[Show abstract][Hide abstract] ABSTRACT: Eating behaviors during childhood are related both to children's diet quality and to their weight status. A better understanding of the determinants of eating behavior during childhood is essential for carrying out effective dietary interventions.
We assessed the contribution of genetic and environmental factors to variations in selected eating behaviors in early and late childhood. Information on eating behaviors came from questionnaires administered to parents of children participating in the Quebec Newborn Twin Study when the twins were 2.5 and 9 years old (n = 692 children). Dichotomous variables were derived and analyzed using structural equation modeling, as part of a classic twin study design. We performed univariate and bivariate longitudinal analyses to quantify sources of variation and covariation across ages, for several eating behavior traits.
We found moderate to strong heritability for traits related to appetite such as eating too much, not eating enough and eating too fast. Univariate analysis estimates varied from 0.71 (95% CI: 0.49, 0.87) to 0.89 (0.75, 0.96) in younger children and from 0.44 (0.18, 0.66) to 0.56 (0.28, 0.78) in older children. Bivariate longitudinal analyses indicated modest to moderate genetic correlations across ages (rA varying from 0.34 to 0.58). Common genetic influences explained 17% to 43% of the phenotypic correlation between 2.5 and 9 years for these appetite-related behaviors. In 9-year-old children, food acceptance traits, such as refusing to eat and being fussy about food, had high heritability estimates, 0.84 (0.63, 0.94) and 0.85 (0.59, 0.96) respectively, while in younger children, the shared environment (i.e., common to both twins) contributed most to phenotypic variance. Variances in meal-pattern-related behaviors were mostly explained by shared environmental influences.
Genetic predispositions explain a large part of the variations in traits related to appetite during childhood, though our results suggest that as children get older, appetite-related behaviors become more sensitive to environmental influences outside the home. Still, for several traits environmental influences shared by twins appear to have the largest relative importance. This finding supports the notion that familial context has considerable potential to influence the development of healthy eating habits throughout childhood.
International Journal of Behavioral Nutrition and Physical Activity 12/2013; 10(1):134. DOI:10.1186/1479-5868-10-134 · 4.11 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The melanin-concentrating hormone receptor 1 (MCHR1) is a G protein-coupled receptor that regulates energy balance and body composition in animal models. Inconsistent effects of MCHR1 polymorphisms on energy homeostasis in humans may partly be attributable to environmental factors.
We examined the effect of 4 single nucleotide polymorphisms (rs133073, rs133074, rs9611386, and rs882111) in the MCHR1 gene on body composition as well as energy-related lifestyle factors (diet and physical activity). We also examined the effect of gene-lifestyle interactions on body composition.
A total of 1153 participants (248 men and 905 women) from the cross-sectional Complex Diseases in the Newfoundland Population: Environment and Genetics (CODING) study were genotyped by using probe-based chemistry validated assays. Diet and physical activity were estimated by using validated frequency questionnaires, and body composition was assessed by using dual-energy X-ray absorptiometry.
Three polymorphisms (rs9611386, rs882111, and rs133073) were associated with differences in body-composition measurements (all P < 0.05). There was an interaction between rs9611386 and carbohydrate intake on total mass and waist circumference (both P ≤ 0.01). There was also an interaction between rs9611386 and body mass index categories (normal weight, overweight, and obese) on energy intakes (P = 0.02). A similar interaction was shown with rs882111 (P = 0.02). Interactions were also observed between each of these polymorphisms (rs9611386, rs882111, and rs133073) and physical activity score on body-composition measurements (all P < 0.05).
These findings suggest that polymorphisms in the MCHR1 gene are associated with differences in body composition and interact with physiologic and energy-related lifestyle factors.
