| Neuroanatomy of body weight control: lessons learned from leptin. | |
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MedLine Citation:
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PMID: 21606602 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Rather than arising from the passive accumulation of excess calories, obesity is a state in which the biologically defended level of body fat stores increases due to defects in the homeostatic process that matches food intake and energy expenditure over time. By deleting leptin receptors from distinct brain regions and neuronal subsets, researchers are beginning to identify the neuroanatomical substrates responsible for this regulation. In this issue of the JCI, Scott et al. demonstrate that loss of leptin receptors in a subset of hindbrain neurons increases food intake in mice, but, unlike what is observed when leptin receptors are deleted from hypothalamic neurons, these mice compensate by increasing energy expenditure and hence do not become obese. Although many brain areas can regulate energy intake and/or energy expenditure, it is likely that only a small subset of neurons actively matches the two over time. It is vital to clarify how this works if we are to improve our understanding of obesity pathogenesis and options available for its treatment. |
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Authors:
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Diana L Williams; Michael W Schwartz |
Publication Detail:
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Type: Comment; Journal Article; Research Support, N.I.H., Extramural Date: 2011-05-23 |
Journal Detail:
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Title: The Journal of clinical investigation Volume: 121 ISSN: 1558-8238 ISO Abbreviation: J. Clin. Invest. Publication Date: 2011 Jun |
Date Detail:
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Created Date: 2011-06-02 Completed Date: 2011-08-17 Revised Date: 2013-05-24 |
Medline Journal Info:
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Nlm Unique ID: 7802877 Medline TA: J Clin Invest Country: United States |
Other Details:
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Languages: eng Pagination: 2152-5 Citation Subset: AIM; IM |
Affiliation:
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Department of Psychology and Program in Neuroscience, Florida State University, Tallahassee, Florida, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Body Weight / physiology* Brain / physiology* Decerebrate State / physiopathology Energy Intake Energy Metabolism / genetics, physiology Feeding Behavior / physiology Homeostasis / genetics, physiology* Humans Hyperphagia / physiopathology Leptin / physiology Mice Mice, Knockout Neurons / physiology Obesity / etiology, physiopathology, therapy Organ Specificity Peptide Hormones / physiology Rats Receptors, Leptin / deficiency, genetics, physiology* |
| Grant Support | |
ID/Acronym/Agency:
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DK035816/DK/NIDDK NIH HHS; DK052989/DK/NIDDK NIH HHS; DK068384/DK/NIDDK NIH HHS; DK078779/DK/NIDDK NIH HHS; DK083042/DK/NIDDK NIH HHS; P30 DK17047/DK/NIDDK NIH HHS; R01 DK083042/DK/NIDDK NIH HHS; R01 DK083042-17/DK/NIDDK NIH HHS; R01 DK090320/DK/NIDDK NIH HHS; U24 DK076126/DK/NIDDK NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Leptin; 0/Peptide Hormones; 0/Receptors, Leptin; 0/leptin receptor, mouse |
| Comments/Corrections | |
Comment On:
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J Clin Invest. 2011 Jun;121(6):2413-21
[PMID:
21606595
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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