Overexpression of p53 Improves Blood Glucose Control in an Insulin Resistant Diabetic Mouse Model.

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

Pancreas

journal_title

Pancreas

authors

Zhang X,Duan W,Lee WN,Zhang Y,Xiang F,Liu Q,Go VL,Xiao GG

doi

10.1097/MPA.0000000000000637

subject

Has Abstract

pub_date

2016-08-01 00:00:00

pages

1010-7

issue

7

eissn

0885-3177

issn

1536-4828

journal_volume

45

pub_type

杂志文章

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