American Journal of Clinical Nutrition 12/2013; 99(2). DOI:10.3945/ajcn.113.073387 · 6.77 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: BACKGROUND: Few twin studies have examined nutrition-related phenotypes among children, and none has investigated energy and macronutrient intakes. OBJECTIVE: The objective was to quantify genetic and environmental influences on variations in energy and macronutrient intakes among children aged 9years. DESIGN: We conducted a nutrition study among children participating in the Quebec Newborn Twin Study, a population-based birth cohort of twins. We derived dietary data from two multiple-pass 24-hour dietary recalls with a parent and his or her child. The analysis employed a classic twin study design and used data from 379 twin pairs. RESULTS: Univariate analyses indicate that heritability for mean daily energy (kcal) and macronutrient (g) intakes was moderate, ranging from 0.34 (95% CI: 0.22, 0.46) to 0.42 (0.31, 0.53). Genetic effects also accounted for 0.28 (0.16, 0.40) of the variance in percent of energy from lipids, while only environmental (shared and unique) effects accounted for the variance in percent of energy from proteins and carbohydrates. The shared environment did not contribute to variations in daily intakes for most of the nutritional variables under study. Multivariate analyses suggest the presence of macronutrient-specific genetic influences for lipids and carbohydrates, estimated at 0.12 (0.04, 0.19) and 0.20 (0.11, 0.29) respectively. CONCLUSIONS: The unique environment (i.e., not shared by family members) has the largest influence on variances in daily energy and macronutrient intakes in 9-year-old children. This finding underscores the need to take obesogenic environments into account when planning dietary interventions for younger populations.
[Show abstract][Hide abstract] ABSTRACT: It was the objective of this study to investigate the relation between vitronectin and plasminogen activator inhibitor (PAI)-1 plasma levels with nine-year incidences of the metabolic syndrome (MetS) and of type 2 diabetes mellitus (T2DM). Baseline plasma concentrations of vitronectin and PAI-1 were measured in 627 healthy participants from the prospective D.E.S.I.R. cohort who subsequently developed MetS (n = 487) and T2DM (n = 182) over a nine-year follow-up (42 presented both) and who were matched with two healthy control subjects each by use of a nested case-control design. Parameters composing the MetS explained about 20% of plasma vitronectin levels. An increase of one standard deviation of vitronectin was associated with increased risks of both the MetS (odds ratio [OR] = 1.21 [1.07 - 1.37], p = 0.003) and T2DM (OR = 1.24 [1.01 - 1.53], p = 0.045). Corresponding ORs for PAI-1 levels were 1.46 [1.27 - 1.68] (p<10(-4)) and 1.40 [1.14 - 1.72] (p = 0.0012). However, the effects of vitronectin and PAI-1 levels on outcomes were not independent. The vitronectin-MetS association was restricted to individuals with low to modest PAI-1 levels (OR = 1.33 [1.14 - 1.54], p = 0.0003) while no association was observed in individuals with high PAI-1 levels (OR = 0.87 [0.68 - 1.10], p = 0.24), the test for interaction being highly significant (p = 0.0009). In conclusion, baseline plasma vitronectin is a marker of incident MetS at nine years. Its predictive ability for MetS and T2DM should not be assessed independently of PAI-1 levels.
Thrombosis and Haemostasis 07/2011; 106(3):416-22. DOI:10.1160/TH11-03-0179 · 4.98 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: First Nations populations in Northwestern Ontario have undergone profound dietary and lifestyle transformations in less than 50 years, which have contributed to the alarming rise in obesity and obesity-related diseases, in particular type 2 diabetes mellitus. Even though the genetic background of First Nations peoples differs from that of the Caucasians, genetics alone cannot explain such a high prevalence in obesity and type 2 diabetes. Modifications in lifestyle and diet are major contributors for the high prevalence of chronic diseases. What remains constant in the literature is the persistent view that locally harvested and prepared foods are of tremendous value to First Nations peoples providing important health and cultural benefits that are increasingly being undermined by western-based food habits. However, the complexities of maintaining a traditional diet require a multifaceted approach, which acknowledges the relationship between benefits, risks and viability that cannot be achieved using purely conventional medical and biological approaches. This brief review explores the biological predispositions and potential environmental factors that contribute to the development of the high incidence of obesity and obesity-related diseases in First Nations communities in Northern Canada. It also highlights some of the complexities of establishing exact physiological causes and providing effective solutions.
