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Leptin as a neuroprotective agent.
- Source :
-
Biochemical and biophysical research communications [Biochem Biophys Res Commun] 2008 Apr 04; Vol. 368 (2), pp. 181-5. Date of Electronic Publication: 2008 Jan 28. - Publication Year :
- 2008
-
Abstract
- Leptin is a hormone produced by adipocytes that regulates satiety (food uptake) and energy homeostasis by activating receptors expressed in neurons of the hypothalamus. Leptin receptors are also found in other brain regions such as the hippocampus and cerebral cortex, and have known roles in regulating neural development and neuroendocrine functions. Recent evidence indicates that leptin could be neuroprotective, enhancing neuronal survival both in vitro and in vivo. Intriguingly, administration of leptin protects against neuronal death in animal models of cerebral ischemic injury and hemiparkisonism. Activation of the Janus kinase (JAK)-signal transducers and activator of transcription (STAT), phosphatidylinositol (PI) 3-kinase and the extracellular signal regulated kinase (ERK) pathways are known downstream events of leptin receptor signaling, all of which are pro-survival and anti-apoptotic. The relative ease of leptin's accessibility to the brain by peripheral administration makes it a potential drug candidate in the development of therapeutics for brain injuries and neurodegeneration.
- Subjects :
- Animals
Brain drug effects
Brain Injuries prevention & control
Humans
Neurodegenerative Diseases prevention & control
Brain metabolism
Brain Injuries drug therapy
Brain Injuries metabolism
Leptin administration & dosage
Neurodegenerative Diseases drug therapy
Neurodegenerative Diseases metabolism
Neuroprotective Agents administration & dosage
Neuroprotective Agents pharmacokinetics
Subjects
Details
- Language :
- English
- ISSN :
- 1090-2104
- Volume :
- 368
- Issue :
- 2
- Database :
- MEDLINE
- Journal :
- Biochemical and biophysical research communications
- Publication Type :
- Academic Journal
- Accession number :
- 18222172
- Full Text :
- https://doi.org/10.1016/j.bbrc.2008.01.063