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An Adipocyte Cell Culture Model to Study the Impact of Protein and Micro-RNA Modulation on Adipocyte Function
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Published on: May 4, 2021

Characterisation of receptor-specific TNFalpha functions in adipocyte cell lines lacking type 1 and 2 TNF receptors

J K Sethi1, H Xu, K T Uysal

  • 1Division of Biological Sciences and Department of Nutrition, Harvard School of Public Health, Boston, MA 02115, USA.

FEBS Letters
|March 10, 2000
PubMed

Insights

Tumour necrosis factor-alpha (TNFalpha) primarily uses TNFR1 to trigger lipolysis and inhibit glucose transport in adipocytes. TNFR2 is not essential for these TNFalpha-mediated effects in fat cells.

Area of Science:

  • Cell Biology
  • Endocrinology
  • Immunology

Background:

  • Tumour necrosis factor-alpha (TNFalpha) is a cytokine with diverse biological roles.
  • TNFalpha acts through two receptors: TNFR1 and TNFR2.
  • Understanding receptor-specific functions in adipocytes is crucial for metabolic research.

Purpose of the Study:

  • To investigate the distinct roles of TNFR1 and TNFR2 in TNFalpha's actions on adipocytes.
  • To characterize TNFalpha-induced lipolysis and glucose transport inhibition mediated by specific TNF receptors.

Main Methods:

  • Development of four preadipocyte cell lines from wild type and TNFR1/TNFR2 knockout mice.
  • Differentiation of cell lines into mature adipocytes.
  • Assessment of TNFalpha-induced lipolysis and insulin-stimulated glucose transport.

Main Results:

  • TNFalpha stimulated lipolysis and inhibited glucose transport in wild type and TNFR2(-/-) adipocytes.
  • These effects were abolished in TNFR1(-/-) and TNFR1(-/-)R2(-/-) adipocytes.
  • TNFR1 is the primary mediator of TNFalpha's effects on adipocyte lipolysis and glucose transport.

Conclusions:

  • TNFalpha-induced lipolysis and inhibition of insulin-stimulated glucose transport are predominantly mediated by TNFR1.
  • TNFR2 is not required for these specific TNFalpha functions in adipocytes.
  • The developed cell lines provide a valuable tool for studying TNF receptor signaling in adipocytes.

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