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  current news   Press   selected story    
     
  8 Feburary 2013  
  Nuclear factor κB (NF-κB) suppresses food intake and energy expenditure in mice by directly activating the Pomc promoter
 
 



Authors
X. Shi1, X. Wang1, Q. Li1, M. Su1, E. Chew1, E. T. Wong2, Z. Lacza3, G. K. Radda1, V. Tergaonkar2,4, and W. Han1,2,4,5.

1 - Singapore Bioimaging Consortium, Agency for Science, Technology and Research (A*STAR), #02-02      Helios, 11 Biopolis Way, Singapore 138667
2 - Institute of Molecular and Cell Biology, Agency for Science, Technology and Research, #3-17 Proteos,      61 Biopolis Drive, Singapore 138673
3 - Department of Human Physiology and Clinical Experimental Research, Semmelweis University,      Budapest, Hungary
4 - Department of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore
5 - Cardiovascular and Metabolic Disorders Program, Duke-National University of Singapore Graduate      Medical School

Published online in Diabetologia on 5 February 2013.

Abstract 
While chronic low-grade inflammation is associated with obesity, acute inflammation reduces food intake and leads to negative energy balance. Although both types of inflammation activate nuclear factor κB (NF-κB) signalling, it remains unclear how NF-κB activation results in opposite physiological responses in the two types of inflammation. The goal of this study was to address this question, and to understand the link between inflammation and leptin signalling.

Figure Legend: Divergent Pomc transcription regulation under acute and chronic inflammatory conditions. Proposed models for the regulation of Pomc transcription under physiological conditions (a), acute inflammation (b) and chronic inflammation (c). CytR, cytokine receptor; LepR, leptin receptor; InsR, insulin receptor; PM, plasma membrane; NE, nuclear envelope.

For more information on Vinay TERGAONKAR's laboratory, please click here.

For more information on Weiping HAN's laboratory, please click here.