Apolipoprotein C-III, n-3 Polyunsaturated Fatty Acids, and “Insulin-Resistant” T−455C APOC3 Gene Polymorphism in Heart Disease Patients: Example of Gene-Diet Interaction

Olivieri, Oliviero; Martinelli, Nicola; Sandri, Marco; Bassi, Antonella; Guarini, Patrizia; Trabetti, Elisabetta; Pizzolo, Francesca; Girelli, Domenico; Friso, Simonetta; Pignatti, Pier Franco; Corrocher, Roberto

doi:10.1373/clinchem.2004.040477

Cited by 46 publications

(30 citation statements)

References 29 publications

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“…In vitro studies have shown a 40-50% insulinmediated decrease in APOC3 gene expression in -455T-containing promoter constructs, which is lost in -455C-containing promoter constructs (37). Moreover, metabolic syndrome patients carrying the -455C allele are at an increased risk of cardiovascular disease (38). These observations suggest that the functional APOC3 SNP at the insulin-response element mediates the widely replicated associations of hypertriglyceridemia and lower HDL cholesterol.…”

Section: Genetic Determinants Of Lipoproteins In Greenlanders Discussionmentioning

confidence: 95%

Common variants APOC3, APOA5, APOE and PON1 are associated with variation in plasma lipoprotein traits in Greenlanders

Lahiry

Ban

Pollex

et al. 2007

International Journal of Circumpolar Health

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Objectives. We undertook studies of the association between common genomic variations in APOC3, APOA5, APOE and PON1 genes and variation in biochemical phenotypes in a sample of Greenlanders. Study design. Genetic association study of quantitative lipoprotein traits. Methods. In a sample of 1,310 adult Greenlanders, fasting plasma lipid, lipoprotein and apolipoprotein (apo) concentrations were assessed for association with known functional genomic variants of APOC3, APOA5, APOE and PON1. For significantly associated polymorphisms, between-genotype differences were examined in closer detail. Results. We found that (1) the APOE restriction isotype was associated with variation in plasma total and LDL cholesterol and apo B (all p<.0001); (2) the APOC3 promoter genotype was associated with variation in plasma triglycerides, HDL cholesterol and apo A-I (all p<.002); (3) the APOA5 codon 19 genotype was associated with variation in plasma triglycerides (p=.027); and (4) the PON1 codon 192 genotype was associated with variation in total and LDL cholesterol and apo B (all p<.05). Conclusions. Taken together, our results suggest that common genetic variations in APOC3, APOA5, APOE and PON1 are associated with significant variation in intermediate traits in plasma lipoprotein metabolism in Greenlanders; the associations are similar to those observed for these variants in other populations. (Int J Circumpolar Health 2007; 66(5): 390-400)

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Section: Genetic Determinants Of Lipoproteins In Greenlanders Discussionmentioning

confidence: 95%

Common variants APOC3, APOA5, APOE and PON1 are associated with variation in plasma lipoprotein traits in Greenlanders

Lahiry

Ban

Pollex

et al. 2007

International Journal of Circumpolar Health

View full text Add to dashboard Cite

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“…Human studies have established that fatty fi sh consumption or increased RBC C 20-22 3 PUFA content is linked to lower triglycerides and plasma ApoCIII (156)(157)(158). Interestingly, patients homozygous for the T-455C variant in the ApoCIII promoter are poorly responsive to the ApoCIII-lowering effect of 3 PUFA ( 158 ).…”

Section: Effects Of 3 Pufa On Endothelial Cells and Infl Ammationmentioning

confidence: 99%

Omega-3 fatty acid supplementation and cardiovascular disease

Jump

Depner

Tripathy

2012

Journal of Lipid Research

194

118

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“…The -455T/C polymorphism in the insulin-responsive element of the apo CIII gene influences TAG and apo CIII concentrations. A formal interactive effect between apo CIII genotype and n-3 PUFAs was confirmed by logistic models in the study of Oliveri et al [127] . Patients homozygous for the -455C apo CIII variant are poorly responsive to the apo C-III-lowering effects of n-3 PUFAs [127] .…”

Section: Gene-nutrient Interactions: Implications For Dietary Fatty Amentioning

confidence: 69%

Gene–Nutrient Interactions in the Metabolic Syndrome

Phillips

Tierney

Roche³

2008

Lifestyle Genomics

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The metabolic syndrome (MetS) is a very common disease associated with an increased risk of type 2 diabetes mellitus and cardiovascular disease. The diverse clinical characteristics of the MetS illustrate the complexity of the disease process, which involves several dysregulated metabolic pathways. Thus, multiple genetic targets must be involved in the pathogenesis and progression of the disease. Research indicates a major role for genetic susceptibility to the MetS. However, the human genome has not changed markedly in the last decade but the prevalence of the condition has increased exponentially, illustrating the importance of gene–environmental interactions. Dietary fat is an important environmental factor which can modify the development of the MetS. Genetic background can interact with habitual dietary fat composition, affecting predisposition to the MetS. Recent research indicates that currently ineffective therapeutic dietary recommendations may require a ‘personalised nutrition’ approach, wherein the genetic profile may determine the responsiveness of patients to specific dietary fatty acid interventions. Understanding the biological impact of gene–nutrient interactions will provide a key insight into the pathogenesis and progression of diet-related polygenic disorders, including the MetS. This review will explore the interactions between genetic background and dietary exposure/nutritional therapy.

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Apolipoprotein C-III, n-3 Polyunsaturated Fatty Acids, and “Insulin-Resistant” T−455C APOC3 Gene Polymorphism in Heart Disease Patients: Example of Gene-Diet Interaction

Cited by 46 publications

References 29 publications

Common variants APOC3, APOA5, APOE and PON1 are associated with variation in plasma lipoprotein traits in Greenlanders

Common variants APOC3, APOA5, APOE and PON1 are associated with variation in plasma lipoprotein traits in Greenlanders

Omega-3 fatty acid supplementation and cardiovascular disease

Gene–Nutrient Interactions in the Metabolic Syndrome

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