International journal of obesity (2005) 12/2010; 34 Suppl 2(supplement 2):S24-31. DOI:10.1038/ijo.2010.236 · 5.00 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: We determined whether single nucleotide polymorphisms (SNPs) previously associated with diabetogenic traits improve the discriminative power of a type 2 diabetes genetic risk score.
Participants (n = 2,751) were genotyped for 73 SNPs previously associated with type 2 diabetes, fasting glucose/insulin concentrations, obesity or lipid levels, from which five genetic risk scores (one for each of the four traits and one combining all SNPs) were computed. Type 2 diabetes patients and non-diabetic controls (n = 1,327/1,424) were identified using medical records in addition to an independent oral glucose tolerance test.
Model 1, including only SNPs associated with type 2 diabetes, had a discriminative power of 0.591 (p < 1.00 x 10(-20) vs null model) as estimated by the area under the receiver operator characteristic curve (ROC AUC). Model 2, including only fasting glucose/insulin SNPs, had a significantly higher discriminative power than the null model (ROC AUC 0.543; p = 9.38 x 10(-6) vs null model), but lower discriminative power than model 1 (p = 5.92 x 10(-5)). Model 3, with only lipid-associated SNPs, had significantly higher discriminative power than the null model (ROC AUC 0.565; p = 1.44 x 10(-9)) and was not statistically different from model 1 (p = 0.083). The ROC AUC of model 4, which included only obesity SNPs, was 0.557 (p = 2.30 x 10(-7) vs null model) and smaller than model 1 (p = 0.025). Finally, the model including all SNPs yielded a significant improvement in discriminative power compared with the null model (p < 1.0 x 10(-20)) and model 1 (p = 1.32 x 10(-5)); its ROC AUC was 0.626.
Adding SNPs previously associated with fasting glucose, insulin, lipids or obesity to a genetic risk score for type 2 diabetes significantly increases the power to discriminate between people with and without clinically manifest type 2 diabetes compared with a model including only conventional type 2 diabetes loci.
[Show abstract][Hide abstract] ABSTRACT: Laminopathies are rare monogenic diseases, some of them exhibiting features of the metabolic syndrome. These diseases are mainly due to mutations in LMNA, encoding A-type lamins. One LMNA polymorphism, rs4641, has been associated with the metabolic syndrome, but results have been controversial. We therefore investigated the effect of single nucleotide polymorphisms (SNPs) in the LMNA gene in combination with four other genes encoding enzymes influencing lamin post-translational maturation on risk of metabolic syndrome (MS). Twenty-three tagging SNPs characterising the haplotypic variability of five genes (LMNA, ICMT, ZMPSTE24, FNTA and FNTB) were genotyped in 3,916 French men and women who took part in the prospective DESIR study. Single locus and haplotype analyses were performed but did not detect any significant association with the risk of MS. No robust interaction between SNPs located in different genes on the risk of MS was identified. In conclusion, we did not observe any convincing evidence that common polymorphisms of the lamina pathway could modulate the risk of MS.
Journal of Molecular Medicine 10/2009; 88(2):193-201. DOI:10.1007/s00109-009-0548-y · 5.11 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Glutathione S-transferases (GSTs) are detoxifying enzymes that contribute to the glutathione-ascorbic acid (vitamin C) antioxidant cycle.
The objective was to determine whether GST genotypes modify the association between dietary vitamin C and serum ascorbic acid.
Nonsmoking men and women (n = 905) between 20 and 29 y of age were participants in the Toronto Nutrigenomics and Health Study. Overnight fasting blood samples were collected to determine serum ascorbic acid concentrations by HPLC and to genotype for deletion polymorphisms in GSTM1 and GSTT1 and an Ile105Val substitution in GSTP1. A 196-item food-frequency questionnaire was used to estimate vitamin C intake.
