SNPMiner Trials by Shray Alag


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Report for SNP rs9939609

Developed by Shray Alag, 2020.
SNP Clinical Trial Gene

There are 11 clinical trials

Clinical Trials


1 The Role of FTO Gene Polymorphism and Insulin Preparation in Overweight/Obesity in Children With Type 1 Diabetes Mellitus

The project aims at assessment of the effect of the FTO gene polymorphism and the type of treatment on the development of overweight/obesity and features of metabolic syndrome in children with type 1 diabetes. Gene polymorphism including some genetic variants may predispose to the development of cardiovascular diseases and their complications. The A allele of the FTO gene predisposing to obesity occurs in approximately 40% of the European population and each copy of this allele can increase BMI by 0.1 Z-score i.e. by 0.4 kg/m2. Insulin therapy in diabetic patients may result in excess body weight gain. Therefore we need studies involving large groups of children and assessing cardiovascular risk factors in type 1 diabetes along with their genetic associations. Patients: The study will include 1500 children with type 1 diabetes, aged 6-18 years. Reference group will be made of 1500 children in whom type 1 diabetes was excluded. The following variables will be assessed in the treatment group: 1) Anthropometric data and questionnaire data: age, sex, body height and weight, body mass index (BMI), waist and hip circumferences, arm and thigh circumferences, family history of overweight/obesity, type 1 or 2 diabetes or cardiovascular disease, 2) Primary disease characteristics: age of the disease onset, treatment regimen, mean daily insulin consumption per kg body weight, brands of insulin products, glycated haemoglobin, BMI from the first 3-6 months following diabetes onset, diet, conversion of these data into actual and ideal calorie intake 3) Laboratory data - lipid profile and blood pressure (average of three measurements). Methodology: Gene polymorphism analysis in the extracted DNA will be made with the real-time PCR method using TaqMan 7900 HT by Applied Biosystems. Correlations between the FTO gene polymorphism and clinical variables such as BMI (including BMI increase since the disease onset), body weight and height, waist and hip circumferences, arm and thigh circumferences, and blood pressure will be assessed by a professional statistician with a specially dedicated software. Moreover parameters such as diet and metabolic control will be assessed. As regards insulin therapy the following variables will be analysed: insulin injection device, therapy regimen (intensive versus functional; brands and types of insulin products: human insulin versus insulin analogue), consumption of insulin. All of the above listed variables will be correlated with the genotypes found in the gene polymorphism analysis. The study has been approved by Bioethics Committee of the Medical University in Białystok. Results: The authors of the project expect that the effect of the FTO gene polymorphism on overweight/obesity and features of metabolic syndrome in children with type 1 diabetes will be shown. Moreover the project will enable assessment of the effect of the therapeutic regimen, including the type of insulin product, on body weight increase in the course of type 1 diabetes treatment in the context of the FTO gene polymorphism. Confirmation of the above associations and identification of a group at risk of excess body weight increase in the course of insulin therapy may help physicians, parents and patients to avoid this complication. Therefore clinical benefit of this project will include identification - based on the genetic assays results - of a group of type 1 diabetic children particularly likely to develop overweight, obesity and other cardiovascular risk factors.

NCT01279161 Type 1 Diabetes Mellitus
MeSH: Diabetes Mellitus Obesity Diabetes Mellitus, Type 1 Pediatric Obesity
HPO: Diabetes mellitus Obesity Type I diabetes mellitus

Particular objective of the project is providing an answer to the question: Are type 1 diabetic children who are carriers of the AA genotype of the FTO gene polymorphism (rs9939609) at risk of more weight gain in the course of insulin therapy when compared to carriers of the TA and TT genotypes of this polymorphism ?

Primary Outcomes

Measure: Identification of the effect of the FTO gene polymorphism on the development of overweight/obesity in insulin treated children

Time: one year

Secondary Outcomes

Measure: • Identification of the effect of the following factors: sex, age, duration of disease, therapy regimen, type of insulin product and degree of metabolic control on the development of overweight/ obesity in insulin treated children

Time: one year

Measure: • Identification of the effect of genetic polymorphism of the FTO gene on the incidence of metabolic syndrome features in insulin treated children.

Time: one year

Measure: • Identification of the effect of genetic polymorphism of the FTO gene on the incidence of overweight, obesity and metabolic syndrome features in children without diabetes.

Time: one year

Measure: • Comparison of frequency distribution of FTO gene polymorphism involved in the pathogenesis of obesity in children with diabetes versus children without diabetes.

Time: one year

2 Polymorphisms in Genes Encoding the Estrogen Metabolism Enzymes and Effects of Hormone Therapy for Oral Low Dose or Not Oral on Variables Related Endothelial Function, Inflammation and Metabolic Profile in Patients in Recent Menopause Study Pharmacogenetic

This is cross-over, randomized clinical trial, with objective to evaluate the effects of low-dose oral hormone therapy and non-oral hormone therapy on endothelial function markers (fibrinogen, von Willebrand factor, c-reactive protein), natriuretic peptide and on anthropometric, metabolic and hormonal variables in early and healthy postmenopausal women and analyzing polymorphisms in the estrogen receptor gene and FTO polymorphisms Patients will be randomized to receive oral hormone treatment or non-oral hormone treatment The investigators hypothesis is that a different genotypes in the receptor estrogen gene and FTO may have an influences on treatment response in metabolic markers and cardiovascular risk

NCT01432028 Postmenopause Drug: Estradiol and Progesterone Drug: Estradiol and Drospirenone

Influence of 2 polymorphisms (rs9939609 and rs8050136) on the effect of different treatment regimens.

Primary Outcomes

Description: Influence of 4 polymorphisms (PVUII, ALUI, RSAI and BSTUI) on the effect of different treatment regimens. Change from Baseline in weight, waist circumference, BMI, systolic and diastolic blood pressure, fasting glucose, glucose at 120 min, Fasting insulin, HOMA, Cholesterol, HDL-c, LDL-c, Triglycerides, Von Willebrand Factor, Fibrinogen, Testosterone and C-reactive protein at six months.

Measure: Polymorphisms of estrogen receptor

Time: six months

Secondary Outcomes

Description: Influence of 2 polymorphisms (rs9939609 and rs8050136) on the effect of different treatment regimens. Change from Baseline in weight, waist circumference, BMI, systolic and diastolic blood pressure, fasting glucose, glucose at 120 min, Fasting insulin,HOMA, Cholesterol, HDL-c, LDL-c, Triglycerides, Von Willebrand Factor, Fibrinogen, Testosterone and C-reactive protein at six months.

