M1-M2 balancing act in white adipose tissue browning - a new role for RIP140

Pu Ste Liu, Yi Wei Lin, Frank H. Burton, Li-Na Wei

Research output: Contribution to journalArticle

16 Scopus citations

Abstract

A“Holy Grail” sought in medical treatment of obesity is to be able to biologically reprogram their adipose tissues to burn fat rather than store it. White adipose tissue (WAT) stores fuel and its expansion underlines insulin resistance (IR) whereas brown adipose tissue (BAT) burns fuel and stimulates insulin sensitivity. These two types of fats seesaw within our bodies via a regulatory mechanism that involves intricate communication between adipocytes and blood cells, particularly macrophages that migrate into adipose deposits. The coregulator, Receptor Interacting Protein 140 (RIP140), plays a key role in regulating this communication. In mice on a high-fat diet, the level of RIP140 in macrophages is dramatically elevated to activate their inflammatory M1 polarization and enhance their recruitment into WAT, facilitating IR. Conversely, lowering the level of RIP140 in macrophages not only reduces M1 macrophages but also expands alternatively polarized, anti-inflammatory M2 macrophages, triggering white adipose tissue browning, fat burning, and restoration of insulin sensitivity. This suggests a potential therapeutic strategy for reversing IR, obesity, and atherosclerotic or even cosmetic fat deposits: therapeutic browning of white adipose deposits by diminishing RIP140 levels in macrophages.

Original languageEnglish (US)
Pages (from-to)146-148
Number of pages3
JournalAdipocyte
Volume4
Issue number2
DOIs
StatePublished - Jan 1 2015

Keywords

  • Brown adipose tissue
  • Inflammation
  • Insulin resistance
  • Macrophage polarization
  • Metabolism
  • RIP140
  • White adipose tissue

Fingerprint Dive into the research topics of 'M1-M2 balancing act in white adipose tissue browning - a new role for RIP140'. Together they form a unique fingerprint.

  • Cite this