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Chromatin Immunoprecipitation of Murine Brown Adipose Tissue
Published on: November 21, 2018
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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
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.
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.
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