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Cellular Aging Contributes to Failure of Cold-Induced Beige Adipocyte Formation in Old Mice and Humans

Daniel C Berry1, Yuwei Jiang1, Robert W Arpke2

  • 1Division of Endocrinology, Department of Internal Medicine, UT Southwestern Medical Center, Dallas, TX 75390, USA.

Cell Metabolism
|November 28, 2016
PubMed

Insights

Aging reduces the ability of white fat progenitor cells to generate energy-burning beige adipocytes. Reversing cellular aging in these cells rejuvenates this process, offering a potential therapy for metabolic health in older adults.

Area of Science:

  • Cellular Biology
  • Metabolic Health
  • Aging Research

Background:

  • Cold exposure activates white adipose tissue progenitor cells to form beige adipocytes, which generate heat and burn energy, presenting a potential anti-obesity and anti-diabesity strategy.
  • The capacity for cold-induced beige adipocyte formation diminishes with age, limiting therapeutic applications for older populations experiencing obesity.

Purpose of the Study:

  • To investigate the cellular mechanisms underlying the age-dependent decline in beige adipocyte formation.
  • To explore strategies for rejuvenating beige progenitor cell function in aged individuals to improve metabolic health.

Main Methods:

  • Analysis of cellular aging (senescence) in murine and human beige progenitor cells from young and aged subjects.
  • Genetic and pharmacological manipulation of the senescence pathway (p38/MAPK-p16Ink4a) in beige progenitor cells.
  • Assessment of cold-induced beiging capacity and glucose sensitivity following interventions.

Main Results:

  • Aging beige progenitor cells exhibit a senescence-like phenotype, explaining their reduced ability to form beige adipocytes.
  • Activating senescence in young cells impaired beiging, while targeting the p38/MAPK-p16Ink4a pathway reversed aging-related dysfunction in aged cells.
  • Rejuvenation of beiging in aged cells led to improved glucose sensitivity.

Conclusions:

  • Cellular senescence is a key factor limiting beige adipocyte formation in aging.
  • Targeting cellular aging pathways, specifically the p38/MAPK-p16Ink4a axis, can restore the beiging potential of aged progenitor cells.
  • Anti-aging and senescence-modulating strategies hold promise for enhancing metabolic health in aging humans.
Keywords:
Ink4a/Arfadiposebeige adipocytescellular agingcold exposuremural cellssenescencethermogenesis

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