The PPARγ-FGF1 axis: An unexpected mediator of adipose tissue homeostasis

Kai Sun; Philipp E. Scherer

doi:10.1038/cr.2012.94

The PPARγ-FGF1 axis: An unexpected mediator of adipose tissue homeostasis

Kai Sun, Philipp E. Scherer

Research output: Contribution to journal › Article › peer-review

17 Scopus citations

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 language	English (US)
Pages (from-to)	1416-1418
Number of pages	3
Journal	Cell Research
Volume	22
Issue number	10
DOIs	https://doi.org/10.1038/cr.2012.94
State	Published - Oct 2012

ASJC Scopus subject areas

Molecular Biology
Cell Biology

Access to Document

10.1038/cr.2012.94

Cite this

@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 = oct,

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

C2 - 22710798

AN - SCOPUS:84867062444

SN - 1001-0602

VL - 22

SP - 1416

EP - 1418

JO - Cell Research

JF - Cell Research

IS - 10

ER -

The PPARγ-FGF1 axis: An unexpected mediator of adipose tissue homeostasis

Abstract

ASJC Scopus subject areas

Access to Document

Other files and links

Fingerprint

Cite this