Standl, M. ; Lattka, E. ; Stach, B.* ; Koletzko, S.* ; Bauer, C.P.* ; von Berg, A.* ; Berdel, D.* ; Krämer, U.* ; Schaaf, B.* ; Roder, S.* ; Herbarth, O.* ; Buyken, A.* ; Drogies, T.* ; Thiery, J.* ; Koletzko, B.* ; Heinrich, J. ; GINIplus Study Group (Heinrich, J. ; Wichmann, H.-E. ; Popescu, M. ; Schoetzau, A. ; Franke, K. ; Mosetter, M. ; Sausenthaler, S. ; Schindler, J. ; Zirngibl, A. ; Thaqi, A. ; Zutavern, A. ; Laubereau, B.) ; LISAplus Study Group (Wichmann, H.-E. ; Bolte, G. ; Belcredi, P. ; Jacob, B. ; Schoetzau, A. ; Schindler, J. ; Höhnke, A. ; Heinrich, J. ; Mosetter, M. ; Franke, K. ; Laubereau, B. ; Sausenthaler, S. ; Thaqi, A. ; Zirngibl, A. ; Zutavern, A.)
     
 
    
        
FADS1 FADS2 gene cluster, PUFA intake and blood lipids in children: Results from the GINIplus and LISAplus studies.
    
    
        
    
    
        
        PLoS ONE 7:e37780 (2012)
    
    
    
		
		
			
				Elevated cholesterol levels in children can be a risk factor for cardiovascular diseases in later life. In adults, it has been shown that blood lipid levels are strongly influenced by polymorphisms in the fatty acid desaturase (FADS) gene cluster in addition to nutritional and other exogenous and endogenous determinants. Our aim was to investigate whether lipid levels are determined by the FADS genotype already in children and whether this association interacts with dietary intake of n-3 fatty acids. METHODS: The analysis was based on data of 2006 children from two German prospective birth cohort studies. Total cholesterol, HDL, LDL and triglycerides were measured at 10 years of age. Six single nucleotide polymorphisms (SNPs) of the FADS gene cluster were genotyped. Dietary n-3 fatty acid intake was assessed by food frequency questionnaire. Linear regression modeling was used to assess the association between lipid levels, n-3 fatty acid intake and FADS genotype. RESULTS: Individuals carrying the homozygous minor allele had lower levels of total cholesterol [means ratio (MR) ranging from 0.96 (p = 0.0093) to 0.98 (p = 0.2949), depending on SNPs] and LDL [MR between 0.94 (p = 0.0179) and 0.97 (p = 0.2963)] compared to homozygous major allele carriers. Carriers of the heterozygous allele showed lower HDL levels [β between -0.04 (p = 0.0074) to -0.01 (p = 0.3318)] and higher triglyceride levels [MR ranging from 1.06 (p = 0.0065) to 1.07 (p = 0.0028)] compared to homozygous major allele carriers. A higher n-3 PUFA intake was associated with higher concentrations of total cholesterol, LDL, HDL and lower triglyceride levels, but these associations did not interact with the FADS1 FADS2 genotype. CONCLUSION: Total cholesterol, HDL, LDL and triglyceride concentrations may be influenced by the FADS1 FADS2 genotype already in 10 year old children. Genetically determined blood lipid levels during childhood might differentially predispose individuals to the development of cardiovascular diseases later in life.
			
			
				
			
		 
		
			
				
					
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        Publikationstyp
        Artikel: Journalartikel
    
 
    
        Dokumenttyp
        Wissenschaftlicher Artikel
    
 
    
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        Schlagwörter
        CORONARY-HEART-DISEASE; PROLIFERATOR-ACTIVATED RECEPTOR; HIGH-DENSITY-LIPOPROTEIN; SINGLE-NUCLEOTIDE POLYMORPHISMS; CARDIOVASCULAR RISK-FACTORS; FATTY-ACID-COMPOSITION; NUTRITIONAL INTERVENTION; VARIANTS; ATHEROSCLEROSIS; ASSOCIATION
    
 
    
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        Sprache
        englisch
    
 
    
        Veröffentlichungsjahr
        2012
    
 
    
        Prepublished im Jahr 
        
    
 
    
        HGF-Berichtsjahr
        2012
    
 
    
    
        ISSN (print) / ISBN
        1932-6203
    
 
    
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	    Band: 7,  
	    Heft: 5,  
	    Seiten: ,  
	    Artikelnummer: e37780 
	    Supplement: ,  
	
    
 
  
        
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            Verlag
            Public Library of Science (PLoS)
        
 
        
            Verlagsort
            Lawrence, Kan.
        
 
	
        
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        Peer reviewed
    
 
     
    
        POF Topic(s)
        30503 - Chronic Diseases of the Lung and Allergies
30501 - Systemic Analysis of Genetic and Environmental Factors that Impact Health
    
 
    
        Forschungsfeld(er)
        Genetics and Epidemiology
    
 
    
        PSP-Element(e)
        G-503900-001
G-504200-001
    
 
    
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        Erfassungsdatum
        2012-06-19