4.5 Article

Temporal specificity of IL-6 knockout in enhancing the thermogenic capability of brown adipose tissue

Journal

JOURNAL OF PHYSIOLOGY AND BIOCHEMISTRY
Volume 78, Issue 3, Pages 619-628

Publisher

SPRINGER
DOI: 10.1007/s13105-021-00847-4

Keywords

IL-6; Brown adipose tissue; Thermogenesis; Glucose homeostasis; Inflammatory cytokines

Funding

  1. Construction Engineering Special Fund of Taishan Scholars [201511023, 201712022]
  2. National Key Research and Development Program of China [2017YFE0129800]
  3. Funds of Shandong Double Tops Program
  4. Natural Science Foundation of Shandong Province, China [ZR2019MC016]
  5. Program for Scientific Research Innovation Team of Young Scholar in Colleges and Universities of Shandong Province [2019KJE009]

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IL-6 plays a regulatory role in the thermogenic capability of brown adipose tissue (BAT). Knockout of IL-6 enhances BAT thermogenesis in young mice and improves glucose homeostasis, but these improvements disappear in elderly mice, possibly due to increased expression of other inflammatory cytokines.
Although interleukin-6 (IL-6) has been regarded as a homeostatic regulator of fat metabolism, its role in brown adipose thermogenesis remains to be further clarified. By using wild-type (WT) and IL-6-knockout (KO) mice, this study aims to investigate whether IL-6 regulates the thermogenic capability of brown adipose tissue (BAT) at both young and elderly stages. We demonstrated that IL-6 KO enhances BAT thermogenesis at a young age, as evidenced by the increased mRNA and protein expression levels of thermogenic genes, and the elevated interscapular surface temperature. The IL-6-KO enhancement of BAT thermogenesis is associated with improved respiratory exchange ratio (RER) and glucose homeostasis at young stages. However, these improvements disappear in elderly KO mice, which is likely attributable to the highly increased expression of other inflammatory cytokines, such as Tnf alpha, Il-1 beta, and Il-10. Our findings indicate that the lack of IL-6 has a temporal-specific contribution to the promotion of BAT thermogenesis.

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