Measure: Polymorphisms in the fat mass-and obesity-associated (FTO) gene

Time: Six Months

Other Outcomes

Description: To assess the effects of oral low-dose and non-oral hormone therapy (HT) on ultra-sensitive C reactive protein (CRP), atrial natriuretic peptide (ANP), and cardiovascular risk factors in postmenopause.

Measure: Effects of hormone therapy on C reactive protein, atrial natriuretic peptide and cardiovascular risk factors in postmenopause.

Time: Six months

3 Obesity in Schoolchildren of Basic Education: a Study of Interdisciplinary Intervention - Phase III

The study aims to evaluate the possible effects of an exercise program, nutritional and psychological, postural orientation and guidance of oral health on body composition, physical activity levels and lifestyle, physical fitness and health and motor performance, the factors risk of cardiovascular disease, eating habits, the cognition levels, the psychological profile, the body posture of children and adolescents with overweight and obesity, considering the presence of risk genotype associated with the development of obesity. In addition, identify the effects of orientation for oral health on the quality of life and healthy oral habits.

NCT02769897 Obesity Adolescent Behavior Behavioral: Physical exercise
MeSH: Obesity
HPO: Obesity

The following parameters will be evaluated: anthropometric (BMI, waist circumference and skinfold thickness); hematologic and biochemical analysis (HDL cholesterol, LDL cholesterol, total cholesterol, triglycerides, glucose, insulin, adiponectin, leptin, resistin, C reative protein, ALT, AST, glycated hemoglobin, IL-6, IL-10, TNF-α, cortisol, irisina, F2 isoprostane and uric acid); polymorphism related to obesity (FTO rs9939609); related-health physical fitness (flexibility; sit and reach test; abdominal strength and cardiorespiratory fitness); postural deviations evaluated by the photogrammetry method - SAPO program.

Primary Outcomes

Description: Body mass index is measured by the weight and height values, applying the formula: weight/(height)²

Measure: Body mass index (kg/m²)

Time: 6 months

4 FTO rs9939609 and PPARy rs1801282 Polymorphisms in Mexican Adolescents With Overweight and Obesity at High Risk for Developing Diabetes

Background and Aims: The presence of the FTO rs9939609 and PPARy rs1801282 polymorphisms suggests changes in energy metabolism; this variation may be responsible for the development of various diseases including obesity. The aim of this study was to identify the presence of these polymorphisms in Mexican adolescents with overweight and obesity at high risk for developing diabetes. Methods and Results: This was a descriptive cross-sectional study, where 71 healthy adolescents (average age of 16) were included. Anthropometric measurements, Body mass index, as well as the determination of glucose, insulin and HOMA index were calculated from all the patients. The FTO rs9939609 and PPARy rs1801282 polymorphisms were determined by real-time PCR.

NCT02886013 Metabolic Syndrome Insulin Resistance
MeSH: Metabolic Syndrome Insulin Resistance
HPO: Insulin resistance

FTO rs9939609 and PPARy rs1801282 Polymorphisms in Mexican Adolescents With Overweight and Obesity at High Risk for Developing Diabetes.

FTO rs9939609 and PPARy rs1801282 Polymorphisms in Mexican Adolescents Background and Aims: The presence of the FTO rs9939609 and PPARy rs1801282 polymorphisms suggests changes in energy metabolism; this variation may be responsible for the development of various diseases including obesity.

The FTO rs9939609 and PPARy rs1801282 polymorphisms were determined by real-time PCR.

Prevalence of the FTO rs9939609 and PPARy rs1801282 polymorphisms..

Primary Outcomes

Description: The aim of this study was to identify the presence of these polymorphisms in Mexican adolescents with overweight and obesity at high risk for developing diabetes.

Measure: Prevalence of the FTO rs9939609 and PPARy rs1801282 polymorphisms.

Time: up to 24 months.

5 Comparison of the Effect of MediterrAsian Diet With Two Different Calorie Restriction on Anthropometric Indices in Carriers of FTO rs9939609 Polymorphism With Overweigh: Toward Personalized Nutrition

Background: Obesity treatment should be individualized since some calorie restricted diet doesn't work for some individuals. Objective: we assess the effect of two different calorie restriction with MediterrAsian diet on weight loss of FTO rs9939609 carriers with overweight. Methods: we recruit 80 healthy overweight participants aged 20-45 years that randomly allocated in two interventional group [group 1: Mediterrasian diet according to adjusted ideal body weight with 500 calories restriction (RD) and group 2: without 500 calories restriction (NRD)+ Moderate physical activity]. Anthropometric indices will be assesses for all participants weekly for two month. The criteria for weight loss is 250-500 grams weekly. Metabolic indices, physical activity and psychologic aspects will be assesses at baseline and the end of the intervention. Dietary adherence will be checked by 24hr recalls at day 0, 30 and 60. At the end of the study, we compare carriers with different alleles (AA+TA and TT) in two intervention groups to find out which calorie restriction is appropriate for each genotype. Significant p-value is less than 0.05.

NCT02940197 Obesity Dietary Modification Behavioral: MediterrAsian diet
MeSH: Overweight

Comparison of the Effect of MediterrAsian Diet With Two Different Calorie Restriction on Anthropometric Indices in Carriers of FTO rs9939609 Polymorphism With Overweigh: Toward Personalized Nutrition.

Comparison of Two Calorie Restricted MediterrAsian Diet on Weight Loss in FTO rs9939609 Overweight Carriers Background: Obesity treatment should be individualized since some calorie restricted diet doesn't work for some individuals.

Objective: we assess the effect of two different calorie restriction with MediterrAsian diet on weight loss of FTO rs9939609 carriers with overweight.

Primary Outcomes

Measure: weight loss

Time: 2 months

6 Using Personalized Nutrigenomics Testing to Mitigate Overweight/Obesity Risk in Two Distinct Patient Populations: A Multicentre Randomized Clinical Intervention Trial

