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Abnormal brown adipose tissue mitochondrial structure and function in IL10 deficiency.

José C de-Lima-Júnior1, Gabriela F Souza1, Alexandre Moura-Assis1

  • 1Laboratory of Cell Signaling, Department of Internal Medicine, University of Campinas, Campinas, São Paulo 13084-970, Brazil; Obesity and Comorbidities Research Center, University of Campinas, Campinas, São Paulo 13084-970, Brazil.

Ebiomedicine
|December 4, 2018
PubMed
Summary

Systemic inflammation, specifically Interleukin-10 (IL10) deficiency, severely impairs brown adipose tissue mitochondria structure and function, leading to cold intolerance. Reducing inflammation partially restored structure but not function.

Keywords:
InflammationInterleukin-10MitochondriaObesityRespirationThermogenesis

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Area of Science:

  • Metabolic disease research
  • Obesity and inflammation studies
  • Brown adipose tissue biology

Background:

  • Inflammation links obesity to insulin resistance and metabolic dysfunction.
  • Brown adipose tissue (BAT) is crucial for energy homeostasis and thermogenesis.
  • The impact of systemic inflammation on BAT structure and function remains unclear.

Purpose of the Study:

  • To investigate the role of Interleukin-10 (IL10) in regulating brown adipose tissue (BAT) structure and function.
  • To determine the effects of IL10 deficiency on mitochondrial integrity and thermogenesis in BAT.
  • To explore the relationship between IL10, mitochondrial function, and inflammation in metabolic health.

Main Methods:

  • Bioinformatic analysis of human and rodent data for IL10-mitochondria-thermogenesis relations.
  • Experimental manipulation of IL10 levels in wild-type and IL10 knockout mice.
  • Assessment of BAT mitochondrial structure using electron microscopy.
  • Measurement of mitochondrial respiration and thermogenic capacity (UCP1-dependent).

Main Results:

  • IL10 knockout mice exhibited severe BAT mitochondrial structural abnormalities (round shape, lost cristae, fragmentation).
  • IL10 deficiency resulted in newborn cold intolerance and impaired UCP1-dependent mitochondrial respiration.
  • Anti-TNFα treatment partially rescued structural but not functional mitochondrial defects.
  • Bioinformatics revealed correlations between IL10, mitochondrial lipid metabolism, and caspase gene expression in humans and mice.

Conclusions:

  • IL10 and systemic inflammation are critical regulators of BAT mitochondrial structure and function.
  • Dysregulation of IL10 impacts BAT's role in energy expenditure and thermogenesis.
  • Targeting IL10 and inflammation may offer therapeutic strategies for metabolic diseases linked to BAT dysfunction.