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Purification of Ubiquitinated p53 Proteins from Mammalian Cells
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The Dysfunctional MDM2-p53 Axis in Adipocytes Contributes to Aging-Related Metabolic Complications by Induction of

Zhuohao Liu1,2, Leigang Jin1,3, Jin-Kui Yang4

  • 1State Key Laboratory of Pharmaceutical Biotechnology, The University of Hong Kong, Hong Kong, People's Republic of China.

Diabetes
|August 23, 2018
PubMed

Insights

Aging adipose tissue dysfunction is linked to the p53 pathway. Loss of the MDM2 protein in fat cells accelerates aging, causing metabolic disease and reduced lifespan in mice.

Area of Science:

  • Aging Biology
  • Metabolic Diseases
  • Adipose Tissue Biology

Background:

  • Adipose tissue aging and loss are common in advanced age, but causes and metabolic impacts are unclear.
  • The murine double minute 2 (MDM2)-p53 pathway regulates tumorigenesis and metabolic health, but its role in adipose tissue aging is unknown.

Purpose of the Study:

  • Investigate the role of the MDM2-p53 axis in adipose tissue aging.
  • Determine the metabolic consequences of MDM2 disruption in adipocytes.

Main Methods:

  • Studied MDM2 levels in aging mouse adipose tissue.
  • Genetically disrupted MDM2 in mouse adipocytes.
  • Assessed metabolic parameters, organ senescence, lifespan, and fat transplantation effects.
  • Analyzed senescence-associated secretory factors' impact on adipocyte differentiation.

Main Results:

  • MDM2 is downregulated in aging mouse adipose tissue.
  • MDM2 disruption in adipocytes induced p53-mediated apoptosis and senescence, causing lipodystrophy and metabolic disorders (type 2 diabetes, NAFLD, hyperlipidemia).
  • MDM2-null mice showed premature aging phenotypes, including organ senescence and shorter lifespan.
  • Fat transplantation improved metabolic health; secreted factors from MDM2-null adipocytes impaired progenitor differentiation.

Conclusions:

  • MDM2 downregulation in adipocytes contributes to adipose tissue aging and metabolic decline.
  • The MDM2-p53 axis is crucial for maintaining adipose tissue function and metabolic homeostasis during aging.
  • Targeting MDM2 in adipocytes may offer therapeutic strategies for age-related metabolic diseases.

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