The PPARγ-FGF1 axis

An unexpected mediator of adipose tissue homeostasis

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

Adipose tissue remodeling is a dynamic process during nutritional fluctuation that plays critical roles in metabolic homeostasis and insulin sensitivity. The process is highly regulated by many factors, including adipokines and cytokines that are locally released within fat pads. In a recent study published in Nature, Jonker and colleagues identified FGF1 as an important mediator that is selectively induced in fat cells by high-fat diet feeding and established the PPARγ-FGF1 axis as a critical pathway that regulates adipose tissue remodeling and ultimately systemic metabolic homeostasis.

Original languageEnglish (US)
Pages (from-to)1416-1418
Number of pages3
JournalCell Research
Volume22
Issue number10
DOIs
StatePublished - Oct 2012

Fingerprint

Fibroblast Growth Factor 1
Peroxisome Proliferator-Activated Receptors
Adipose Tissue
Homeostasis
Nutritional Physiological Phenomena
Adipokines
Critical Pathways
High Fat Diet
Adipocytes
Insulin Resistance
Cytokines

ASJC Scopus subject areas

  • Cell Biology
  • Molecular Biology

Cite this

The PPARγ-FGF1 axis : An unexpected mediator of adipose tissue homeostasis. / Sun, Kai; Scherer, Philipp E.

In: Cell Research, Vol. 22, No. 10, 10.2012, p. 1416-1418.

Research output: Contribution to journalArticle

@article{d751164f50aa4c63ab343ba230ec8e9a,
title = "The PPARγ-FGF1 axis: An unexpected mediator of adipose tissue homeostasis",
abstract = "Adipose tissue remodeling is a dynamic process during nutritional fluctuation that plays critical roles in metabolic homeostasis and insulin sensitivity. The process is highly regulated by many factors, including adipokines and cytokines that are locally released within fat pads. In a recent study published in Nature, Jonker and colleagues identified FGF1 as an important mediator that is selectively induced in fat cells by high-fat diet feeding and established the PPARγ-FGF1 axis as a critical pathway that regulates adipose tissue remodeling and ultimately systemic metabolic homeostasis.",
author = "Kai Sun and Scherer, {Philipp E.}",
year = "2012",
month = "10",
doi = "10.1038/cr.2012.94",
language = "English (US)",
volume = "22",
pages = "1416--1418",
journal = "Cell Research",
issn = "1001-0602",
publisher = "Nature Publishing Group",
number = "10",

}

TY - JOUR

T1 - The PPARγ-FGF1 axis

T2 - An unexpected mediator of adipose tissue homeostasis

AU - Sun, Kai

AU - Scherer, Philipp E.

PY - 2012/10

Y1 - 2012/10

N2 - Adipose tissue remodeling is a dynamic process during nutritional fluctuation that plays critical roles in metabolic homeostasis and insulin sensitivity. The process is highly regulated by many factors, including adipokines and cytokines that are locally released within fat pads. In a recent study published in Nature, Jonker and colleagues identified FGF1 as an important mediator that is selectively induced in fat cells by high-fat diet feeding and established the PPARγ-FGF1 axis as a critical pathway that regulates adipose tissue remodeling and ultimately systemic metabolic homeostasis.

AB - Adipose tissue remodeling is a dynamic process during nutritional fluctuation that plays critical roles in metabolic homeostasis and insulin sensitivity. The process is highly regulated by many factors, including adipokines and cytokines that are locally released within fat pads. In a recent study published in Nature, Jonker and colleagues identified FGF1 as an important mediator that is selectively induced in fat cells by high-fat diet feeding and established the PPARγ-FGF1 axis as a critical pathway that regulates adipose tissue remodeling and ultimately systemic metabolic homeostasis.

UR - http://www.scopus.com/inward/record.url?scp=84867062444&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84867062444&partnerID=8YFLogxK

U2 - 10.1038/cr.2012.94

DO - 10.1038/cr.2012.94

M3 - Article

VL - 22

SP - 1416

EP - 1418

JO - Cell Research

JF - Cell Research

SN - 1001-0602

IS - 10

ER -