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Is the endotoxin-complement cascade the major driver in lipedema?

Ilja L Kruglikov1, Philipp E Scherer2

  • 1Scientific Department, Wellcomet GmbH, Karlsruhe, Germany.

Trends in Endocrinology and Metabolism: TEM
|April 30, 2024
PubMed
Summary

Lipedema may stem from bacterial endotoxins (LPS) accumulating in fat tissue, causing inflammation and expansion. Managing endotoxemia could potentially improve lipedema symptoms and slow disease progression.

Keywords:
MMP14caveolin-1complement pathwaylipedemamembrane attack complexpregnancy

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Area of Science:

  • Endocrinology
  • Immunology
  • Metabolic Disorders

Background:

  • Lipedema is a poorly understood adipose tissue disorder.
  • It involves symmetrical fat deposition in proximal extremities.
  • The exact cause of lipedema remains unclear.

Purpose of the Study:

  • To propose a novel hypothesis for the underlying cause of lipedema.
  • To investigate the role of bacterial lipopolysaccharides (LPS) and endotoxemia in lipedema pathogenesis.
  • To suggest potential therapeutic targets for lipedema management.

Main Methods:

  • This study is primarily theoretical, proposing a mechanism based on existing knowledge.
  • It integrates concepts of adipose tissue biology, immunology, and microbiology.
  • Future research directions are suggested.

Main Results:

  • A selective accumulation of bacterial lipopolysaccharides (LPS) in gluteofemoral white adipose tissue (WAT) is proposed as a trigger for lipedema.
  • A malfunctioning complement system, in conjunction with LPS, is suggested to induce low-grade inflammation and uncontrollable fat expansion.
  • Endotoxemia is highlighted as a prevalent condition in lipedema patients.

Conclusions:

  • Lipedema pathogenesis may involve LPS accumulation and endotoxemia.
  • Targeting endotoxemia presents a potential strategy for managing lipedema.
  • Further research into the role of endotoxemia in lipedema is warranted.