There are 3 clinical trials
There are many substances naturally present in the mouth that may help us taste fat in food. Two of these substances (lipases and CD36) will be examined in this study. The presence of fat in food increases food tastiness, therefore people often over-eat high-fat foods and gain weight. The purpose of this study is to determine if blocking lipases and some genetic variations in the CD36 gene will make fatty food less tasty so that people eat less. Our hypothesis is that Orlistat and a particular gene will increase one's ability to detect fat.
Hypothesis: SNPs that associate with reduced CD36 expression will be associated with higher FFA and TAG detection thresholds To test this hypothesis we will measure triolein and oleic acid taste detection thresholds in subjects who carry of the common CD36 e-SNP rs1761667 (i.e. a SNP that significantly reduces CD36 level and has a minor allele frequency of 38-48%).
Description: We will measure oleic acid detection levels as a marker of subjects' ability to detect free fatty acids. Oleic acid taste detection thresholds were separately assessed using a three-alternative forced-choice (i.e. 3-AFC) ascending concentration.
Measure: Oleic Acid Detection Level Time: Ranges from 5 days after screening to several weeks, pending availablity of participant.Description: We will measure triolein detection levels as a marker of subjects' ability to detect triglyceride. Triolein taste detection thresholds were separately assessed using a three-alternative forced-choice (i.e. 3-AFC) ascending concentration.
Measure: Triolein Detection Time: Ranges from 5 days after screening to several weeks, pending availablity of participant.Background: Cardiovascular diseases are the major health problem worldwide and the understanding of genetic contributions on the development of cardiovascular diseases is increasing significantly. The CD36 is a protein associated with uptake of oxidized forms of LDL and the single nucleotide polymorphism (SNP) rs1761667 A/G in the CD36 gene is correlated with increased consumption of total fat. The transcription factor STAT3 is released during the inflammatory acute phase response and the SNP rs8069645 G/A in the STAT3 gene is associated with abdominal obesity and higher intake of saturated fat. Studies have been shown the benefits of the Mediterranean diet in secondary prevention of cardiovascular disease and these dietary patterns have been often studied with nutrigenetic approach; these studies, however, are often limited to European populations, making it difficult to generalize to different populations. Hypothesis: Different dietary approaches may similarly influence in modifying metabolic, inflammatory and anthropometric profile, especially among patients with coronary arterial disease (CAD). The genetic interaction with environmental factors such as the nutrient intake, and the prescription of a different diet according to individual genotype, could influence the development and/or the treatment of cardiovascular diseases. Objective: To evaluate the effect of three dietary approaches on metabolic, inflammatory and anthropometric profile in patients with CAD and possible interactions with polymorphisms in CD36 and STAT3 genes.
The CD36 is a protein associated with uptake of oxidized forms of LDL and the single nucleotide polymorphism (SNP) rs1761667 A/G in the CD36 gene is correlated with increased consumption of total fat.
rs1761667 G>A.
Polymorphism rs1761667 G>A in the CD36 gene.
Interaction between dietary intervention, rs1761667 and rs8069645.
Description: LDL-cholesterol, in mg/dL
Measure: LDL Time: twelve weeksDescription: total cholesterol (TC), in mg/dL)
Measure: TC Time: twelve weeksDescription: non-HDL-cholesterol, in mg/dL
Measure: NHDL Time: twelve weeksDescription: HDL-cholesterol, in mg/dL
Measure: HDL Time: twelve weeksDescription: serum triglyceride, in mg/dL
Measure: TG Time: twelve weeksDescription: Triglycerides/fasting glucose index, calculated according to (fasting triglycerides [mg/dL] x fasting glucose [mg/dL])/2
Measure: TyG index Time: twelve weeksDescription: glycated hemoglobin (HbA1C), in %
Measure: HbA1C Time: twelve weeksDescription: fasting glucose, in mg/dL
Measure: FG Time: twelve weeksDescription: serum insulin, in UI/mL
Measure: Insulin Time: twelve weeksDescription: Homeostatic Model Assessment for Insulin Resistance (HOMA-IR), calculated according to fasting insulin (microU/L) x fasting glucose (nmol/L)/22.5
Measure: HOMA-IR Time: twelve weeksDescription: CRP-us, in mg/dL; IL-6, in mg/dL; IL-10, in mg/dL
Measure: inflammatory profile Time: twelve weeksDescription: body weight, in kg;
Measure: BW Time: twelve weeksDescription: body mass index (BMI), in kg/m2, calculated according to weight (kg)/height*height (m)
Measure: BMI Time: twelve weeksDescription: waist circumference, in cm
Measure: WC Time: twelve weeksDescription: neck circumference, in cm
Measure: NC Time: twelve weeksDescription: Lipid Accumulation Product Index (in cm.mmol.l), calculated for men: men (waist circumference [WC] - 65) x triglycerides (TG), and women (WC - 58) x TG
Measure: LAP index Time: twelve weeksDescription: Deep-Abdominal-Adipose-Tissue Index (in cm2), calculated for men (- 382.9 + [1.09 x weight] + [6.04 x waist circumference (WC)] + [- 2.29 x body mass index (BMI)]) and women (- 278 + [- 0.86 x weight] + [5.19 x WC])
Measure: DAAT index Time: twelve weeksDescription: Visceral Adiposity Index (log), calculated for men (waist circumference (WC)/[39 + (1.88 x body mass index (BMI)) x (triglycerides (TG)/1.03) x (1.31/HDL)]) and women (WC/[36.58 + (1.89 x BMI) x (TG/0.81) x (1.53/HDL)])
Measure: VAI index Time: twelve weeksDescription: plasma fatty acids, in percentage
Measure: PFA Time: twelve weeksDescription: plasma monocytes, in percentage
Measure: Mon Time: twelve weeksDescription: Polymorphism rs1761667 G>A in the CD36 gene
Measure: rs1761667 G>A Time: baselineDescription: Polymorphism rs8069645 A>G in the STAT3 gene
Measure: rs8069645 A>G Time: baselineDescription: Interaction between dietary intervention, rs1761667 and rs8069645
Measure: Interaction diet * genotype Time: twelve weeksA cross-sectional quantitative study will be carried out; recruiting female, Caucasian participants aged 18-65 years. The relevance of candidate gene studies is disputed. Research has shown associations between genotype and total fat intake. However, food preference is often described as a result of exposure to food types during upbringing. Many single nucleotide polymorphisms (SNP) have been associated with fat taste sensitivity, the majority of research shows that with a reduced sensitivity comes a higher total fat consumption. This study aims to assess the relationship between rs1761667 genotype, body mass index, fat intake, fat taste sensitivity and fat taste preference.
This study aims to assess the relationship between rs1761667 genotype, body mass index, fat intake, fat taste sensitivity and fat taste preference.