Document Detail


Transgenic expression of n-3 fatty acid desaturase (fat-1) in C57/BL6 mice: Effects on glucose homeostasis and body weight.
MedLine Citation:
PMID:  19396841     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The fat-1 gene, derived from Caenorhabditis elegans, encodes for a fatty acid n-3 desaturase. In order to study the potential metabolic benefits of n-3 fatty acids, independent of dietary fatty acids, we developed seven lines of fat-1 transgenic mice (C57/BL6) controlled by the regulatory sequences of the adipocyte protein-2 (aP2) gene for adipocyte-specific expression (AP-lines). We were unable to obtain homozygous fat-1 transgenic offspring from the two highest expressing lines, suggesting that excessive expression of this enzyme may be lethal during gestation. Serum fatty acid analysis of fat-1 transgenic mice (AP-3) fed a high n-6 unsaturated fat (HUSF) diet had an n-6/n-3 fatty acid ratio reduced by 23% (P < 0.025) and the n-3 fatty acid eicosapentaenoic acid (EPA) concentration increased by 61% (P < 0.020). Docosahexaenoic acid (DHA) was increased by 19% (P < 0.015) in white adipose tissue. Male AP-3-fat-1 line of mice had improved glucose tolerance and reduced body weight with no change in insulin sensitivity when challenged with a high-carbohydrate (HC) diet. In contrast, the female AP-3 mice had reduced glucose tolerance and no change in insulin sensitivity or body weight. These findings indicate that male transgenic fat-1 mice have improved glucose tolerance likely due to increased insulin secretion while female fat-1 mice have reduced glucose tolerance compared to wild-type mice. Finally the inability of fat-1 transgenic mice to generate homozygous offspring suggests that prolonged exposure to increased concentrations of n-3 fatty acids may be detrimental to reproduction.
Authors:
Shaonin Ji; Robert W Hardy; Philip A Wood
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Journal of cellular biochemistry     Volume:  107     ISSN:  1097-4644     ISO Abbreviation:  J. Cell. Biochem.     Publication Date:  2009 Jul 
Date Detail:
Created Date:  2009-06-30     Completed Date:  2009-10-26     Revised Date:  2013-06-02    
Medline Journal Info:
Nlm Unique ID:  8205768     Medline TA:  J Cell Biochem     Country:  United States    
Other Details:
Languages:  eng     Pagination:  809-17     Citation Subset:  IM    
Copyright Information:
2009 Wiley-Liss, Inc.
Affiliation:
Department of Genetics, University of Alabama at Birmingham, 35294, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Body Weight*
Caenorhabditis elegans Proteins / genetics,  pharmacology*
Fatty Acid Desaturases / genetics,  pharmacology*
Fatty Acids, Omega-3 / pharmacology*
Female
Glucose / metabolism*
Glucose Intolerance
Homeostasis*
Male
Mice
Mice, Inbred C57BL
Mice, Transgenic
Reproduction
Sex Factors
Grant Support
ID/Acronym/Agency:
P30 CA13148/CA/NCI NIH HHS; R-21 DK66517/DK/NIDDK NIH HHS; R21 DK066517-02/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Caenorhabditis elegans Proteins; 0/Fatty Acids, Omega-3; 0/fat-1 protein, C elegans; 50-99-7/Glucose; EC 1.14.19.-/Fatty Acid Desaturases
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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