The investigators hypothesize that compared to the provision of population-based lifestyle advice, providing DNA-based lifestyle advice via personalized nutrigenomics testing (PNT) to two distinct patient populations (Family Health Team patients receiving a lifestyle counselling intervention and transplant recipients) will lead to greater reductions in percent body fat. In addition, it will motivate them to adopt healthier dietary and physical activity habits through changes in attitudes and/or subjective norms and/or behavioural control, lead to greater fat loss (kg), increased percent lean mass and therefore improve health and quality of life outcomes for both patient populations. In addition, it is hypothesized that dietary strategies related to the intake of one or more dietary components of interest will mitigate post-transplant weight gain associated with three SNPs of interest. This is a randomized clinical intervention trial involving a total of four groups of patients (n = 400). The two main patient groups include overweight or obese, stable transplant recipients and overweight or obese patients who are attending group counselling sessions at the East Elgin Family Health Team. Within these two main groups, there will be two sub-groups. Patients will be randomized to receive either PNT or standard nutrition intervention (SNI). Baseline data will be conducted consisting of a food frequency questionnaire and three-day food records using a validated multiple pass method. Bioelectrical Impedance Analysis (BIA) will be conducted to assess body composition and to derive percent body fat and lean mass. Weight and height will be measured using a weigh scale and stadiometer. Attitudes, subjective norms and behavioural control will be assessed using a Theory of Planned Behaviour Questionnaire. Those patients randomized to the PNT group will be instructed on a tailored nutrition care plan and physical activity recommendations based on their individual genetic profile. At the same time, the SNI group will be instructed on general nutrition and physical activity recommendations for weight loss, which include the use of dietary strategies from the standard tool ('Just the Basics') used by registered dietitians for transplant patients and the GLB program for patients attending the East Elgin Family Health Team sessions. Monthly email reminders or phone calls (depending on patient preference) will be sent to transplant recipients as a reminder of their nutrition and physical activity plan. Reminders of nutrition and physical activity goals for the Family Health Team participants are incorporated into the GLB program. Three months, six months and twelve months after baseline data collection and individual nutrition interventions, baseline data will be repeated. After the study is complete, participants in the SNI group will be offered a nutrigenomics report and consultation with a registered dietitian. A paired t-test or repeated measures ANOVA will be used to assess within group change from baseline to each follow-up time point for: BMI, body fat, lean mass, and dietary intake. A repeated measures ANOVA will be used to test between group differences from baseline to each follow-up time point for: BMI, body fat, lean mass, and dietary intake. If significant mean differences are detected, a Tukey's post hoc test will be used to compare differences by group. Statistical significance will be determined by P < 0.05. General linear regression models will be used to assess interactions between each genotype of interest and each dietary component of interest on BMI and body composition from baseline to each follow-up time point.

NCT03015012 Transplant-Related Disorder Overweight and Obesity Genetic: Personalized Nutrigenomics Testing (PNT) Other: Standard Nutrition Intervention (SNI)
MeSH: Obesity Overweight
HPO: Obesity

Nutrigenomics (nutrition-genetic) interactions between ACE gene variants at rs4343, FTO gene variants at rs1558902 (in strong linkage disequilibrium with rs9939609) and MC4R (rs571312) to mitigate risk of post-transplant weight gain will be assessed for transplant recipients in the PNT group.. Inclusion Criteria: - TRANSPLANT PATIENTS: Adults greater than or equal to age 18, non-pregnant, non-lactating, attending Canadian Transplant Association meetings, BMI ≥ 25kg/m2, ≥1 year stable (not being treated for transplant rejection or infection) post-transplant, having access to a computer with email or a telephone at least one day per week and English speaking.

Primary Outcomes

Description: Change in body composition (body fat percentage as the primary outcome) will be assessed using BIA which will provide information on fat mass, lean mass, and water weight

Measure: Change in Body Fat Percentage

Time: 3 months, 6 months, 12 months

Secondary Outcomes

Description: Change in dietary intake will be assessed using pre- and post- dietary data collected using 3-day food records, and a past-month online food frequency questionnaire.

Measure: Change in Dietary Intake

Time: 3 months, 6 months, 12 months

Description: Change in physical activity will be assessed using pre- and post- physical activity data collected using a 7-day physical activity recall. Metabolic equivalents will then be calculated from this data.

Measure: Change in Physical Activity

Time: 3 months, 6 months, 12 months

Description: Change in these key components of the Theory of Planned Behaviour (TPB) will be assessed using a TPB questionnaire.

Measure: Change in Attitudes, Subjective Norms and Behavioural Control

Time: Pre- and post- lifestyle intervention (baseline), 3 months, 6 months, 12 months

Description: Change in body composition will be assessed using BIA which will provide information on fat mass, lean mass, and water weight

Measure: Change in Body Composition

Time: 3 months, 6 months, 12 months

Description: Change in BMI will be measured using weight and height data collected using a weigh scale and stadiometer

Measure: BMI

Time: 3 months, 6 months, 12 months

Description: Change in weight will be measured using a weigh scale

Measure: Weight

Time: 3 months, 6 months, 12 months

Other Outcomes

Description: Nutrigenomics (nutrition-genetic) interactions between ACE gene variants at rs4343, FTO gene variants at rs1558902 (in strong linkage disequilibrium with rs9939609) and MC4R (rs571312) to mitigate risk of post-transplant weight gain will be assessed for transplant recipients in the PNT group.

Measure: Nutrigenomics Interactions

Time: 3 months, 6 months, 12 months

7 Effect of Exercise on Appetite, Energy Intake, Butyrylcholinesterase Activity and Gut Peptides in Men With Variants of the Obesity-linked FTO rs9939609 Polymorphism

Using a database of individuals with FTO genetic data, the study aims to assess the appetite, energy intake, butyrylcholinesterase, gut hormone responses to a bout of moderate- to high intensity exercise in individuals with genetic variations in the FTO gene.

NCT03025347 Appetitive Behavior Other: Control Other: Exercise

Effect of Exercise on Appetite, Energy Intake, Butyrylcholinesterase Activity and Gut Peptides in Men With Variants of the Obesity-linked FTO rs9939609 Polymorphism.

Inclusion Criteria: - non-smoker, not currently dieting, weight stable for >3 months (self-reported), no personal history of cardiovascular disease, metabolic disease or dyslipidaemia, European ancestry, no psychiatric or medical condition Exclusion Criteria: - food allergies, dislike or intolerance of study foods and drinks, irregular eating patterns, use of medication that could influence hormone concentrations Inclusion Criteria: - non-smoker, not currently dieting, weight stable for >3 months (self-reported), no personal history of cardiovascular disease, metabolic disease or dyslipidaemia, European ancestry, no psychiatric or medical condition Exclusion Criteria: - food allergies, dislike or intolerance of study foods and drinks, irregular eating patterns, use of medication that could influence hormone concentrations Appetitive Behavior The fat mass and obesity-associated gene (FTO) rs9939609 A allele is related to obesity, greater food intake and impaired postprandial reduction of ghrelin.

Exercise acutely suppresses levels of ghrelin and appetite, yet whether the response differs in people with or without the rs9939609 A allele is unknown.

This study assessed the effect of exercise on appetite, appetite-regulatory hormones and energy intake in variants of the FTO rs9939609 polymorphism.

Cohort The investigators initially recruited 202 subjects to a database and measured FTO rs9939609 genotype.

From these subjects, 12 individuals homozygous for the 'obesity-risk' rs9939609 A allele and 12 homozygous for the T allele were recruited.

