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Published on: January 7, 2018
Overexpression of p53 Improves Blood Glucose Control in an Insulin Resistant Diabetic Mouse Model
Xuemei Zhang1, Wei Duan, Wai-Nang Paul Lee
1From the *The Medical College of Dalian University, Dalian Economic and Technical Development Zone; †Affiliated Zhongshan Hospital of Dalian University, Dalian, China; ‡Metabolomics Core, LA Biomed, David Geffen School of Medicine, University of California Los Angeles, Torrance; §Department of Medicine, David Geffen School of Medicine at University of California Los Angeles, Los Angeles, CA; ∥School of Pharmaceutical Science and Technology at Dalian University of Technology, Dalian, China; and ¶Department of Medicine and Medical Microbiology, Creighton University, Omaha, NE.
Objective:
This paper aimed to assess the physiological effects of p53 on glucose homeostasis in vivo.
Methods:
A recombinant adenoviral p53 (rAd-p53) vector was administered to insulin-resistant diabetic mice. Intraperitoneal glucose tolerance test was performed in all groups of mice. Changes in fasting blood glucose, serum triglycerides, C-peptide, and insulin concentrations in treated and untreated mice were measured. Analyses of the target genes related to glucose metabolism were performed.
Results:
Treatment with the rAd-p53 improved glucose control in a dose- and time-dependent manner and lowered significantly the fasting blood glucose, the serum triglycerides, and improved tolerance test of glucose as compared to control. Lowered blood glucose was associated with up-regulation of genes in the glycogenesis pathways, and down-regulation of genes in the gluconeogenesis pathways in the liver. Overexpressions of GLUT2, GK, PPAR-γ, and insulin receptor precursor were also observed in the liver and the pancreas of treated animals.
Conclusions:
Activation of p53-mediated glucose metabolism led to insulin-like antidiabetic effect in the mouse model especially by changing hepatic insulin sensitivity in the diabetic mouse model.
