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Year : 2012  |  Volume : 16  |  Issue : 9  |  Page : 534-542

Leptin, diabetes, and the brain

Diabetes and Obesity Center of Excellence, Department of Medicine, University of Washington, Seattle, WA, USA

Correspondence Address:
Gregory J Morton
UW Medicine at South Lake Union, 850 Republican St, Box - 358055, Seattle, WA 98195
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Source of Support: This work was supported by grants from the National Institutes of Health (NIH) to GJM (DK-089056), the Nutrition Obesity Research Unit (NORC, P30 DK-035816) the Diabetes and Metabolism Training Grant (T32 DK-0007247) at the University of Washington, and an American Heart Association Scientist Development Grant to GJM. , Conflict of Interest: None

DOI: 10.4103/2230-8210.105568

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Diabetes is a major worldwide problem. Despite some progress in the development of new antidiabetic agents, the ability to maintain tight glycemic control in order to prevent renal, retinal, and neuropathic complications of diabetes without adverse complications still remains a challenge. Recent evidence suggests, however, that in addition to playing a key role in the regulation of energy homeostasis, the adiposity hormone leptin also plays an important role in the control of glucose metabolism via its actions in the brain. This review examines the role of leptin action in the central nervous system and the mechanisms whereby leptin mediates its effects to regulate glucose metabolism. These findings suggest that defects or dysfunction in leptin signaling may contribute to the etiology of diabetes and raise the possibility that either leptin or downstream targets of leptin may have therapeutic potential for the treatment of diabetes.

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