CNS leptin and insulin action in the control of energy homeostasis

Authors

  • Bengt F. Belgardt,

    1. Department of Mouse Genetics and Metabolism, Institute for Genetics, Center for Molecular Medicine, Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, Second Department for Internal Medicine University of Cologne, and Max Planck Institute for the Biology of Ageing, Cologne, Germany
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  • Jens C. Brüning

    1. Department of Mouse Genetics and Metabolism, Institute for Genetics, Center for Molecular Medicine, Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, Second Department for Internal Medicine University of Cologne, and Max Planck Institute for the Biology of Ageing, Cologne, Germany
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Address for correspondence: Jens C. Brüning, M.D., Institute for Genetics and Center for Molecular Medicine (CMMC), Department of Mouse Genetics and Metabolism, Zülpicher Str. 47a, 50674 Cologne, Germany. jens.bruening@uni-koeln.de

Abstract

The obesity and diabetes pandemics have made it an urgent necessity to define the central nervous system (CNS) pathways controlling body weight, energy expenditure, and fuel metabolism. The pancreatic hormone insulin and the adipose tissue–derived leptin are known to act on diverse neuronal circuits in the CNS to maintain body weight and metabolism in a variety of species, including humans. Because these homeostatic circuits are disrupted during the development of obesity, the pathomechanisms leading to CNS leptin and insulin resistance are a focal point of research. In this review, we summarize the recent findings concerning the mechanisms and novel neuronal mediators of both insulin and leptin action in the CNS.

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