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Updated: Apr 17, 2026

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
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Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis

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ATM Regulates Adipocyte Differentiation and Contributes to Glucose Homeostasis

Masatoshi Takagi1, Hatsume Uno2, Rina Nishi1

  • 1Department of Pediatrics and Developmental Biology, Graduate School of Medicine, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan.

Cell Reports
|February 17, 2015
PubMed

Insights

Ataxia-telangiectasia (A-T) impairs adipocyte differentiation, leading to insulin resistance. This study reveals the ATM protein

Area of Science:

  • Molecular Biology
  • Metabolic Diseases
  • Genetics

Background:

  • Ataxia-telangiectasia (A-T) is a rare genetic disorder.
  • A-T patients can develop diabetes mellitus, but underlying mechanisms are unclear.
  • The role of ATM in glucose metabolism and adipogenesis is poorly understood.

Purpose of the Study:

  • To investigate the molecular mechanisms linking ATM deficiency to glucose intolerance in A-T.
  • To explore the role of ATM in adipocyte differentiation and insulin resistance.

Main Methods:

  • Comparison of Atm-/- and Atm+/+ mice.
  • In vitro studies of adipocyte differentiation in Atm-/- cells.
  • Analysis of key transcription factors (C/EBPα, PPARγ, C/EBPβ) and ATM signaling pathways.

Main Results:

  • Atm-/- mice exhibited insulin resistance, reduced subcutaneous adipose tissue, and lower serum adiponectin.
  • Atm-/- cells showed impaired adipocyte differentiation due to reduced C/EBPα and PPARγ induction.
  • ATM activation was linked to differentiation stimuli, involving ATM binding to C/EBPβ and p300 for C/EBPα regulation.

Conclusions:

  • ATM deficiency contributes to glucose intolerance and insulin resistance in A-T.
  • ATM plays a critical role in regulating adipocyte differentiation and glucose metabolism.
  • Findings provide insights into A-T pathogenesis and potential therapeutic targets for metabolic dysfunction.

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