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Lysyl oxidase and adipose tissue dysfunction.

Emilie Pastel1, Emily Price1, Kajsa Sjöholm2

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Lysyl oxidase (LOX) increases with obesity and is upregulated by hypoxia and inflammation in adipose tissue. Diabetes and hyperglycemia did not affect LOX levels, suggesting specific triggers for fibrosis development.

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Area of Science:

  • Biochemistry
  • Cell Biology
  • Metabolic Research

Background:

  • Lysyl oxidase (LOX) is vital for collagen crosslinking and fibrosis.
  • Fibrosis, marked by excess collagen, is a feature of dysfunctional adipose tissue (AT) in obesity and type 2 diabetes.
  • This study investigates LOX in human AT, particularly in relation to obesity and diabetes.

Purpose of the Study:

  • To comprehensively characterize lysyl oxidase (LOX) expression and activity in human adipose tissue (AT).
  • To investigate the relationship between LOX, obesity, and type 2 diabetes.
  • To explore the mechanisms underlying LOX regulation in AT, including hypoxia, leptin, glucose, and inflammation.

Main Methods:

  • Analyzed LOX mRNA expression in omental and abdominal subcutaneous AT from individuals with varying BMI and diabetes status.
  • Assessed LOX expression and activity in AT explants under hypoxia, leptin, and glucose treatment.
  • Evaluated in vivo LOX response to acute inflammation (lipopolysaccharide) in healthy men.
  • Quantified mRNA using RT-qPCR.

Main Results:

  • LOX expression was elevated in obesity and correlated with BMI.
  • High concentrations of leptin suppressed LOX expression in vitro.
  • Hypoxia and lipopolysaccharide-induced inflammation increased LOX expression in AT, independent of macrophage infiltration.
  • Diabetes status and hyperglycemia did not significantly affect LOX levels.

Conclusions:

  • LOX expression in adipose tissue is increased in obesity.
  • Hypoxia and inflammation are key mechanisms driving LOX upregulation in obese adipose tissue.
  • LOX is not directly affected by diabetes or hyperglycemia in adipose tissue, despite its role in fibrosis.