2. Academic Validation
  3. Loss of MER Tyrosine Kinase Attenuates Adipocyte Hypertrophy and Leads to Enhanced Thermogenesis in Mice Exposed to High-Fat Diet

Loss of MER Tyrosine Kinase Attenuates Adipocyte Hypertrophy and Leads to Enhanced Thermogenesis in Mice Exposed to High-Fat Diet

  • Cells. 2024 Nov 18;13(22):1902. doi: 10.3390/cells13221902.
Krisztina Köröskényi 1 2,  László Sós 3,  Melinda Rostás 3,  Albert Bálint Papp 3,  Endre Kókai 1 4,  Éva Garabuczi 5,  Dávid Deák 6,  Lívia Beke 7,  Gábor Méhes 7,  Zsuzsa Szondy 1 2
Affiliations

Affiliations

  • 1 Division of Dental Biochemistry, Department of Basic Medical Sciences, Faculty of Dentistry, University of Debrecen, 4032 Debrecen, Hungary.
  • 2 Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary.
  • 3 Doctoral School of Dental Sciences, Faculty of Dentistry, University of Debrecen, 4032 Debrecen, Hungary.
  • 4 Department of Medical Chemistry, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary.
  • 5 Department of Integrative Health Sciences, Institute of Health Sciences, Faculty of Health Sciences, University of Debrecen, 4032 Debrecen, Hungary.
  • 6 Laboratory Animal Facility, Life Science Building, University of Debrecen, 4032 Debrecen, Hungary.
  • 7 Department of Pathology, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary.
PMID: 39594650 DOI: 10.3390/cells13221902
Abstract

Obesity is characterized by low-grade inflammation that originates predominantly from the expanding visceral adipose tissue, in which adipocytes respond to lipid overload with hypertrophy, and consequently die by Apoptosis. Recruited adipose tissue macrophages (ATMs) take up the excess lipids and remove the dead cells; however, long-term exposure to high concentrations of lipids alters their phenotype to M1-like ATMs that produce pro-inflammatory cytokines and resistin leading to Insulin resistance and Other obesity-related pathologies. Mer tyrosine kinase is expressed by macrophages and by being an efferocytosis receptor, and by suppressing inflammation, we hypothesized that it might play a protective role against obesity. To our surprise, however, the loss of Mer protected mice against high-fat diet (HFD)-induced obesity. We report in this paper that Mer is also expressed by adipocytes of both white and brown adipose tissues, and while its activity facilitates adipocyte lipid storage both in vitro and in vivo in mice exposed to HFD, it simultaneously attenuates thermogenesis in the brown adipose tissue contributing to its 'whitening'. Our data indicate that Mer is one of the adipocyte tyrosine kinase receptors, the activity of which contributes to the metabolic decision about the fate of excess lipids favoring their storage within the body.

Keywords

Mer tyrosine kinase; adipocyte; obesity; thermogenesis.

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