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Isolation and Culture of Human Mature Adipocytes Using Membrane Mature Adipocyte Aggregate Cultures (MAAC)
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An inflammatory micro-environment promotes human adipocyte apoptosis

Michaela Keuper1, Matthias Blüher, Michael R Schön

  • 1Division of Pediatric Endocrinology, Diabetes and Obesity Unit, Department of Pediatrics and Adolescent Medicine, Ulm University, Eythstr. 24, 89075 Ulm, Germany.

Molecular and Cellular Endocrinology
|April 20, 2011
PubMed

Insights

Macrophages in obesity worsen inflammation by inducing insulin resistance and fat cell (adipocyte) apoptosis. This creates a harmful cycle, increasing local and systemic inflammation.

Area of Science:

  • Cell Biology
  • Immunology
  • Metabolic Disease

Background:

  • Obesity involves macrophage infiltration into adipose tissue, driving inflammation.
  • Fat cell apoptosis is implicated in initiating macrophage recruitment.
  • Understanding the inflammatory micro-environment's impact on fat cells is crucial.

Purpose of the Study:

  • To investigate the interaction between macrophages and adipocytes in an inflammatory context.
  • To determine how macrophage-secreted factors affect adipocyte insulin signaling and survival.
  • To explore the link between insulin resistance and adipocyte apoptosis.

Main Methods:

  • Co-culture of human THP-1 macrophages and SGBS adipocytes.
  • Analysis of insulin signaling pathways, including Akt phosphorylation.
  • Assessment of adipocyte apoptosis induction.

Main Results:

  • Macrophage factors induced insulin resistance and inhibited insulin-stimulated Akt phosphorylation in adipocytes.
  • Adipocyte apoptosis was induced by macrophage-secreted factors, especially in direct co-culture.
  • Inhibition of Akt2 sensitized adipocytes to macrophage-induced apoptosis, linking insulin resistance and apoptosis sensitivity.

Conclusions:

  • Macrophages induce adipocyte apoptosis, representing a novel interaction.
  • A feed-forward cycle exists where macrophages exacerbate inflammation by promoting insulin resistance and adipocyte death.
  • This interaction highlights a mechanism contributing to obesity-associated inflammation.

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