A gene-diet interaction on serum ascorbic acid was observed for GSTM1 (P = 0.04) and GSTT1 (P = 0.01) but not for GSTP1 (P = 0.83). The odds ratio (95% CI) for serum ascorbic acid deficiency (<11 micromol/L) was 3.20 (1.88, 5.44) for subjects who did not meet the Recommended Dietary Allowance of vitamin C compared with those who did. The corresponding odds ratios (95% CIs) were 2.17 (1.10, 4.28) and 12.28 (4.26, 33.42), respectively, for individuals with the GSTT1*1/*1 +*1/*0 (functional) and GSTT1*0/*0 (null) genotypes and 2.29 (0.96, 5.45) and 4.03 (2.01, 8.09), respectively, for the GSTM1*1/*1+GSTM1*1/*0 and GSTM1*0/*0 genotypes.
The recommended intake of vitamin C protects against serum ascorbic acid deficiency, regardless of genotype. Individuals with GST null genotypes had an increased risk of deficiency if they did not meet the Recommended Dietary Allowance for vitamin C, which suggests that the GST enzymes protect against serum ascorbic acid deficiency when dietary vitamin C is insufficient.
American Journal of Clinical Nutrition 09/2009; 90(5):1411-7. DOI:10.3945/ajcn.2009.28327 · 6.77 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Aims/hypothesis
Laminopathies are rare monogenic diseases, some of them exhibiting features of the metabolic syndrome. These diseases are mainly due to mutations in LMNA, encoding A-type lamins. The LMNA_rs4641 polymorphism has been associated with the metabolic syndrome, but results have been controversial. We therefore investigated the effect of single nucleotide polymorphisms (SNPs) in the LMNA gene in combination with four other genes encoding enzymes influencing lamin post-translational maturation on risk of metabolic syndrome (MetS).
Twenty-three tagging SNPs characterizing the haplotypic variability of 5 genes (LMNA, ICMT, ZMPSTE24, FNTA, FNTB) were genotyped in 3916 French men and women who took part in the prospective DESIR study.
LMNA_rs4641 was found to interact with ZMPSTE24_rs2284447 to influence the risk of MetS (P = 0.006). Among carriers of the ZMPSTE24_rs2284447 minor T allele, those also carrying the minor T allele for LMNA_rs4641 had a decreased risk of MetS (OR=0.53 [0.31-0.90], p = 0.01). The effect of LMNA_rs4641 on MetS was also found to be modulated by the FNTA_rs10958736 (P=0.001). Among carriers of the A allele for the FNTA_rs10958736 SNP, those also carrying the minor T allele at LMNA_rs4641 had an increased risk of MetS (OR = 1.68 [1.20-2.36], P = 0.002).
We observed that the effect of the LMNA_rs4641 polymorphism on risk of MetS was modulated by other polymorphisms in genes influencing lamin A post-translational maturation. Our findings emphasize the need to examine the complex interplay between genes influencing a given biological system.
[Show abstract][Hide abstract] ABSTRACT: We previously showed that polymorphisms in the tumor necrosis factor (TNF)-alpha gene, which is regulated by nuclear factor kappa B (NF-kappaB), modify the association between dietary polyunsaturated fatty acid (PUFA) intake and circulating HDL-cholesterol. Our objective was to determine whether a common polymorphism in the NFKB1 gene (-94Ins/Del ATTG) interacts with PUFA intake to affect HDL-cholesterol in two distinct populations. Participants were diabetes-free young adults (n=593) and older individuals with diet-treated type 2 diabetes (n=103). The NF-kappaB polymorphism modified the association between dietary PUFA intake and HDL-cholesterol in both populations (p=0.02 and 0.005 for interaction). Among individuals with the Ins/Ins genotype, each 1% increase in energy from PUFA was associated with a 0.03+/-0.01 mmol/L (p for slope=0.009) and 0.06+/-0.02 mmol/L (p=0.02) increase in HDL-cholesterol among participants from the diabetes-free and diabetic populations. An inverse relationship was observed among those with the Del/Del genotype, which was significantly different from that of the Ins/Ins groups in both populations (p=0.02 and 0.006). No effects were observed for the Ins/Del genotype in either population (p>0.05). These findings show that this functional polymorphism in the NF-kB gene modifies the association between PUFA intake and plasma HDL-cholesterol in two distinct populations.
