PPAR-γ is a major driver of the accumulation and phenotype of adipose tissue Treg cells View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2012-06

AUTHORS

Daniela Cipolletta, Markus Feuerer, Amy Li, Nozomu Kamei, Jongsoon Lee, Steven E. Shoelson, Christophe Benoist, Diane Mathis

ABSTRACT

Obesity and type-2 diabetes have increased markedly over the past few decades, in parallel. One of the major links between these two disorders is chronic, low-grade inflammation. Prolonged nutrient excess promotes the accumulation and activation of leukocytes in visceral adipose tissue (VAT) and ultimately other tissues, leading to metabolic abnormalities such as insulin resistance, type-2 diabetes and fatty-liver disease. Although invasion of VAT by pro-inflammatory macrophages is considered to be a key event driving adipose-tissue inflammation and insulin resistance, little is known about the roles of other immune system cell types in these processes. A unique population of VAT-resident regulatory T (Treg) cells was recently implicated in control of the inflammatory state of adipose tissue and, thereby, insulin sensitivity. Here we identify peroxisome proliferator-activated receptor (PPAR)-γ, the 'master regulator' of adipocyte differentiation, as a crucial molecular orchestrator of VAT Treg cell accumulation, phenotype and function. Unexpectedly, PPAR-γ expression by VAT Treg cells was necessary for complete restoration of insulin sensitivity in obese mice by the thiazolidinedione drug pioglitazone. These findings suggest a previously unknown cellular mechanism for this important class of thiazolidinedione drugs, and provide proof-of-principle that discrete populations of Treg cells with unique functions can be precisely targeted to therapeutic ends. More... »

PAGES

549

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/nature11132

DOI

http://dx.doi.org/10.1038/nature11132

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1047004921

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/22722857


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