| First Author | Chen S | Year | 2014 |
| Journal | Mol Endocrinol | Volume | 28 |
| Issue | 12 | Pages | 1987-98 |
| PubMed ID | 25333514 | Mgi Jnum | J:218284 |
| Mgi Id | MGI:5617114 | Doi | 10.1210/me.2014-1164 |
| Citation | Chen S, et al. (2014) Control of hepatic gluconeogenesis by the promyelocytic leukemia zinc finger protein. Mol Endocrinol 28(12):1987-98 |
| abstractText | The promyelocytic leukemia zinc finger (PLZF) protein is involved in major biological processes including energy metabolism, although its role remains unknown. In this study, we demonstrated that hepatic PLZF expression was induced in fasted or diabetic mice. PLZF promoted gluconeogenic gene expression and hepatic glucose output, leading to hyperglycemia. In contrast, hepatic PLZF knockdown improved glucose homeostasis in db/db mice. Mechanistically, peroxisome proliferator-activated receptor gamma coactivator 1alpha and the glucocorticoid receptor synergistically activated PLZF expression. We conclude that PLZF is a critical regulator of hepatic gluconeogenesis. PLZF manipulation may benefit the treatment of metabolic diseases associated with gluconeogenesis. |
