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,
2 - Institute of Molecular and Cell Biology, Agency for Science,
Technology and Research, #3-17 Proteos,
61 Biopolis Drive,
3 - Department of Human Physiology and Clinical Experimental Research, Semmelweis University,
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.
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.