Primary Outcomes

Description: Measured using ELISA from venous blood samples

Measure: Plasma acylated ghrelin concentrations (N=24)

Time: 24 hours

Description: Measured using ELISA from venous blood samples

Measure: Plasma desacyl ghrelin concentrations (N=24)

Time: 24 hours

Description: Measured using visual analogue scales

Measure: Subjective appetite (N=24)

Time: 24 hours

Description: Measured at laboratory-based meals

Measure: Ad-libitum energy intake (N=24)

Time: 24 hours

Description: Measured using Ellman's reagent protocol

Measure: Plasma butyrylcholinesterase activity (N=24)

Time: First hour of main trial (three samples).

Secondary Outcomes

Description: Measured using ELISA from venous blood samples

Measure: Plasma total glucagon-like peptide 1 concentrations (N=24)

Time: 24 hours

Description: Measured using ELISA from venous blood samples

Measure: Plasma total peptide yy concentrations (N=24)

Time: 24 hours

Description: Measured using ELISA from venous blood samples

Measure: Plasma leptin concentrations (N=24)

Time: Baseline (fasting) sample

8 Influence of Polymorphysms in the Fto and Ppar Gen Genes, Systemic Inflammation and Oxidative Stress in the Magnitude of Weight Loss Induced by Intermittent or Moderate Continuous High Intensity Training Programs

The study focuses on the influence of polymorphism in the FTO genes rs9939609 and PPARᵧ Pro12Ala, oxidative stress and systemic inflammation on changes in body composition and rest metabolism induced by HIIT and continuous aerobic programs in obese or overweight individuals.

NCT03568773 Overweight and Obesity Chronic Disease Other: High-intensity interval training Other: Aerobic exercise moderate intensity Other: Control Group
MeSH: Overweight Weight Loss Chronic Disease
HPO: Decreased body weight Weight loss

Influence of Genetic and Physiological in Weight Loss The study focuses on the influence of polymorphism in the FTO genes rs9939609 and PPARᵧ Pro12Ala, oxidative stress and systemic inflammation on changes in body composition and rest metabolism induced by HIIT and continuous aerobic programs in obese or overweight individuals.

Thus, the objective of the study is to analyze the influence of polymorphism in the genes FTO rs9939609 and PPARᵧ Pro12Ala, oxidative stress and systemic inflammation on changes in body composition and rest metabolism induced by continuous and continuous aerobic programs.

Primary Outcomes

Description: The procedure used for analysis is done using a Dual Energy Radiological Absortiometry (DEXA) equipment. The measurement of the body fat and fat free mass percentage measure is obtained by means of a full body scan using the LUNAR PRODIGY DF + 14.319 Radiation (Madison, WI) brand device, following manufacturer's protocols. The body mass is evaluated by means of a balance (Sanny®, São Bernardo do Campo - São Paulo, Brazil), with the volunteer barefoot and in orthostatic position using a Toledo scale sensitive to 100 g. The stature is evaluated by a stadiometer with a tape calibrated at 0.1 of the same mark. Waist circumference and other body perimeters are measured with a 0.1 cm Anthropometric Tape (Sanny®, São Bernardo do Campo - São Paulo, Brazil). Weight and height data are used to calculate BMI using the equation adopted by the WHO: BMI = (Weight / (Stature) 2).

Measure: Body Composition. The changes are being evaluated.

Time: Before the intervention protocol and 48 hours immediately after the last exercise session.

Secondary Outcomes

Description: The metabolic rate was measured using a gas spirometry analyzer. After having fasted from 8:00 pm the previous day, the volunteers were referred to the laboratory shortly after the awakening and were invited to remain seated in a thermoneutral environment for 30 minutes. For the next 30 minutes, VO2, VCO2, VE and RER were monitored until variations of no more than 10% occurred when five-minute intervals were compared. Once this steady state was obtained, these variables were recorded for five minutes. The calculation of the resting metabolic rate is done according to Macdonald (1990).

Measure: Metabolic Rate of Rest. The changes are being evaluated.

Time: Before the intervention protocol and 48 hours immediately after the last exercise session.

Description: Collections of 10 ml of blood from the antecubital vein will be performed early in the morning, with fasting from 10 to 12 hours. The collections will be done 24 hours before, in the 6th week and after the intervention period. They will remain seated for 10 minutes for subsequent collection. Five milliliters of blood will be placed in EDTA-containing test tubes, protected from light and gently homogenized by inversion. The other 5ml will be placed in tubes without anticoagulants. They will then be centrifuged at 3,000 rpm for 10 min. The plasma or serum will be separated, placed in eppendorf tubes and refrigerated at -20 ° C until analysis. All analyzes will be carried out using a commercial kit of the Labtest brand (Minas Gerais-Brazil). The analyzes will be carried out on serum samples using commercial Labtest kits (Minas Gerais, Brazil), following the manufacturer's recommendations and on a Labmax 240 premium automatic analyzer (Lagoa Santa-MG, Brazil).

Measure: Lipid and Glycemic Profile. The changes are being evaluated.

Time: The collections will be done 24 hours before, in the 6th week and 48 hours after the end of the intervention.

Description: 10 ml of blood will be collected in the beginning of the morning, with fasting of 10 to 12 hours, being done 24 hours before, in the 6th week and after the intervention period. Five milliliters of blood will be placed in test tubes containing EDTA and protected from light and the other 5ml will be placed in tubes without anticoagulants and centrifuged at 3,000 rpm for 10 min. The plasma or serum will be separated, placed in eppendorf tubes and refrigerated at -20 ° C until analyzed by a commercial kit of the Labtest brand (Minas Gerais, Brazil). For this, 250 μl of sample will be added to KCl and incubated in a water bath (37 ° / 60 minutes). The mixture will be precipitated with 35% AA perchloric acid and centrifuged at 14,000 rpm for 10 minutes at 4 ° C. The supernatant will be transferred to eppendorfs and 400μl of 0.6% thiobarbituric acid is added and incubated at 95-100 ° C for 30minutes. The material will be read in a spectrophotometer at a wavelength of 532nm.

Measure: Oxidative stress (Malondialdehyde). The changes are being evaluated.

Time: The collections will be done 24 hours before, in the 6th week and 48 hours after the end of the intervention.

Description: 10 ml of blood will be collected in the beginning of the morning, with fasting of 10 to 12 hours, being done 24 hours before, in the 6th week and after the intervention period. Five milliliters of blood will be placed in test tubes containing EDTA and protected from light and the other 5ml will be placed in tubes without anticoagulants and centrifuged at 3,000 rpm for 10 min. The plasma or serum will be separated, placed in eppendorf tubes and refrigerated at -20 ° C until analyzed by a commercial kit of the Labtest brand (Minas Gerais, Brazil). The evaluation of the total antioxidant capacity will be performed through DPPH. For analysis, 100 μl of plasma will be added to 3.9 ml of vortexed DPPH solution, set to stand for 30 minutes and then centrifuged at 10,000 rpm for 15 minutes at 20 ° C. The supernatant will be used for spectrophotometer reading at 515 nm wavelength, using distilled white water. The result will be expressed as a percentage of antioxidant activity.

