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Central Leptin Receptor Action and Resistance in Obesity
  1. Christian Bjørbæk, PhD
  1. From the Division of Endocrinology and Metabolism, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA.
  1. Received June 26, 2009, and in revised form August 4, 2009.
  2. Accepted for publication August 4, 2009.
  3. Reprints: Christian Bjørbæk, PhD, Division of Endocrinology and Metabolism, Department of Medicine, Beth Israel Deaconess Medical Center, 330 Brookline Ave, E/CLS-734, Boston, MA 02215. E-mail: cbjorbae{at}bidmc.harvard.edu.
  4. Supported by grants from the American Diabetes Association and The Richard and Susan Smith Family Foundation Pinnacle Program Project (7-05-PPG-02), the National Institutes of Health (DK60673 and DK65743), the Endocrine Society (all to C.B.), and the Boston Obesity Nutrition Research Center (DK46200). In addition, this symposium was supported in part by a grant from the National Center for Research Resources (R13 RR023236).

Abstract

The discovery of leptin in 1994 has led to remarkable advances in obesity research. We now know that leptin is a cytokinelike hormone that is produced in adipose tissue and plays a pivotal role in regulation of energy balance and in a variety of additional processes via actions in the central nervous system. This symposium review covers current understandings of neuronal leptin receptor signaling and mechanisms of obesity-related leptin resistance in the central nervous system and provides recent insights into the regulation of peripheral glucose balance by central leptin action in rodents.

Key Words
  • leptin
  • receptor
  • hypothalamus
  • signaling
  • POMC
  • neurons
  • obesity
  • diabetes
  • rodents

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