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Adipose Tissue Dysfunction Occurs Independently of Obesity in Adipocyte-Specific Oncostatin Receptor Knockout Mice

Jacqueline M Stephens1, Jennifer L Bailey2, Hardy Hang1

  • 1Adipocyte Biology Laboratory, Pennington Biomedical Research Center, Baton Rouge, Louisiana, USA.

Obesity (Silver Spring, Md.)
|September 19, 2018
PubMed
Abstract

Insights

Loss of the oncostatin M receptor (OSMR) in fat cells impairs insulin sensitivity and increases inflammatory adipokines. Intact OSMR signaling is vital for maintaining adipose tissue immune cell balance.

Area of Science:

  • Metabolic research
  • Adipose tissue biology
  • Immunology

Background:

  • Adipose tissue plays a crucial role in metabolic health.
  • Oncostatin M receptor (OSMR) signaling is implicated in various cellular functions.
  • The specific role of adipocyte OSMR in metabolic homeostasis is not fully understood.

Purpose of the Study:

  • To investigate the phenotypic consequences of adipocyte-specific OSMR loss in mice.
  • To determine the impact of OSMR deficiency on adipose tissue function and inflammation.

Main Methods:

  • Comparison of chow-fed adipocyte-specific OSMR knockout (FKO) mice with littermate controls.
  • Assessment of tissue weights, insulin sensitivity, and adipokine production in epididymal fat (eWAT) and serum.
  • In vitro analysis of adipocyte response to oncostatin M and gene expression.

Main Results:

  • No significant differences in body weight, fasting glucose, or eWAT weight between genotypes.
  • Reduced insulin responsiveness in the eWAT of OSMRFKO mice.
  • Elevated levels of pro-inflammatory adipokines (e.g., C-reactive protein, lipocalin 2, ICAM-1) in eWAT and serum of OSMRFKO mice.
  • Increased leukocyte infiltration in the eWAT of OSMRFKO mice.

Conclusions:

  • Adipocyte-specific OSMR loss leads to adipose tissue dysfunction and increased inflammation.
  • Intact adipocyte OSMR signaling is essential for maintaining immune cell homeostasis within adipose tissue.

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