Hypothalamic inflammation in obesity and metabolic disease
Alexander Jais1,2,3 and Jens C. Brüning1,2,3,4
1Department of Neuronal Control of Metabolism, Max Planck Institute for Metabolism Research, Cologne, Germany.
2Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), University Hospital Cologne, Cologne, Germany.
3Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD) and Center for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany.
4National Center for Diabetes Research (DZD), Neuherberg, Germany.
Address correspondence to: Jens C. Brüning, Max Planck Institute for Metabolism Research, Gleueler Str. 50, 50931 Cologne, Germany. Phone: 49.221.4726202; E-mail: bruening@sf.mpg.de.
Find articles by Jais, A. in: JCI | PubMed | Google Scholar
1Department of Neuronal Control of Metabolism, Max Planck Institute for Metabolism Research, Cologne, Germany.
2Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), University Hospital Cologne, Cologne, Germany.
3Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD) and Center for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany.
4National Center for Diabetes Research (DZD), Neuherberg, Germany.
Address correspondence to: Jens C. Brüning, Max Planck Institute for Metabolism Research, Gleueler Str. 50, 50931 Cologne, Germany. Phone: 49.221.4726202; E-mail: bruening@sf.mpg.de.
Find articles by Brüning, J. in: JCI | PubMed | Google Scholar
First published January 3, 2017 - More info
J Clin Invest. 2017;127(1):24–32. doi:10.1172/JCI88878.
Copyright © 2017, American Society for Clinical Investigation
Over the last years, hypothalamic inflammation has been linked to the development and progression of obesity and its sequelae. There is accumulating evidence that this inflammation not only impairs energy balance but also contributes to obesity-associated insulin resistance. Elevated activation of key inflammatory mediators such as JNK and IκB kinase (IKK) occurs rapidly upon consumption of a high-fat diet, even prior to significant weight gain. This activation of hypothalamic inflammatory pathways results in the uncoupling of caloric intake and energy expenditure, fostering overeating and further weight gain. In addition, these inflammatory processes contribute to obesity-associated insulin resistance and deterioration of glucose metabolism via altered neurocircuit functions. An understanding of the contributions of different neuronal and non-neuronal cell types to hypothalamic inflammatory processes, and delineation of the differences and similarities between acute and chronic activation of these inflammatory pathways, will be critical for the development of novel therapeutic strategies for the treatment of obesity and metabolic syndrome.
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ISSN: 0021-9738 (print), 1558-8238 (online)