[Show abstract][Hide abstract] ABSTRACT: Genetic polymorphisms in tumor necrosis factor-alpha (TNF-alpha) modify the association between polyunsaturated fatty acids (PUFA) and plasma high-density lipoprotein (HDL) cholesterol in a population with type 2 diabetes. The objective of this study was to determine whether this gene x diet interaction is observed in a diabetes-free population and whether it is due to n-3 or n-6 PUFA.
Subjects (n = 595) were aged 20-29 years and genotyped for the TNF-alpha -238G>A and TNF-alpha -308G>A polymorphisms. Diet was assessed using a food frequency questionnaire. Subjects were grouped as having no minor A allele at both the -238 and -308 positions (0/0), or one minor A allele at either the -238 (1/0) or the -308 (0/1) position.
TNF-alpha genotypes modified the association between dietary PUFA and HDL-cholesterol concentrations (p = 0.04 for interaction). Among individuals with the 0/0 genotype, total PUFA was positively associated with HDL-cholesterol in both men (p = 0.008) and women (p = 0.03), and for both n-6 (p = 0.004) and n-3 (p = 0.04) PUFA. However, an inverse relationship was observed among men carrying the 1/0 genotype (p = 0.005).
These findings demonstrate that TNF-alpha genotypes modify the association between dietary PUFA and HDL-cholesterol and provide further evidence that inflammation is involved in the reverse cholesterol transport.
Journal of Nutrigenetics and Nutrigenomics 07/2008; 1(5):215-23. DOI:10.1159/000149825 · 2.00 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Glucose sensing in the brain has been proposed to be involved in regulating food intake, but the mechanism is not known. Glucose transporter type 2 (GLUT2)-null mice fail to control their food intake in response to glucose, suggesting a potential role for this transporter as a glucose sensor in the brain. Here we show that individuals with a genetic variation in GLUT2 (Thr110Ile) have a higher daily intake of sugars in two distinct populations. In the first population, compared with individuals with the Thr/Thr genotype, carriers of the Ile allele had a significantly higher intake of sugars as assessed from 3-day food records administered on two separate visits (visit 1: 112 +/- 9 vs. 86 +/- 4 g/day, P = 0.01; visit 2: 111 +/- 8 vs. 82 +/- 4 g/day, P = 0.003), demonstrating within-population reproducibility. In a second population, carriers of the Ile allele also reported consuming a significantly greater intake of sugars (131 +/- 5 vs. 115 +/- 3 g/day, P = 0.007) over a 1-mo period as measured from a food frequency questionnaire. GLUT2 genotypes were not associated with fat, protein, or alcohol intake in either population. These observations were consistent across older and younger adults as well as among subjects with early Type 2 diabetes and healthy individuals. Taken together, our findings show that a genetic variation in GLUT2 is associated with habitual consumption of sugars, suggesting an underlying glucose-sensing mechanism that regulates food intake.
[Show abstract][Hide abstract] ABSTRACT: Heterogeneity in circulating lipid concentrations in response to dietary polyunsaturated fatty acids (PUFAs) may be due, in part, to genetic variations. Tumor necrosis factor-alpha (TNF-alpha) is a proinflammatory cytokine that can induce hyperlipidemia and is known to be modulated by dietary PUFAs.