Measure: Oxidative stress (Total antioxidant capacity). The changes are being evaluated.

Time: The collections will be done 24 hours before, in the 6th week and 48 hours after the end of the intervention.

Description: 10 ml of blood will be collected in the beginning of the morning, with fasting of 10 to 12 hours, being done 24 hours before, in the 6th week and after the intervention period. Five milliliters of blood will be placed in test tubes containing EDTA and protected from light and the other 5ml will be placed in tubes without anticoagulants and centrifuged at 3,000 rpm for 10 min. The plasma or serum will be separated, placed in eppendorf tubes and refrigerated at -20 ° C until analyzed by a commercial kit of the Labtest brand (Minas Gerais, Brazil). The concentration of hs-CRP will be quantified by immunoturbidimetry in serum samples. Calibration will use the Calibra Calibrator from Labtest (Calibra Plus PCR-ultra - Ref-345). Absorbance will be obtained on the Labmax 240 premium automatic analyzer at 540 nm wavelength. The concentrations of hs-CRP will be determined by the commercial kit (Labtest, Minas Gerais, Brazil) according to the manufacturer's instructions.

Measure: Systemic Inflammation (Plasma ultra-sensitive C-reactive protein). The changes are being evaluated.

Time: The collections will be done 24 hours before, in the 6th week and 48 hours after the end of the intervention.

Description: 10 ml of blood will be collected in the beginning of the morning, with fasting of 10 to 12 hours, being done 24 hours before, in the 6th week and after the intervention period. Five milliliters of blood will be placed in test tubes containing EDTA and protected from light and the other 5ml will be placed in tubes without anticoagulants and centrifuged at 3,000 rpm for 10 min. The plasma or serum will be separated, placed in eppendorf tubes and refrigerated at -20 ° C until analyzed by a commercial kit of the Labtest brand (Minas Gerais, Brazil). The A1GPA concentration will be quantified by immunoturbidimetry using the commercial kit (Labtest, Minas Gerais, Brazil) as per manufacturer's instructions. Calibration will use the Calibra Calibrator from Labtest (Calibra Plus Protein - Ref-346). The absorbance will be obtained in the Labmax 240 premium automatic analyzer (Lagoa Santa-MG, Brazil), at wavelength 340nm.

Measure: Systemic Inflammation (Analysis of alpha-1-glycoprotein acid). The changes are being evaluated.

Time: The collections will be done 24 hours before, in the 6th week and 48 hours after the end of the intervention.

Description: Oral cell samples were collected through a mouthwash for 60 seconds of 5 ml of 3% sucrose solution. The resulting contents of the mouthwash were transferred to a 15 ml tube, which immediately afterwards was placed in a solution of TNE (17 mM Tris-HCl pH 8.0, 50 mM NaCl and 7 mM EDTA), diluted to 66% alcohol and autoclaved distilled water.After this, the extraction and genotyping process followed the recommendations of Saiki et al. (1985)

Measure: DNA Extraction and Genotyping

Time: The genetic collection will be made in the 6th week of the intervention.

9 A Replicated Crossover Study to Explore Individual Variability of Appetite Responses to a Standardised Meal and Any Moderating Influence of the FTO Gene

The aim of this study is to examine the interindividual variability of subjective and hormonal appetite responses to a standardised meal in healthy men and explore any moderating influence of the fat mass and obesity associated gene (FTO). Participants homozygous for the obesity risk A allele (AA) or low risk T allele (TT) of FTO rs9939609 will complete two fasted control and two standardised meal (5025 kJ energy, 47% carbohydrate, 9% protein, 44% fat) conditions in randomised sequences. Ratings of perceived appetite and venous blood samples will be taken before and after the interventions. Interindividual differences in appetite responses and the potential moderating influence of the FTO gene will be examined using bivariate correlations and linear mixed modelling.

NCT03771690 Appetitive Behavior Obesity Genetic Predisposition to Disease Behavioral: Standardised meal
MeSH: Disease Susceptibility Genetic Predisposition to Disease

Participants homozygous for the obesity risk A allele (AA) or low risk T allele (TT) of FTO rs9939609 will complete two fasted control and two standardised meal (5025 kJ energy, 47% carbohydrate, 9% protein, 44% fat) conditions in randomised sequences.

Inclusion Criteria: - Homozygous minor allele (AA) or major allele (TT) FTO rs9939609 genotype; - Non-smoker; - Weight stable for the previous 3 months.

Exclusion Criteria: - Heterozygous FTO rs9939609 genotype (i.e., AT); - Any medical conditions (e.g., diabetes, coagulation or bleeding disorders); - Taking any medication that might influence appetite, fat metabolism or blood glucose; - Dieting or restrained eating behaviours; - Any food allergies.

A total of 18 healthy men will be recruited according to their FTO rs9939609 genotype: 9 homozygous minor allele (AA) and 9 homozygous major allele (TT).

Primary Outcomes

Description: Control adjusted pre-to-post change in plasma acylated ghrelin concentration

Measure: Acylated ghrelin concentration

Time: 1 hour (Plasma samples will be collected at 0 hour (pre) and 1 hour (post))

Secondary Outcomes

Description: Control adjusted pre-to-post change in plasma total peptide YY concentration

Measure: Total peptide YY concentration

Time: 1 hour (Plasma samples will be collected at 0 hour (pre) and 1 hour (post))

Description: Control adjusted pre-to-post change in plasma insulin concentration

Measure: Insulin concentration

Time: 0.5 hour (Plasma samples will be collected at 0 hour (pre) and 0.5 hour (post))

Description: Control adjusted pre-to-post change in plasma glucose concentration

Measure: Glucose concentration

Time: 0.5 hour (Plasma samples will be collected at 0 hour (pre) and 0.5 hour (post))

Description: Control adjusted pre-to-post change in rating of perceived hunger. Perceived hunger will be measured using a 100 mm visual analogue scale anchored at 0, 'I am not hungry at all', and 100, 'I have never been more hungry'.

Measure: Rating of perceived hunger

Time: 1 hour (Visual analogue scales will be completed at 0 hour (pre) and 1 hour (post))

Description: Control adjusted pre-to-post change in rating of perceived satisfaction. Perceived satisfaction will be measured using a 100 mm visual analogue scale anchored at 0, 'I am completely empty', and 100, 'I cannot eat another bite'.

