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American Journal of Clinical Nutrition, Vol. 86, No. 5, 1524-1529, November 2007
© 2007 American Society for Nutrition

ORIGINAL RESEARCH COMMUNICATION

Interaction between dietary fat intake and the cholesterol ester transfer protein TaqIB polymorphism in relation to HDL-cholesterol concentrations among US diabetic men1,2,3

Tricia Y Li, Cuilin Zhang, Folkert W Asselbergs, Lu Qi, Eric Rimm, David J Hunter and Frank B Hu

1 From the Department of Nutrition, Harvard School of Public Health, Boston, MA (TYL, CZ, FWA, LQ, ER, and FBH); the Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA (ER, DJH, and FBH); the Department of Epidemiology, Harvard School of Public Health, Boston, MA (ER, DJH, and FBH); the Department of Cardiology, University Medical Center Groningen, Groningen, Netherlands (FWA); and the Epidemiology Branch, Division of Epidemiology, Statistics, and Prevention Research, National Institute of Child Health and Human Development, Bethesda, MD (CZ)

2 Supported by awards from the National Institutes of Health (HL 65582 and HL 35464).

3 Address reprint requests and correspondence to FB Hu, Department of Nutrition and Epidemiology, Harvard School of Public Health, 665 Huntington Avenue, Boston, MA 02115. E-mail: nhbfh{at}channing.harvard.edu.


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Background: 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.

Objective: We examined the association between the CETP TaqIB polymorphism and plasma HDL concentrations and evaluated whether this association was modified by dietary fat intake.

Design: 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.

Results: After adjustment for age, smoking, alcohol consumption, fasting status, hemoglobin A1c, 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).

Conclusion: 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.

Key Words: Cholesterol ester transfer protein • CETP • genetics • polymorphism • dietary fat • HDL cholesterol • diabetes


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Low plasma concentrations of HDL cholesterol are an important component of dyslipidemia in diabetes and have been associated with an increased risk of cardiovascular disease (1). Plasma HDL concentrations are determined by both environmental and genetic factors (2, 3). Findings from several studies suggest that polymorphisms in the cholesteryl ester transfer protein (CETP) (4), hepatic lipase (5), and apolipoprotein A-I/CIII/A-IV (6) genes are major sources of genetically determined variation in plasma HDL-cholesterol concentrations. Of these gene products, CETP, a hydrophobic glycoprotein manufactured in the liver, is predominantly bound to HDL in blood and is responsible for the transfer of cholesteryl esters from HDL to VLDL and LDL in exchange for triacylglycerol and thereby a decrease in plasma HDL (7). In addition, CETP eliminates cholesterol by transporting it from peripheral tissues to the liver for metabolism and excretion in bile by promoting reverse cholesterol transport (8). Thus, CETP can have both proatherogenic and antiatherogenic roles, depending on the metabolic setting (9, 10).

Several studies have documented a significant association between polymorphisms in the human CETP gene and plasma CETP and HDL concentrations (11). One of the most studied polymorphisms, TaqIB in the CETP gene, is a silent mutation of intron 1 detected by enzyme TaqIB as a restriction-fragment length polymorphism. In a recent meta-analysis (12), HDL concentrations in individuals with B2B2 were 0.11 (95% CI: 0.10, 0.12) mmol/L higher than in individuals with B1B1. In addition, plasma HDL concentrations and CETP activity are determined by environmental factors such as dietary fat intake (13). Less is known, however, about potential interactions between CETP gene polymorphisms and dietary factors in determining HDL concentrations. In this study, we aimed to investigate the role of the CETP TaqIB polymorphism in determining plasma HDL concentrations and whether the associations were modified by dietary factors in US diabetic men.


   SUBJECTS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
Study population
Details of the Health Professionals' Follow-Up Study (HPFS) were reported elsewhere (14). Briefly, the HPFS is a prospective cohort study of etiologies of heart disease, cancer, and other major chronic diseases in 51 529 US male health professionals aged 40–75 y at study baseline in 1986 (14). Lifestyle factors and health outcomes were obtained by questionnaires every 2 y. Dietary information has been collected every 4 y with a food-frequency questionnaire (FFQ), and 18 159 study participants provided blood samples between 1993 and 1999 (most in 1993–1994), 1000 of whom received a diagnosis of definite type 2 diabetes at baseline or during follow-up until 1998 (most before or within 2 y after blood collection). The present study included 780 diabetic men who did not report a diagnosis of angina pectoris, myocardial infarction, coronary bypass surgery, or stroke on any of the biennial questionnaires before blood collection. Men who developed cardiovascular diseases during follow-up were further excluded, which left 603 participants in the final analytic population in the present study; 96% of these diabetic men were white.

