Interaction between dietary fat intake and the cholesterol ester transfer protein TaqIB polymorphism in relation to HDL-cholesterol concentrations among US diabetic men.
ABSTRACT A low plasma HDL-cholesterol concentration is a major characteristic of diabetic dyslipidemia. HDL concentrations are determined by both environmental factors and genetic factors. Cholesterol ester transfer protein (CETP) plays an important role in the regulation of HDL metabolism, and the TaqIB polymorphism of the CETP gene has been associated with elevated HDL concentrations.
We examined the association between the CETP TaqIB polymorphism and plasma HDL concentrations and evaluated whether this association was modified by dietary fat intake.
We followed 780 diabetic men aged 40-75 y who participated in the Health Professionals Follow-Up Study since its initiation in 1986. The participants had confirmed type 2 diabetes and were free of cardiovascular disease at the time blood was drawn.
After adjustment for age, smoking, alcohol consumption, fasting status, hemoglobin A(1c), physical activity, total energy intake, and body mass index, HDL concentrations were significantly higher in men with the B2B2 or B1B2 genotype than in those with the B1B1 genotype (adjusted x +/- SE: 37.9 +/- 0.02, 40.3 +/- 0.01, and 42.6 +/- 0.02 mg/dL for B1B1, B1B2, and B2B2, respectively; P for trend = 0.0004). This inverse association of the B1 allele with plasma HDL concentrations existed for those with a high consumption of animal fat (P for interaction = 0.02), saturated fat (P for interaction = 0.02), and monounsaturated fat (P for interaction = 0.04).
These data confirmed a significant effect of the CETP Taq1 gene on HDL concentrations and suggested a potential interaction between the CETP TaqIB polymorphism and intake of dietary fat on plasma HDL concentration.
- [Show abstract] [Hide abstract]
ABSTRACT: The aims of this review were to examine the rationale for investigating the interaction between genes and the environment and to discuss recent studies into the interactions of genes and environmental modulators that are relevant to cardiovascular disease and its principle risk factors. Studies that have focused on smoking, alcohol and coffee consumption, and physical activity have all been observational studies and have involved relatively large samples. However, they tended to examine single genes and failed to take into account interactions with other genes or associated environmental factors. Both observational and interventional studies have been used to explore the interaction between genes and diet, with interventional studies being much smaller. Of the gene– diet interactions reported, two important highlights are, firstly, the confirmation that the apolipoprotein A-V gene (APOA5) is involved in triglyceride metabolism and is modulated by dietary factors and, secondly, the discovery that apolipoprotein A-II (APOA2) modulates food intake and the risk of obesity. The study of gene-environment interactions is an active and vital area of research. While the technical barriers to carrying out genetic studies are rapidly being overcome, studies are still hampered by the substantial difficulty of including comprehensive and reliable data on environmental factors. Progress in this area depends on involving large study populations across a range of geographical regions, as well as on employing a more comprehensive, standardized and precise approach to acquiring information about environmental factors.Revista Española de Cardiología Suplementos 01/2009; 9(2). DOI:10.1016/S1131-3587(09)71503-1
Dataset: Nutrigenomics and Metabolic Syndrome[Show abstract] [Hide abstract]
ABSTRACT: The metabolic syndrome (MetS) is a clinical entity of substantial heterogeneity, represented by the cooccurrence of multiple metabolic and vascular disorders, which are risk factors for both type 2 diabetes mellitus and atherosclerotic cardiovascular diseases. The constellation of clinical complications associated to the MetS illustrates the complexity of the disease process, which involves several dysregulated metabolic pathways. Thus, multiple genetic targets as well as gene-environmental interactions must be involved in the pathogenesis and progression of the MetS. The application of molecular biology techniques and the success of the Human Genome Project have opened a new era for molecular nutrition and medicine. In this context, different candidate genes have been implicated in the pathogenesis of this syndrome. The interactions between the most relevant gene polymorphisms affecting the metabolic syndrome and nutritional intake are under investigation. Indeed, different gene polymorphisms have been MetS syndrome related features, such as LIPC, PPARγ, APOA5, PLIN, ADIPOQ, FABP2, etc., but also to be a key issue in the therapeutical approach. Indeed, a number of studies are in course to understand the interplay between body weight, fat distribution, insulin sensitivity, physical inactivity, dietary habits and genetic predisposition, to be able to optimize and personalize the nutritional treatment of the MetS.
- [Show abstract] [Hide abstract]
ABSTRACT: We examine the reasons for investigating gene-environment interactions and address recent reports evaluating interactions between genes and environmental modulators in relation to cardiovascular disease and its common risk factors. Studies focusing on smoking, physical activity, and alcohol and coffee consumption are observational and include relatively large sample sizes. They tend to examine single genes, however, and fail to address interactions with other genes and other correlated environmental factors. Studies examining gene-diet interactions include both observational and interventional designs. These studies are smaller, especially those including dietary interventions. Among the reported gene-diet interactions, it is important to highlight the strengthened position of APOA5 as a major gene that is involved in triglyceride metabolism and modulated by dietary factors, and the identification of APOA2 as a modulator of food intake and obesity risk. The study of gene-environment interactions is an active and much needed area of research. Although technical barriers of genetic studies are rapidly being overcome, inclusion of comprehensive and reliable environmental information represents a significant shortcoming of genetics studies. Progress in this area requires inclusion of larger populations but also more comprehensive, standardized, and precise approaches to capturing environmental information.Current Opinion in Lipidology 05/2008; 19(2):158-67. DOI:10.1097/MOL.0b013e3282f6a809 · 5.80 Impact Factor