Document Detail


Synphilin-1 alters metabolic homeostasis in a novel Drosophila obesity model.
MedLine Citation:
PMID:  22828940     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
AIMS: The pathogenesis of obesity remains incompletely understood. Drosophila have conserved neuroendocrine and digestion systems with human and become an excellent system for studying energy homeostasis. Here, we reported a novel obesity Drosophila model, in which expression of human protein, synphilin-1 (SP1), in neurons fosters positive energy balance.
SUBJECTS AND METHODS: To further understand the actions of SP1 in energy balance control, the upstream activation sequence UAS/GAL4 system was used to generate human SP1 transgenic Drosophila. We characterized a human SP1 transgenic Drosophila by assessing SP1 expression, fat lipid deposition, food intake and fly locomotor activity to determine the major behavioral changes and their consequences in the development of the obesity-like phenotype.
RESULTS: Overexpression of SP1 in neurons, but not peripheral cells, increased the body weight of flies compared with that of non-transgenic controls. SP1 increased food intake but did not affect locomotor activity. SP1 increased the levels of triacylglycerol, and the size of fat body cells and lipid droplets, indicating that SP1 increased lipid-fat disposition. Survival studies showed that SP1 transgenic flies were more resistant to food deprivation. SP1 regulated lipin gene expression that may participate in SP1-induced fat deposition and starvation resistance.
CONCLUSION: These studies demonstrate that SP1 expression affects energy homeostasis in ways that enhance positive energy balance and provide a useful obesity model for future pathogenesis and therapeutic studies.
Authors:
J Liu; T Li; D Yang; R Ma; T H Moran; W W Smith
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2012-07-17
Journal Detail:
Title:  International journal of obesity (2005)     Volume:  36     ISSN:  1476-5497     ISO Abbreviation:  Int J Obes (Lond)     Publication Date:  2012 Dec 
Date Detail:
Created Date:  2012-12-11     Completed Date:  2013-05-15     Revised Date:  2013-12-05    
Medline Journal Info:
Nlm Unique ID:  101256108     Medline TA:  Int J Obes (Lond)     Country:  England    
Other Details:
Languages:  eng     Pagination:  1529-36     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Animals, Genetically Modified
Blotting, Western
Carrier Proteins / metabolism*
Disease Models, Animal
Drosophila / metabolism
Eating*
Energy Metabolism*
Female
Homeostasis
Humans
Lipid Metabolism*
Male
Motor Activity
Nerve Tissue Proteins / metabolism*
Neurons / metabolism*
Obesity / metabolism*
Up-Regulation
Weight Gain
Grant Support
ID/Acronym/Agency:
DK083410/DK/NIDDK NIH HHS; R01 DK083410/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Carrier Proteins; 0/Nerve Tissue Proteins; 0/SNCAIP protein, human
Comments/Corrections
Erratum In:
Int J Obes (Lond). 2012 Dec;36(12):1592

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