Measure: Rating of perceived satisfaction

Time: 1 hour (Visual analogue scales will be completed at 0 hour (pre) and 1 hour (post))

Description: Control adjusted pre-to-post change in rating of perceived fullness. Perceived fullness will be measured using a 100 mm visual analogue scale anchored at 0, 'Not full at all', and 100, 'Totally full'.

Measure: Rating of perceived fullness

Time: 1 hour (Visual analogue scales will be completed at 0 hour (pre) and 1 hour (post))

Description: Control adjusted pre-to-post change in rating of perceived prospective food consumption. Perceived prospective food consumption will be measured using a 100 mm visual analogue scale anchored at 0, 'Nothing at all', and 100, 'A lot'. consumption

Measure: Rating of perceived prospective food consumption

Time: 1 hour (Visual analogue scales will be completed at 0 hour (pre) and 1 hour (post))

10 Effects of Exercise Intervention and Confounding Factors on Type II Diabetic Muscles

The aim of the first year of this three-year plan is to analyze and compare the muscle quality of lower limb muscle (microcirculation, muscle performance and mechanical characteristics) and maximal aerobic exercise capacity in treadmill exercise tests for diabetic and non-diabetic cases. The hypotheses are:1) the muscle quality of lower limb muscle and maximal aerobic exercise capacity are different between participate with diabetic and non-diabetic, 2) the effect of the three-month aerobic exercise intervention or home exercise on the characteristics of the muscle quality are different , and 3) intrinsic factors (such as age, BMI, and HDL) and characteristics of specific FTO genes are influenced the training outcomes.

NCT03869411 Diabetes and Healthy Control FTO Gene Expression Aerobic Exercise Intervention or Home Exercise Pre-training and Post-training Behavioral: supervised aerobic exercise or home-based aerobic exercise

rs9939609 SNP analysis, record as TT or TA or AA type.

Primary Outcomes

Description: elastography was used, units on kPa

Measure: index of muscle stiffness

Time: Change from Baseline muscle quality at 3 months

Description: Dynamometer was used to measure muscle strength, units on kilograms

Measure: muscle strength of knee extensor and plantarflexor

Time: Change from Baseline functional performance at 3 months

Description: B mode sonography was used, units on mm/s

Measure: Relative sliding of muscles

Time: Change from Baseline muscle quality at 3 months

Description: Near-infrared spectroscopy was used to measure oxygen saturation on muscle, units on percentage

Measure: muscle microcirculation

Time: Change from Baseline muscle quality at 3 months

Description: Bruce treadmill protocol was used in the maximal exercise testing, maximum rate of oxygen consumption record as ml/kg/min

Measure: maximum rate of oxygen consumption

Time: Baseline

Secondary Outcomes

Description: rs9939609 SNP analysis, record as TT or TA or AA type

Measure: characteristics of specific FTO genes

Time: Baseline

Description: self report the ability of walking one-fourth of a mile, record as degree of difficulty: none, some difficulty, much difficulty, inability

Measure: physical activity level

Time: Change from Baseline functional performance at 3 months

Description: weight and height will be combined to report BMI in kg/m^2

Measure: BMI

Time: Change from Baseline functional performance at 3 months

Description: Hemoglobin A1c (HbA1c), unit on percentage

Measure: blood glucose level

Time: Change from Baseline functional performance at 3 months

Description: total cholesterol, units on mg/dL

Measure: blood cholesterol

Time: Change from Baseline functional performance at 3 months

11 Impact of FTO Gene Variants and Lifestyle Factors on Obesity Traits in a Turkish Population

Studies have shown that the effect of fat mass and obesity-associated (FTO) gene on obesity is modulated by lifestyle factors. Hence, we aimed to determine whether two single nucleotide polymorphisms (SNPs) in the FTO gene are associated with obesity and to assess whether these associations were modified by lifestyle factors. The study included 200 obese and 200 non-obese individuals from Turkey. Our study suggests that the effect of the SNPs on obesity traits is likely to be influenced by lifestyle factors in this Turkish population.

NCT04205318 Obesity Diet Habit Genetic Predisposition
MeSH: Obesity Disease Susceptibility Genetic Predisposition to Disease
HPO: Obesity

FTO SNPs rs9939609 and rs10163409.

Primary Outcomes

Description: FTO SNPs rs9939609 and rs10163409

Measure: Genetic analysis of two SNPs at FTO gene

Time: up to 36 weeks

Description: Body mass index, waist circumference, hip circumference, body composition

