Abstract:
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.
journal_name
Pancreasjournal_title
Pancreasauthors
Zhang X,Duan W,Lee WN,Zhang Y,Xiang F,Liu Q,Go VL,Xiao GGdoi
10.1097/MPA.0000000000000637subject
Has Abstractpub_date
2016-08-01 00:00:00pages
1010-7issue
7eissn
0885-3177issn
1536-4828journal_volume
45pub_type
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