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Yeast As a Chassis for Developing Functional Assays to Study Human P53
14:57

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

P53 and cellular glucose uptake

Alejandro J de la Torre1, Daniela Rogoff, Perrin C White

  • 1Division of Pediatric Endocrinology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9063, USA.

Endocrine Research
|August 4, 2012
PubMed
Abstract

Insights

Inhibition of tumor protein p53 (p53) blunts glucose uptake in liver cells but not fat cells. However, p53 knockout mice show normal glucose homeostasis, suggesting complex roles in glucose metabolism.

Area of Science:

  • Cellular Biology
  • Molecular Biology
  • Metabolism

Background:

  • Tumor protein p53 (p53) is a critical transcription factor responding to cellular stress.
  • Limited glucose availability is a known stressor that can activate p53.
  • The precise role of p53 in regulating glucose uptake remains incompletely understood.

Purpose of the Study:

  • To investigate the hypothesis that modulating p53 levels affects cellular glucose uptake.
  • To determine the impact of p53 inhibition on insulin-stimulated glucose uptake in hepatocytes and adipocytes.
  • To assess the in vivo effects of p53 knockout on glucose homeostasis.

Main Methods:

  • Primary mouse hepatocytes and 3T3-L1 adipocytes were treated with p53 siRNA to suppress p53 expression.
  • Insulin-stimulated glucose uptake was measured in treated and control cells.
  • Western blotting assessed Glut 1, Glut 2, and phosphorylated AKT levels.
  • p53 knockout and wild-type mice underwent glucose and insulin tolerance tests.

Main Results:

  • p53 siRNA significantly reduced p53 mRNA in hepatocytes, leading to a blunted insulin-stimulated glucose uptake compared to controls.
  • In contrast, p53 knockdown had no effect on insulin-stimulated glucose uptake in 3T3-L1 adipocytes.
  • No significant differences were observed in Glut 1, Glut 2, or p-AKT levels between groups.
  • p53 knockout mice exhibited normal glycemic responses in tolerance tests.

Conclusions:

  • p53 inhibition demonstrates tissue-specific effects, impairing hepatic glucose uptake while sparing adipocytes.
  • Complete knockout of p53 does not appear to disrupt overall glucose homeostasis in lean mice.
  • Further research is needed to elucidate the mechanisms linking p53 expression to hepatocyte glucose uptake.

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