| Knockdown of NPY expression in the dorsomedial hypothalamus promotes development of brown adipocytes and prevents diet-induced obesity. | |
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MedLine Citation:
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PMID: 21531339 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Hypothalamic neuropeptide Y (NPY) has been implicated in control of energy balance, but the physiological importance of NPY in the dorsomedial hypothalamus (DMH) remains unclear. Here we report that knockdown of NPY expression in the DMH by adeno-associated virus-mediated RNAi reduced fat depots in rats fed regular chow and ameliorated high-fat diet-induced hyperphagia and obesity. DMH NPY knockdown resulted in development of brown adipocytes in inguinal white adipose tissue through the sympathetic nervous system. This knockdown increased uncoupling protein 1 expression in both inguinal fat and interscapular brown adipose tissue (BAT). Consistent with the activation of BAT, DMH NPY knockdown increased energy expenditure and enhanced the thermogenic response to a cold environment. This knockdown also increased locomotor activity, improved glucose homeostasis, and enhanced insulin sensitivity. Together, these results demonstrate critical roles of DMH NPY in body weight regulation through affecting food intake, body adiposity, thermogenesis, energy expenditure, and physical activity. |
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Authors:
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Pei-Ting Chao; Liang Yang; Susan Aja; Timothy H Moran; Sheng Bi |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural |
Journal Detail:
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Title: Cell metabolism Volume: 13 ISSN: 1932-7420 ISO Abbreviation: Cell Metab. Publication Date: 2011 May |
Date Detail:
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Created Date: 2011-05-02 Completed Date: 2011-09-05 Revised Date: 2012-05-07 |
Medline Journal Info:
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Nlm Unique ID: 101233170 Medline TA: Cell Metab Country: United States |
Other Details:
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Languages: eng Pagination: 573-83 Citation Subset: IM |
Copyright Information:
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Copyright © 2011 Elsevier Inc. All rights reserved. |
Affiliation:
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Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adipocytes, Brown
/
cytology*,
metabolism Adipose Tissue, White / cytology, metabolism Animals Body Weight* Cells, Cultured Dependovirus / genetics Diet, Atherogenic* Down-Regulation Eating Energy Metabolism Glucose / metabolism Glucose Tolerance Test Homeostasis Hypothalamus / metabolism* Immunoblotting Insulin / pharmacology Ion Channels / genetics, metabolism Male Mitochondrial Proteins / genetics, metabolism Neuropeptide Y / physiology* Obesity / etiology, metabolism, prevention & control* RNA, Messenger / genetics Rats Rats, Sprague-Dawley Reverse Transcriptase Polymerase Chain Reaction Signal Transduction |
| Grant Support | |
ID/Acronym/Agency:
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DK074269/DK/NIDDK NIH HHS; R01 DK074269-01A1/DK/NIDDK NIH HHS; R01 DK074269-02/DK/NIDDK NIH HHS; R01 DK074269-03/DK/NIDDK NIH HHS; R01 DK074269-04/DK/NIDDK NIH HHS; R01 DK074269-04S1/DK/NIDDK NIH HHS; R01 DK074269-05/DK/NIDDK NIH HHS; R01 DK087888-02/DK/NIDDK NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Insulin; 0/Ion Channels; 0/Mitochondrial Proteins; 0/Neuropeptide Y; 0/RNA, Messenger; 0/mitochondrial uncoupling protein; 50-99-7/Glucose |
| Comments/Corrections | |
Comment In:
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Cell Metab. 2011 May 4;13(5):493-4
[PMID:
21531331
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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