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Inactivation of Minar2 in mice hyperactivates mTOR signaling and results in obesity

Saran Lotfollahzadeh1, Chaoshuang Xia2, Razie Amraei3

  • 1Renal Section, Department of Medicine, Boston University Chobanian & Avedisian School of Medicine, Boston, MA, USA.

Molecular Metabolism
|May 28, 2023
PubMed
Abstract

Insights

Major intrinsically disordered NOTCH2-associated receptor2 (MINAR2) negatively regulates mTORC1, impacting obesity and metabolism. Loss of MINAR2 leads to increased body fat and impaired glucose tolerance, highlighting its role in metabolic disorders.

Area of Science:

  • Metabolic research
  • Obesity research
  • Adipocyte biology

Background:

  • Obesity is a complex metabolic disorder linked to chronic diseases like type 2 diabetes.
  • The protein Major intrinsically disordered NOTCH2-associated receptor2 (MINAR2) is understudied regarding its role in obesity and metabolism.

Purpose of the Study:

  • To determine the impact of Minar2 on adipose tissues and obesity.
  • To elucidate the molecular mechanisms by which Minar2 influences adipocyte function and overall metabolism.

Main Methods:

  • Generation of Minar2 knockout (KO) mice.
  • Comprehensive molecular, proteomic, biochemical, and histopathological analyses.
  • In vitro studies using cell cultures (HEK-293 cells) and adipocytes.

Main Results:

  • Minar2 inactivation in mice led to increased body fat and hypertrophic adipocytes.
  • Minar2 KO mice exhibited obesity, impaired glucose tolerance, and metabolic dysfunction on a high-fat diet.
  • Minar2 interacts with Raptor, inhibiting mTORC1 activation; Minar2 deficiency results in mTOR hyperactivation.

Conclusions:

  • Minar2 is identified as a novel physiological negative regulator of mTORC1.
  • Minar2 plays a key role in regulating obesity and associated metabolic disorders.
  • Impaired MINAR2 expression or activation may contribute to obesity and related diseases.
Keywords:
DiabetesMinar2ObesityRaptormTORmTORC1

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