Measure: Anthropometric measurements

Time: up to 36 weeks

Description: lipid profile, glucose, insulin, adiponectin

Measure: Biochemical measurements

Time: up to 36 weeks


HPO Nodes


Obesity
Genes 465
PDE6A IDH3A ALG13 CANT1 PRKAR1A WDR34 PCARE EIF2S3 RP1 CTSH RAI1 LZTFL1 MTFMT TTC8 PPARG ANOS1 IQSEC2 IQSEC2 C8ORF37 TMEM67 RNPC3 MKRN3 FLRT3 MYT1L SNRNP200 BBS4 IFT172 CEP19 PROKR2 EMD EYS SLC25A4 LEPR KIDINS220 THOC2 PCSK1 PRPF4 ARL6 USP9X RDH12 IGF1 IFT172 ARL3 SOX10 PDE11A FGFR3 NR2E3 CUL4B RAB23 PAX6 ARL2BP DYRK1B GNAS PRPF31 PNPLA6 PRCD RLBP1 FTO KLF11 TBX1 BLK INPP5E HIRA CYP7A1 TMEM43 DHDDS BBS5 MLXIPL LEP CLIP2 WNT4 IFT140 RP2 REEP6 EP300 FHL1 PDE4D SH2B1 CNGA1 CNNM2 PAK3 TNFSF4 IQSEC2 SDCCAG8 MOG TRAPPC9 SDC3 HLA-DQB1 TBL2 POMC ALMS1 PTCHD1 PRPH2 PSMD12 SH3KBP1 SNORD115-1 HSD11B1 ARVCF PRPF8 POMC GUCA1B ATRX SEC24C POMGNT1 ZNF365 SUFU ARMC5 CLCN4 HACE1 RBMX KIAA1549 SLC9A7 SH2B1 IFT27 GNAS EIF2S3 JMJD1C FGF17 COMT MKS1 ZNF81 HERC2 SKI CYP19A1 MKKS SOX2 SLC7A7 GTF2I AKT2 MID2 SIM1 SMARCB1 DNMT3A ENPP1 PRPF6 ZNF408 PRDM16 FGFR1 PROM1 ERMARD BBS10 AIP NPAP1 BEST1 GATA4 BBS1 TUB P4HTM TBX3 KMT2A BBS7 GABRD GP1BB WDR11 RP9 GNAS XRCC4 PAX6 SDCCAG8 RBP3 ADRB3 GNAS PAX4 NSMF NPHP1 RAI1 ATP6AP2 GNAS-AS1 USP8 MAK KCNJ18 CCDC141 IMPDH1 PDSS1 NIPBL ADNP DPYD SETD2 NR0B2 MED12 NDN FAM161A HESX1 NRL BBS10 GHRL DUSP6 LAS1L MKKS P2RY11 BBS5 MEGF8 ZNF711 RREB1 H6PD HESX1 SIN3A CNKSR2 KIDINS220 BBS12 FRMPD4 IFT74 TRIM32 BLK AFF4 POGZ ALB GABRA3 TSPAN7 SLC10A7 SYNE2 CREBBP GNAS RPS6KA3 OFD1 IFT172 APC2 PRKAR1A RPGR BBS9 SNORD116-1 IL1RAPL1 OTX2 NSD1 HACE1 PCSK1 FGFR1 SETD2 BAZ1B EHMT1 ZNF41 INS PROK2 POU3F4 IFT88 PDE6B GNAS ABCC8 RGR ARL13B KMT2D GHR GNAS NEK2 RFC2 CA4 LIPE RERE MAPK8IP3 RHO SCAPER BPTF RAP1A DLG3 BBS9 PCNT LEP IGFALS CRB1 RPS6KA3 TBX1 NEUROD1 CEP164 GTF2IRD1 SIM1 MECP2 ARX SMC3 PHIP TRIP12 CARTPT NTRK2 HDAC8 AGTR2 SEMA3A BRAF AHR PWRN1 OFD1 SETD5 ADNP LZTFL1 PROK2 KISS1R CEP290 HS6ST1 CDHR1 DEAF1 MAN1B1 RAP1B CTNNB1 USP8 BBS2 GCK UPF3B ELN MAN1B1 PTEN TRIM32 MKS1 ROM1 BBS2 LEPR KCNJ11 MRAP2 PRPF3 PDGFB LRAT TRAF3IP1 HDAC8 SPRY4 ELN SRY FEZF1 VPS13B TACR3 KIF7 TAF1 RAB23 FOXP1 HDAC8 CERKL CLRN1 AGRP BBS2 MOG TOPORS ARNT2 ARHGEF6 FMR1 USP27X SHANK3 XYLT1 VPS13B SMAD4 UFD1 EGF UCP3 BBS12 IFT172 SNRPN CACNA1S USH2A HNF1A ACADVL ADRB2 MEGF8 C8ORF37 APOE WDPCP IGF1R CCDC141 NIN IPW MAGEL2 GDI1 NF2 HGSNAT ARL6 HUWE1 SEMA4A EHMT1 SYP IDH3B PRMT7 CEP290 PCNT SH2B1 HDAC4 ADCY3 TTC8 CHD7 AKT2 ABCA4 LMNA HCRT MC4R DMD ZNF513 CRX SYNE1 XYLT1 BDNF TBX3 MC3R KLHL7 DCC SPG11 TTC8 POMC ALMS1 FTSJ1 PDX1 KDM6A LIMK1 BBIP1 BBS7 RPE65 CCDC28B EXOC6B BBIP1 AHI1 ARMC5 AGBL5 PDE4D TULP1 SMC1A DHX38 CEL ARL6 MAGEL2 PROKR2 HLA-DRB1 MKRN3-AS1 SHOX RAD21 IMPG2 ZNF711 C8ORF37 IFT27 PWAR1 PNKP FGF8 HNF4A CDH23 BBS1 WT1 GNAS MTTP ZBTB20 KIZ APPL1 FLII IL17RD SPATA7 MERTK TCF20 MECP2 CXORF56 LMNA BBS4 SLC7A14 SOX3 MC4R LAS1L KCNAB2 CUL4B PDE6G ARHGEF18 SAG RAB39B STX16 UBE3A ACSL4 TBX1 MCM3AP TUB ATRX FSCN2 PHF6 TRAPPC9 PHF6 WT1 CNGB1 HCFC1
Diabetes mellitus
Genes 523
PDE6A IDH3A UBR1 IER3IP1 SPINK1 HNF1B PCARE ND1 OPA1 RP1 AGPAT2 TRNS1 MMP2 TTC8 PDX1 TGIF1 TREX1 CDON CFTR MKRN3 GCK INS PPARG HYMAI COX2 XRCC4 SNRNP200 NUBPL PTRH2 CEP19 NDUFB10 PROKR2 EYS LMNA TRNQ MAPK8IP1 LEPR TCF7L2 NSMCE2 PRPF4 ARL6 RDH12 ARL3 FGF8 GCK KDSR CEL DISP1 NR2E3 NDUFAF5 ARL2BP ERGIC1 PLAGL1 PRPF31 PNPLA6 NDUFV2 COX3 PRCD RLBP1 WFS1 KLF11 TRNL1 PDX1 NDUFA11 BLK KCNJ11 GPD2 SLC19A2 DHDDS MLXIPL LEP CLIP2 BMP2 BRCA2 TRNF IFT140 LMNA RP2 REEP6 NDUFS2 PDX1 PDE4D LIG4 RETN CNGA1 GLI2 NDP PNPLA2 EDA CYTB LHX1 PRSS1 NPM1 IFIH1 TBL2 ALMS1 GCK PRPH2 HAMP DCAF17 ABCC8 SNORD115-1 PRPF8 ENPP1 GUCA1B MEN1 MST1 NEUROD1 POMGNT1 