Dietary obesity-induced Egr-1 in adipocytes facilitates energy storage via suppression of FOXC2

Jifeng Zhang; Yuan Zhang; Tingwan Sun; Fang Guo; Shengping Huang; Menisha Chandalia; Nicola Abate; Daping Fan; Hong Bo Xin; Y. Eugene Chen; Mingui Fu

doi:10.1038/srep01476

Dietary obesity-induced Egr-1 in adipocytes facilitates energy storage via suppression of FOXC2

Jifeng Zhang, Yuan Zhang, Tingwan Sun, Fang Guo, Shengping Huang, Menisha Chandalia, Nicola Abate, Daping Fan, Hong Bo Xin, Y. Eugene Chen, Mingui Fu

Pharmacology

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

36 Scopus citations

Abstract

The molecular mechanism to regulate energy balance is not completely understood. Here we observed that Egr-1 expression in white adipose tissue (WAT) was highly correlated with dietary-induced obesity and insulin resistance both in mice and humans. Egr-1 null mice were protected from diet-induced obesity and obesity-associated pathologies such as fatty liver, insulin resistance, hyperlipidemia and hyperinsulinemia. This phenotype can be largely explained by the increase of energy expenditure in Egr-1 null mice. Characterization of these mice revealed that the expression of FOXC2 and its target genes were significantly elevated in white adipose tissues, leading to WAT energy expenditure instead of energy storage. Altogether, these studies suggest an important role for Egr-1, which, by repressing FOXC2 expression, promotes energy storage in WAT and favored the development of obesity under high energy intake.

Original language	English (US)
Article number	1476
Journal	Scientific reports
Volume	3
DOIs	https://doi.org/10.1038/srep01476
State	Published - 2013

ASJC Scopus subject areas

General

Access to Document

10.1038/srep01476

Cite this

@article{564950cac75d48c8a090191fa1afa02d,

title = "Dietary obesity-induced Egr-1 in adipocytes facilitates energy storage via suppression of FOXC2",

abstract = "The molecular mechanism to regulate energy balance is not completely understood. Here we observed that Egr-1 expression in white adipose tissue (WAT) was highly correlated with dietary-induced obesity and insulin resistance both in mice and humans. Egr-1 null mice were protected from diet-induced obesity and obesity-associated pathologies such as fatty liver, insulin resistance, hyperlipidemia and hyperinsulinemia. This phenotype can be largely explained by the increase of energy expenditure in Egr-1 null mice. Characterization of these mice revealed that the expression of FOXC2 and its target genes were significantly elevated in white adipose tissues, leading to WAT energy expenditure instead of energy storage. Altogether, these studies suggest an important role for Egr-1, which, by repressing FOXC2 expression, promotes energy storage in WAT and favored the development of obesity under high energy intake.",

author = "Jifeng Zhang and Yuan Zhang and Tingwan Sun and Fang Guo and Shengping Huang and Menisha Chandalia and Nicola Abate and Daping Fan and Xin, {Hong Bo} and {Eugene Chen}, Y. and Mingui Fu",

note = "Funding Information: We thank Drs. Jian Liang, Angie Bookout, Vicky Lin, Ms. Norma Anderson and Donna Floyd for technical helps on animal experiments. We also thank Drs. David J. Mangelsdorf and Steven A. Kliewer for helpful discussion. M.F. is a recipient of a Junior Faculty Award from American Diabetes Association (ADA). This work was supported by ADA (7-03-JF-18 to M.F.) and National Institutes Health Grants (HL068878 and HL03676 to Y.E.C., DK072158 to N.A. & M.C.).",

year = "2013",

doi = "10.1038/srep01476",

language = "English (US)",

volume = "3",

journal = "Scientific reports",

issn = "2045-2322",

publisher = "Nature Publishing Group",

}

TY - JOUR

T1 - Dietary obesity-induced Egr-1 in adipocytes facilitates energy storage via suppression of FOXC2

AU - Zhang, Jifeng

AU - Zhang, Yuan

AU - Sun, Tingwan

AU - Guo, Fang

AU - Huang, Shengping

AU - Chandalia, Menisha

AU - Abate, Nicola

AU - Fan, Daping

AU - Xin, Hong Bo

AU - Eugene Chen, Y.

AU - Fu, Mingui

N1 - Funding Information: We thank Drs. Jian Liang, Angie Bookout, Vicky Lin, Ms. Norma Anderson and Donna Floyd for technical helps on animal experiments. We also thank Drs. David J. Mangelsdorf and Steven A. Kliewer for helpful discussion. M.F. is a recipient of a Junior Faculty Award from American Diabetes Association (ADA). This work was supported by ADA (7-03-JF-18 to M.F.) and National Institutes Health Grants (HL068878 and HL03676 to Y.E.C., DK072158 to N.A. & M.C.).

PY - 2013

Y1 - 2013

N2 - The molecular mechanism to regulate energy balance is not completely understood. Here we observed that Egr-1 expression in white adipose tissue (WAT) was highly correlated with dietary-induced obesity and insulin resistance both in mice and humans. Egr-1 null mice were protected from diet-induced obesity and obesity-associated pathologies such as fatty liver, insulin resistance, hyperlipidemia and hyperinsulinemia. This phenotype can be largely explained by the increase of energy expenditure in Egr-1 null mice. Characterization of these mice revealed that the expression of FOXC2 and its target genes were significantly elevated in white adipose tissues, leading to WAT energy expenditure instead of energy storage. Altogether, these studies suggest an important role for Egr-1, which, by repressing FOXC2 expression, promotes energy storage in WAT and favored the development of obesity under high energy intake.

AB - The molecular mechanism to regulate energy balance is not completely understood. Here we observed that Egr-1 expression in white adipose tissue (WAT) was highly correlated with dietary-induced obesity and insulin resistance both in mice and humans. Egr-1 null mice were protected from diet-induced obesity and obesity-associated pathologies such as fatty liver, insulin resistance, hyperlipidemia and hyperinsulinemia. This phenotype can be largely explained by the increase of energy expenditure in Egr-1 null mice. Characterization of these mice revealed that the expression of FOXC2 and its target genes were significantly elevated in white adipose tissues, leading to WAT energy expenditure instead of energy storage. Altogether, these studies suggest an important role for Egr-1, which, by repressing FOXC2 expression, promotes energy storage in WAT and favored the development of obesity under high energy intake.

UR - http://www.scopus.com/inward/record.url?scp=84875825672&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84875825672&partnerID=8YFLogxK

U2 - 10.1038/srep01476

DO - 10.1038/srep01476

M3 - Article

C2 - 23502673

AN - SCOPUS:84875825672

SN - 2045-2322

VL - 3

JO - Scientific reports

JF - Scientific reports

M1 - 1476

ER -

Dietary obesity-induced Egr-1 in adipocytes facilitates energy storage via suppression of FOXC2

Abstract

ASJC Scopus subject areas

Access to Document

Other files and links

Fingerprint

Cite this