The objective was to determine whether TNF-alpha genotypes modify the association between dietary PUFA intake and serum lipid concentrations.
The study involved 53 men and 56 women aged 42-75 y with type 2 diabetes. Dietary intakes were assessed with the use of a 3-d food record, and blood samples were collected to determine fasting serum lipids. DNA was isolated from blood for genotyping by polymerase chain reaction-restriction fragment length polymorphism for the TNF-alpha -238G-->A and -308G-->A polymorphisms.
PUFA intake was positively associated with serum HDL cholesterol in carriers of the -238A allele (beta = 0.06 +/- 0.03 mmol/L per 1% of energy from PUFAs; P = 0.03), but negatively associated in those with the -238GG genotype (beta = -0.03 +/- 0.01, P = 0.03) (P = 0.004 for interaction). PUFA intake was inversely associated with HDL cholesterol in carriers of the -308A allele (beta = -0.07 +/- 0.02, P = 0.002), but not in those with the -308GG genotype (beta = 0.02 +/- 0.02, P = 0.13) (P = 0.001 for interaction). A stronger gene x diet interaction was observed when the polymorphisms at the 2 positions (-238/-308) were combined (P = 0.0003). Similar effects were observed for apolipoprotein A-I, but not with other dietary fatty acids and serum lipids.
TNF-alpha genotypes modify the relation between dietary PUFA intake and HDL-cholesterol concentrations. These findings suggest that genetic variations affecting inflammation may explain some of the inconsistencies between previous studies relating PUFA intake and circulating HDL.
American Journal of Clinical Nutrition 09/2007; 86(3):768-74. · 6.77 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Inflammatory markers predict memory dysfunction in elderly patients, but their contribution to memory deficits in adults with Type 2 diabetes mellitus (T2DM) is less well understood. The present study determined whether specific single-nucleotide polymorphisms in the promoter region of tumor necrosis factor-alpha (TNF-alpha) predict verbal memory in older patients with T2DM. Immediate and delayed verbal memory were assessed using word list and paragraph recall tests in a cohort of subjects with T2DM during 2 sessions, separated by 48 weeks. The presence of the TNF-alpha-238A allele, which has been shown to decrease gene expression, consistently predicted better baseline performance and protected against memory decline over a period of 48 weeks. Therefore, inflammatory mediators may be important modulators of memory function in individuals with T2DM.
[Show abstract][Hide abstract] ABSTRACT: Tumor necrosis factor alpha (TNF-alpha) is a proinflammatory cytokine that impairs insulin action and alters lipid metabolism. We investigated the effects of genetic polymorphisms of TNF-alpha on circulating biomarkers of insulin resistance and lipid metabolism during an 8-hour metabolic profile test and a 2-hour oral glucose tolerance test in subjects with type 2 diabetes mellitus. Subjects (N = 123) recruited were type 2 diabetic men (n = 56) and women (n = 67) aged 36 to 75 years with a body mass index of at least 25 kg/m(2). Blood samples were collected to determine postprandial changes in circulating lipid levels and biomarkers of insulin resistance. Subjects were genotyped by polymerase chain reaction-restriction fragment length polymorphism for the TNF-alpha -238G>A, -308G>A, and -863C>A polymorphisms. Compared with subjects who were homozygous for the -238G allele, carriers of the -238A allele had an altered ability to suppress postprandial free fatty acids as shown by an increased net incremental area under the curve (0.26 +/- 2.44 vs -1.33 +/- 2.71 mEq h(-1) L(-1), P = .002) during the 8-hour metabolic profile test. This effect was observed in obese (1.04 +/- 2.42 vs -1.68 +/- 2.70 mEq h(-1) L(-1), P = .0004) but not in non-obese (-0.63 +/- 2.20 vs -0.95 +/- 2.71 mEq h(-1) L(-1), P = .6) individuals. Among obese subjects, carriers of the -308A allele had greater insulin resistance as estimated by the homeostasis model assessment of insulin resistance index (4.36 +/- 2.83 vs 2.85 +/- 1.75, P = .01), but no differences were observed among non-obese subjects (2.19 +/- 1.24 vs 1.97 +/- 0.90, P = .6). Our findings suggest that the -238G>A and -308G>A polymorphisms of TNF-alpha alter circulating free fatty acids and insulin resistance in obese subjects with type 2 diabetes mellitus.
