期刊论文

Chen, Y. Eugene

英文

Scientific Reports

2045-2322

2013

3

1

1476

10.1038/srep01476

American Diabetes Association (ADA)American Diabetes Association [7-03-JF-18]; National Institutes HealthUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USA [HL068878, HL03676, DK072158]; NATIONAL HEART, LUNG, AND BLOOD INSTITUTEUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USANIH National Heart Lung & Blood Institute (NHLBI) [R01HL068878, R01HL068878, R01HL068878, R01HL068878, R01HL068878, R01HL068878, R01HL068878, R01HL068878, R01HL068878, R01HL068878, R01HL068878, R01HL068878, R01HL068878, R01HL068878, R01HL068878, R01HL068878, R01HL068878, R01HL068878, R01HL068878, R01HL068878, R01HL068878, R01HL068878, R01HL068878] Funding Source: NIH RePORTER; NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASESUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USANIH National Institute of Diabetes & Digestive & Kidney Diseases (NIDDK) [R01DK072158, R01DK072158, R01DK072158, R01DK072158, R01DK072158] Funding Source: NIH RePORTER

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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...