Diagnosis of type 2 diabetes
On the basis of diagnostic criteria proposed by the National Diabetes Data Group (15), a diagnosis of diabetes was established when at least one of the following criteria was reported on a supplementary questionnaire sent to all men who reported a diagnosis of diabetes on any biennial follow-up questionnaire: 1) one or more classic symptoms (excessive thirst, polyuria, weight loss, hunger, or coma) plus a fasting plasma glucose concentration of ≥140 mg/dL or a random plasma glucose concentration of ≥200 mg/dL, 2) ≥2 elevated plasma glucose concentrations on different occasions (fasting ≥140 mg/dL and/or random ≥200 mg/dL and/or ≥200 mg/dL after ≥2 h on oral-glucose-tolerance testing) in the absence of symptoms, or 3) treatment with hypoglycemic medication (insulin or oral hypoglycemic agents). We used the National Diabetes Data Group criteria to define diabetes because most of our cases received a diagnosis before the release of the American Diabetes Association criteria (16). Men with type 1 diabetes were excluded. A validation study in a subsample of the HPFS showed that our supplementary questionnaire is highly reliable in confirming a diabetes diagnosis (17).

Ascertainment of diet and lifestyle factors and anthropometric measurements
The average nutrient intake was derived from the semiquantitative FFQ administered in 1994. For each food, a commonly used unit or portion size was specified, and participants were asked how often, on average, they consumed that amount of each food over the previous year. Nutrient density for total, saturated, monounsaturated, polyunsaturated, and trans unsaturated fats was calculated as energy derived from dietary fat divided by total dietary energy. The dietary questionnaire has been evaluated in detail for reproducibility and validity within the HPFS (18). After adjustment for energy and deattenuation for within person variation, Pearson's correlation coefficients between the questionnaire and the average of 2 single-week diet records 6 mo apart were 0.67 for total, 0.75 for saturated, 0.37 for polyunsaturated, and 0.68 for monounsaturated fat. The correlation between the reported alcohol intakes in the FFQ and the average of two 1-wk diet records was 0.86 (19).

Each participant was asked to report his height to the closest inch at baseline and his current weight in pounds at baseline and on each biennial questionnaire. Self-reports of body weight have been shown to be highly correlated with technician-measured weights (r = 0.97) in the HPFS participants (20). We calculated body mass index (BMI) as the ratio of weight (kg) to squared height (m); the latter was assessed in 1986 only.

Participants also provided information biennially on their cigarette smoking status, aspirin use, and physical activity. Physical activity (MET-hours/wk) was calculated by using the reported time spent on various activities, weighting each activity by its intensity level. History of hypertension and hypercholesterolemia was determined from self-reports preceding the blood collection. Family history of coronary heart disease was reported in 1986. Alcohol intake was estimated with a dietary questionnaire in 1994.

Blood collection
Each interested participant was sent a blood collection kit containing instructions and supplies (blood tubes, tourniquet, gauze, adhesive bandages, and needles). The participants made arrangements for blood to be drawn. Blood samples were collected into three 10-mL liquid EDTA-containing blood tubes, placed on ice packs stored in styrofoam containers, and returned to our laboratory via overnight courier; >95% of the samples arrived within 24 h. After receipt, the chilled blood was centrifuged; separated into plasma, erythrocytes, and buffy coat; and stored in continuously monitored nitrogen freezers at temperatures not higher than –130 °C. We requested information on the date and time of the blood sample drawing and the time elapsed since the preceding meal to identify nonfasting (<8 h) subjects.

Laboratory methods
All lipid profiles were assayed in the laboratory of Nader Rifai (The Children's Hospital, Boston, MA), which is certified by the NHLBI/CDC Lipid Standardization program. All assays except the enzyme-linked immunosorbent assay and the radioimmunoassay were done with the Hitachi 911 analyzer (Roche Diagnostics, Indianapolis, IN). Concentrations of total cholesterol, triacylglycerols, and HDL were analyzed simultaneously with enzymatic assays with CVs of 1.7%, 1.8%, and 2.5%, respectively. LDL cholesterol was determined by a homogenous direct method (Genzyme, Cambridge, MA) with a CV < 3.1%. Apolipoprotein (apo) B-100 was measured with an immunoturbidimetric technique (Roche Diagnostics) with a CV of 4.3%, and lipoprotein(a) with a latex-enhanced immunoturbidimetric method (Denka Sieken, Tokyo, Japan) with a CV of 2.6%. The method used to measure hemoglobin A1c (Hb A1c) was based on turbidimetric immunoinhibition using hemolyzed packed red cells. The intraassay CV for Hb A1c values of 5.5% and 9.1% were 1.9 and 3.0%, respectively.

