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Updated: Apr 21, 2026

Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells
Published on: February 21, 2018
Control of hepatic gluconeogenesis by the promyelocytic leukemia zinc finger protein
Siyu Chen1, Jinchun Qian, Xiaoli Shi
1Jiangsu Key Laboratory for Molecular and Medical Biotechnology and College of Life Sciences (S.C., J.Q., X.S., T.G., T.L., C.L.), Nanjing Normal University, Nanjing, Jiangsu 210023, China; and State Key Laboratory of Natural Medicines (C.L.), China Pharmaceutical University, Nanjing, Jiangsu 210009, China.
Abstract:
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 γ coactivator 1α 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.
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