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Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
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Cell Specific Gene Expression

Multicellular organisms contain a variety of structurally and functionally distinct cell types, but the DNA in all the cells originated from the same parent cells. The differences in the cells can be attributed to the differential gene expression. Liver cells, whose functions include detoxification of blood, production of bile to metabolize fats, and synthesis of proteins essential for metabolism, must express a specific set of genes to perform their functions. Gene expression also varies with...
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Related Experiment Video

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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
Summary

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.

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  • 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.