Genotyping
DNA was extracted from the buffy coat fraction of centrifuged blood with the QLAmp Blood Kit (Qiagen, Chatsworth, CA). All samples were genotyped by using the ABI PRISM 7900HT Sequence Detection System (Applied Biosystems, Foster City, CA) in 384-well format. Amplification conditions on an AB 9700 dual-plate thermal cycler (Applied Biosystems) were as follows: 1 cycle at 95 °C for 10 min, followed by 50 cycles at 92 °C for 15 s and at 58 °C for 1 min. TaqMan primers and probes were designed for the CETP aq1 T polymorphism (rs708272), on the reverse strand, by using the Primer Express Oligo Design software v2.0 (ABI PRISM). Replicate quality-control samples (10%) were included and genotyped with ≥99% concordance. Genotype frequencies did not deviate from Hardy-Weinberg equilibrium in this population (P > 0.10).

Statistical analysis
Frequency distributions for the characteristics of the study subjects were examined according to CETP genotype. Student's t tests and chi-square tests were used for comparisons of means and proportions. When the overall difference was statistically significant, Tukey's test was used to identify significant differences between the 3 genotype groups.

Generalized linear models were used to compare geometric crude and age-adjusted mean concentrations of plasma lipids across the CETP TaqIB genotype groups. In addition, a multivariate model was fitted to adjust further for factors that may influence plasma lipid concentrations: fasting status (>8 h), physical activity (in quartiles), cigarette smoking (never, past, and current smoker), alcohol consumption (nondrinker and 0.1–4.9, 5.0–9.9, and ≥10.0 g/d), BMI (<25.0, 25.0–29.9, and ≥30.0), hypertension, and duration of diabetes. Concentrations of triacylglycerols were computed only in samples from subjects who fasted for ≥8 h before the blood drawing (n = 417).

Stratified analyses were conducted to examine whether the association between the CETP TaqIB polymorphism and plasma HDL concentrations was modified by self-reported dietary fat intake (high or low, dichotomized according the median values). Interactions between CETP TaqIB genotype and dietary and lifestyle factors were assessed by using a cross-product term between genotypes and the aforementioned factors. Statistical significance was evaluated with a Wald test for the interaction after adjustment for multiple covariates. All reported P values were 2-tailed, and statistical significance was defined at the {alpha} = 0.05 level. All analyses were performed with SAS version 9.1 software (SAS Institute, Cary, NC).


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
Characteristics of the diabetic men according to genotype are presented in Table 1Go. The genotype frequencies of B1B1, B1B2, and B2B2 among the cohort were 31.8%, 50.3%, and 17.9%, respectively, which did not deviate from Hardy-Weinberg equilibrium. Compared with diabetic men with the B1B1genotype, those with the B1B2 or B2B2 genotype were more likely to have a history of hypertension; those with the B2B2 genotype consumed less polyunsaturated fat.


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  		TABLE 1. Baseline characteristics of diabetic men without cardiovascular disease according to cholesterol ester transfer protein (CETP) TaqIB genotype1

 
Age- and multivariate-adjusted mean lipid concentrations across the CETP TaqIB genotypes are shown in Table 2Go. Plasma HDL concentrations were strongly and significantly associated with the CETP TaqIB polymorphism. The multivariate-adjusted mean (±SE) HDL concentrations for men with the B1B1, B1B2, and B2B2 genotypes were 37.9 ± 0.02, 40.3 ± 0.01, and 42.6 ± 0.02 mg/dL, respectively (P for trend = 0.0004). No significant association between the CETP TaqIB genotypes and other lipid concentrations was observed.


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  		TABLE 2. Age- and multivariate-adjusted lipid concentrations according to cholesterol ester transfer protein (CETP) genotype TaqIB in diabetic men1

 
In addition, we observed a strong interaction between CETP TaqIB polymorphisms and total fat, animal fat, saturated fat, and monounsaturated fat intakes on HDL concentrations (P for interaction = 0.003, 0.02, 0.02, and 0.04, respectively) (Table 3Go). The associations between CETP TaqIB polymorphism and HDL were more evident in diabetic patients who had higher intakes of total fat, animal fat, saturated fat, and monounsaturated fat than in those with lower intakes. We observed no significant interaction between CETP TaqIB polymorphism and intakes of vegetable fat, polyunsaturated fat, and dietary cholesterol in association with plasma HDL concentrations.


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  		TABLE 3. Interaction of dietary fat consumption with the cholesterol ester transfer protein (CETP) genotypes in relation to HDL concentrations

 
Considering that altered CETP activity and plasma HDL concentrations have been shown to be related to other lifestyle factors, including physical activity, BMI, and alcohol consumption, we further examined whether these factors modulated the observed association between this polymorphism and plasma HDL concentrations. No significant interactions between these factors and this polymorphism in relation to HDL concentrations were observed (P for interaction > 0.10 for all). We conducted a sensitivity analysis to evaluate the CETP TaqIB polymorphism with HDL and interaction with dietary fat only among 96% of the white population. In addition, we restricted our analysis to those men who were not taking lipid-lowering medicine at the time of blood drawing. Similar results were observed for both analyses.