[Show abstract][Hide abstract] ABSTRACT: Background: Low circulating sex hormone-binding globulin (SHBG) concentrations have been associated with the presence of several features of the metabolic syndrome in both men and women. Nutritional factors including dietary lipids and fibers in particular have been suggested to modulate plasma SHBG levels. Methods: The primary objective of the present study was to investigate the effect of an oat bran-rich supplement in conjunction with the National Cholesterol Education Program (NCEP) Step 1 diet (< 30% of total energy from fat, < 10% of energy from saturated fat, and < 300 mg cholesterol per day) on plasma SHBG levels in 35 overweight premenopausal women. Subjects (age 38.6 ± 7.4 years) had normal menstrual cycles and were tested in the midluteal phase. Since no effect of the oat bran supplement was observed on plasma SHBG levels, data were analyzed according to the 6-week NCEP Step 1 diet. Results: The NCEP Step 1 nutritional intervention caused a significant decrease in energy intake (-11%, p < 0.05), percent fat intake (-10%, p < 0.005), as well as saturated (-20%, p < 0.005) and monounsaturated (-10%, p < 0.05) fatty acid intake. Body mass index (BMI) decreased slightly but significantly (from 29.2 ± 4.5 to 28.8 ± 4.3 kg/m2, p < 0.005). Plasma SHBG levels increased significantly (from 70.6 ± 17.7 to 79.9 ± 15.3 pmol/L, p < 0.0005) following the 6-week NCEP Step 1 diet, whereas plasma insulin levels were not modified significantly. Significant correlations were observed between the change in plasma SHBG levels and baseline BMI (r = 0.36, p < 0.04), as well as baseline (r = -0.42, p < 0.05) and postintervention (r = -0.35, p < 0.05) HDL cholesterol levels. Conclusions: We observed that a 6-week NCEP Step 1 diet significantly increased plasma SHBG levels, despite the finding that fasting insulin was not modified. Further studies are needed to elucidate physiological mechanisms underlying a direct effect of dietary composition on SHBG production by the liver.
Metabolic syndrome and related disorders 03/2007; 5(1):22-33. DOI:10.1089/met.2006.0005 · 1.98 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Food preferences are influenced by a number of factors such as personal experiences, cultural adaptations and perceived health benefits. Taste, however, is the most important determinant of how much a food is liked or disliked. Based on the response to bitter-tasting compounds such as phenylthiocarbamide (PTC) or 6-n-propylthiouracil (PROP), individuals can be classified as supertasters, tasters or nontasters. Sensitivity to bitter-tasting compounds is a genetic trait that has been recognized for more than 70 years. Genetic differences in bitter taste perception may account for individual differences in food preferences. Other factors such as age, sex and ethnicity may also modify the response to bitter-tasting compounds. There are several members of the TAS2R receptor gene family that encode taste receptors on the tongue, and genetic polymorphisms of TAS2R38 have been associated with marked differences in the perception of PTC and PROP. However, the association between TAS2R38 genotypes and aversion to bitter-tasting foods is not clear. Single nucleotide polymorphisms in other taste receptor genes have recently been identified, but their role in bitter taste perception is not known. Establishing a genetic basis for food likes/dislikes may explain, in part, some of the inconsistencies among epidemiologic studies relating diet to risk of chronic diseases. Identifying populations with preferences for particular flavors or foods may lead to the development of novel food products targeted to specific genotypes or ethnic populations.
Forum of nutrition 02/2007; 60:176-82. DOI:10.1159/0000107194