期刊
METABOLISM-CLINICAL AND EXPERIMENTAL
卷 64, 期 1, 页码 13-23出版社
W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1016/j.metabol.2014.09.010
关键词
Leptin signaling; Leptin transport; Neuronal circuits; Energy homeostasis
资金
- NIH [R01-DK092587, P20-RR02195, P30-DK072476, R01-DK081563]
- NATIONAL CENTER FOR RESEARCH RESOURCES [P20RR021945] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK081563, P30DK072476, R01DK092587] Funding Source: NIH RePORTER
The cloning of leptin in 1994 was an important milestone in obesity research. In those days obesity was stigmatized as a condition caused by lack of character and self-control. Mutations in either leptin or its receptor were the first single gene mutations found to cause morbid obesity, and it is now appreciated that obesity is caused by a dysregulation of central neuronal circuits. From the first discovery of the leptin deficient obese mouse (ob/ob), to the cloning leptin (ob aka lep) and leptin receptor (db aka lepr) genes, much has been learned about leptin and its action in the central nervous system. The initial high hopes that leptin would cure obesity were quickly dampened by the discovery that most obese humans have increased leptin levels and develop leptin resistance. Nevertheless, leptin target sites in the brain represent an excellent blueprint for distinct neuronal circuits that control energy homeostasis. A better understanding of the regulation and interconnection of these circuits will guide and improve the development of safe and effective interventions to treat obesity. This review will highlight our current knowledge about the hormone leptin, its signaling pathways and its central actions to mediate distinct physiological functions. (C) 2015 Elsevier Inc. All rights reserved.
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