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
In this study of diabetic men, plasma HDL concentrations were significantly higher in subjects with the B2 allele (B2B2 or B1B2 genotype) than in those with the B1B1 genotype in a dose-dependent manner. Furthermore, this association was significantly modulated by dietary fat intake. The beneficial effects of the CETP TaqIB B2 allele on HDL concentrations were more evident in men with higher intakes of total fat, animal fat, saturated fat, and monounsaturated fat.

The TaqIB variant in the CETP gene has been investigated extensively in genetic association studies investigating the relation between CETP activity and lipids because of the high frequency of the variant allele of this polymorphism in whites and its strong association with HDL concentrations. However, data concerning the relation between the CETP TaqIB polymorphism and plasma HDL concentrations in diabetic patients are sparse. Our findings are generally consistent with a relatively large body of literature documenting elevated plasma HDL concentration in association with the B2 allele in the general population (12). The TaqIB, located in intron 1, was suggested to act as a marker for a functional C->A polymorphism in the promoter region of the CETP gene, located 629 base pairs upstream from the transcription start site (21). This –629C->A variant has been shown to directly affect CETP promoter activity and, subsequently, HDL concentrations (22).

Our study indicated that the association between CETP TaqIB polymorphism and HDL was more evident in diabetic patients with a higher intake of total fat, animal fat, saturated fat, and monounsaturated fat. The mechanism underlying such modification effects of dietary fat is unclear. Data about the effect modification of dietary factors on the relation between CETP polymorphisms and HDL in humans are limited. Aitken et al (23) did not observe the interaction between CETP TaqIB genotype and changes in dietary fat in regulating HDL concentrations in their feeding study, which is hampered by small sample size and, subsequently, limited power to detect statistical significance. In animal studies, saturated fatty acid increased CETP activity (24-27) and a high-fat diet can increase HDL concentrations (28). Human studies have demonstrated that higher saturated fat intake increased CETP activity in both men and women with normal cholesterol (29-31). Moreover, there were great interindividual variations in HDL concentrations in response to a high-fat diet, probably because of genetic variations (32). It is plausible that interactions between dietary fat and the CETP polymorphism in association with HDL concentrations through their effects on CETP activity. Our data show that the B2 allele is associated with higher HDL concentrations in subjects with a lower carbohydrate consumption, which agrees with the present findings because lower carbohydrate intakes are usually correlated with higher fat intakes because of caloric balance.

Several potential limitations must be considered when interpreting the results of the present study. First, CETP activity was not measured directly; therefore, we were not able to directly assess the effect of the CETP TaqIB gene polymorphism on CETP activity. Second, subclasses of HDL particles were not measured in our study. Both the composition and concentration of HDL particles are modulated by CETP. It has been suggested that the smaller size HDL3 rather than total HDL may be a more sensitive marker for the effect of the CETP TaqIB polymorphism on HDL metabolism (33, 34). However, we observed a positive association between the CETP TaqIB polymorphism and HDL metabolism even when we used this less sensitive marker. In addition, we cannot exclude the possibility that the observed association between the CETP TaqIB polymorphism and HDL metabolism arose from its linkage disequilibrium with other variations, such as –629C->A, which is located on the promoter of the CETP gene and has been associated with CETP activity (22).

In summary, we observed that the CETP TaqIB polymorphism interacts with dietary total fat, saturated fat, and monounsaturated fat in determining plasma HDL concentrations. Additional observational and intervention studies are warranted to replicate these findings and further explore the biological mechanisms underlying the observed significant gene-diet interactions.


   ACKNOWLEDGMENTS
 
The authors' responsibilities were as follows—TYL: contributed to the study concept and design, data analysis, statistical support, and manuscript writing and editing; CZ, FWA, DJH, and LQ: contributed to the study concept and design, statistical support, and manuscript writing and editing; ER: contributed to the study concept and design, data collection, statistical support, and manuscript writing and editing; and FBH: helped obtain funding and contributed to the study concept and design, data analysis, statistical support, and manuscript writing and editing. FWA was a research fellow of the Netherlands Heart Foundation (2003T010) and the Dutch Inter University Cardiology Institute Netherlands at the time of the study. FBH was partly supported by an American Heart Association Established Investigator Award. None of the other authors had a conflict of interest to disclose.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 

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Received for publication February 9, 2007. Accepted for publication June 28, 2007.





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