Innate immunity orchestrates adipose tissue homeostasis

Yi Wei Lin, Li-Na Wei

Research output: Contribution to journalReview articlepeer-review

5 Scopus citations

Abstract

Obesity is strongly associated with multiple diseases including insulin resistance, type 2 diabetes, cardiovascular diseases, fatty liver disease, neurodegenerative diseases and cancers, etc. Adipose tissue (AT), mainly brown AT (BAT) and white AT (WAT), is an important metabolic and endocrine organ that maintains whole-body homeostasis. BAT contributes to non-shivering thermogenesis in a cold environment; WAT stores energy and produces adipokines that fine-tune metabolic and inflammatory responses. Obesity is often characterized by over-expansion and inflammation of WAT where inflammatory cells/mediators are abundant, especially pro-inflammatory (M1) macrophages, resulting in chronic low-grade inflammation and leading to insulin resistance and metabolic complications. Macrophages constitute the major component of innate immunity and can be activated as a M1 or M2 (anti-inflammatory) phenotype in response to environmental stimuli. Polarized M1 macrophage causes AT inflammation, whereas polarized M2 macrophage promotes WAT remodeling into the BAT phenotype, also known as WAT browning/beiging, which enhances insulin sensitivity and metabolic health. This review will discuss the regulation of AT homeostasis in relation to innate immunity.

Original languageEnglish (US)
Article number20170013
JournalHormone Molecular Biology and Clinical Investigation
Volume31
Issue number1
DOIs
StatePublished - Jul 26 2017

Bibliographical note

Funding Information:
Research funding: This work was supported by NIH grants DK54733, DK60521, DK54733–11S, DK60521–12S1, and the Dean’s Commitment and the Distinguished McKnight Professorship of University of Minnesota to LNW. The authors declare no competing financial interests.

Keywords

  • RIP140
  • adipose tissue
  • browning/beiging
  • innate immunity
  • macrophage
  • metabolic disease
  • microbiota

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