is unregulated hepatic glucose production (HGP). Insulin suppresses HGP by phosphorylating CBP and disassembling the CREB-CBP complex from gluconeogenic genes. p300 is closely related to CBP; but in contrast to CBP, p300 binds constitutively to CREB due to the absence of phosphorylation site found in CBP. In a phosphorylation-competent p300(G442S) knock-in mouse model, we demonstrate that HGP is now exquisitely sensitive to insulin suppression. p300(G422S) and hepatic-deleted p300 mice exhibited significant lower blood glucose levels in the fasted and post-prandial states, indicating a role for p300 in maintaining basal HGP. |