HNF4A PTPN1 PPP1R3A FXN AIP KIAA1549 IGF2BP2 NKX2-5 EIF2S3 COX1 SLC29A3 ND5 SUFU CDKN2A HERC2 FXN CYP19A1 STAT3 MKKS SOX2 LIPC INSR GTF2I TDGF1 GCGR HMGA2 TWNK HFE TRNH HLA-DRB1 CORIN PRPF6 ZNF408 FGFR1 PROM1 FOS ZMPSTE24 PEX1 CPA1 HNF4A NPAP1 NDUFAF3 DLL1 BEST1 TRNK TRNL1 POLG CAV1 XRCC4 ND2 TUB CP SLC2A2 KRAS EFL1 NDUFS1 HNF1A SIX3 POLR3A RP9 TRNE AKT2 NODAL PPARG XRCC4 ND1 NDUFS4 GATA6 WRN DCAF17 TTC7A AKT2 RBP3 POC1A PAX4 RTEL1 NDUFA6 TRNS1 KCNJ11 INSR GJB3 INS CASR USP8 MAK FOXC2 FOXP3 HNF1B GATA3 IMPDH1 APOA5 LIPE TRNL1 LEMD3 IL6 PRKAR1A FGFR1 NDN COX1 FAM161A HESX1 INSR NRL NDUFS6 ABCC8 TRNC CFTR GJA1 PRKACA NDUFB9 TRNW COX3 TTPA GPR101 PLAGL1 TIMMDC1 GJA1 WRAP53 RNASEH2A HNF4A COX2 PAX4 FOXRED1 PAX4 DKC1 RRM2B SMAD4 BLK TMEM126B ND5 NDUFAF1 FLT1 KCNJ11 MAFA GATA6 IL2RA CLCNKB NDUFAF2 CTRC PPARG OFD1 IFT172 SPINK1 PRKAR1A RPGR ATM SNORD116-1 OTX2 NDUFA1 ZFYVE26 NDUFB3 BAZ1B PRSS2 BSCL2 ABCC8 INS WFS1 IFT88 PDE6B GAS1 ABCC8 ABCC8 RGR PALLD ND4 STOX1 GNAS NEK2 RFC2 CA4 HYMAI CTRC LIPE RHO MMP14 SCAPER NOP10 ITPR3 GCK SLC19A2 NHP2 HNF1B CRB1 PEX6 TWNK TRNQ NEUROD1 GTF2IRD1 ABCC8 ND6 DNAJC3 POLD1 GJB4 SPINK1 PARN BSCL2 VANGL1 SLC29A3 PDE11A PTPN22 PTF1A BRAF AHR PWRN1 HYMAI TRNV GLRX5 USB1 HLA-DQB1 ITCH SBDS TRNK GPR35 PRSS2 PROK2 STAT1 NSMCE2 CTNS PIK3R1 NDUFAF4 CDHR1 ZFP57 ATP6 TRNW PTF1A CTNNB1 AIP EIF2AK3 POLA1 GCK TRNE ELN NEUROG3 CISD2 GLIS3 DNAJC21 CAVIN1 ELMO2 PTCH1 ROM1 ZFP57 BBS2 LEPR LRP6 KCNJ11 PRKACA PRPF3 SLC25A4 DNM1L GCK HJV LRAT WFS1 HNF1B TP53 PNPLA2 ELN IRS2 NDUFV1 ND6 PRSS1 CERKL CLRN1 PPARG BBS2 MOG TOPORS ARNT2 FOXH1 RAC1 HNF4A PLIN1 TP53 TRNF NDUFB11 EIF2AK3 CFTR SNRPN USH2A KCNJ11 HNF1A STAT3 C8ORF37 APOE FUZ LMNB2 IGF1R TRNS2 LMNA IPW POLG2 PDX1 TERC SLC16A2 INS CAV1 NDUFS7 AR LMNA HGSNAT KLF11 SEMA4A FOXP3 CIDEC CTC1 PLIN1 IDH3B PCNT PEX10 GCK SPINK1 APPL1 HNF1A ZIC2 ABCA4 FBN1 ZNF513 TRNS2 CRX STUB1 NEUROD1 KLHL7 CISD2 PSTPIP1 ALMS1 LMNA PDX1 LIMK1 HNF1A RPE65 BRCA1 RNASEH2B CCDC28B STAT1 AHI1 AIRE ARMC5 NDUFS3 AGBL5 PDE4D TULP1 SHH DHX38 IL2RA HMGA1 CEL NDUFS8 ATM DNAJC3 INS MAGEL2 HNF1A EDA2R HFE MKRN3-AS1 SLC12A3 SLC30A8 UBR1 ND1 IMPG2 KCNJ11 PWAR1 CNOT1 ADAR BLM PDE8B PDX1 HNF4A IRS1 RNASEH2C INSR PIK3R1 CDH23 BBS1 TCF4 ZMPSTE24 ZBTB20 KIZ TINF2 KCTD1 WFS1 SRP54 APPL1 ND3 WFS1 PRSS1 SPATA7 AGPAT2 HBB MERTK WRN KCNJ11 PALB2 HNF1A LMNA PAX4 SARS2 SLC7A14 SOX3 MC4R PDE6G LMNA ARHGEF18 SAG AMACR MTNR1B CP CNBP PLCD1 CTRC FSCN2 TERT SAMHD1 CNGB1
Weight loss
Genes 318
COL5A2 GPC3 MPL COL12A1 BCL10 BIRC3 CCR1 AK2 DNAJC13 SNCA ABCC8 LMNA ERCC4 RBBP8 JAK2 PALLD BRCA2 ND4 RFWD3 RNF168 TYMP HMBS HYMAI PTEN LIPA TYMP HLA-B SLC25A11 SUCLA2 SNCA ATRIP BMPR1A FAN1 TRNQ MPL IRF2BP2 HMGCL CYP24A1 WT1 PML ERCC4 FANCI GCK KDSR GJB4 LRRK2 MECP2 TSHR TET2 RARA HTT MAD2L2 ERCC3 CENPE IFNGR1 NOD2 COL6A2 FANCF SDHA TRAIP HLA-DQB1 NOD2 POLG MDH2 GPR35 FANCA CEP152 HLA-DPA1 IL12B SLX4 CHEK2 SLC11A1 SDHB ERCC5 TRIM37 TRIM28 COL6A3 CDH23 MAFB PANK2 BRCA2 HLA-B TRNF POU6F2 TBL1XR1 FIP1L1 SEMA3C BCL2 JAK2 NDP PALB2 JPH3 BCOR HLA-DPB1 ZFP57 HLCS TP53 FANCE IL10 KCNJ18 SDHD FANCM COL5A1 MAX DIS3L2 BMPR1A TP53 ACAT1 IL12A-AS1 THPO KRT10 IL12A NABP1 MC2R CALR IL23R MST1 FH FANCG PCNT MLH3 CCND1 JPH3 TMEM127 ND6 SLC39A4 NUMA1 WT1 SDHC SDHA ACADM ND5 AVP DLST SEMA3D TP53 TRPV4 TSHR FLI1 EIF2AK3 PMS1 SDHB CDKN2A STAT3 PRNP NBN POLG ECE1 DCTN1 REST CACNA1S SDHAF1 ATP7B KCNJ11 NRTN IGH F5 STAT3 PTPN22 TXNRD2 TRIP13 AKT1 FOXP1 JAK2 MLH1 TRNH HLA-DRB1 PMS2 SDHAF2 PDX1 INS LRP12 NNT SLC9A6 RRM2B FOXP3 DCTN1 ERAP1 TP53 SLC52A3 TRNL1 STAT6 PRNP GATA4 MSH6 RET KIF1B ERCC4 FANCB KRAS RAD51 IGH VHL FANCD2 VPS13A KRAS TRNS2 MSH2 BCL6 SDHC GATA2 EDNRB ATM PRKAR1A BRCA1 RHBDF2 PIK3CA KRT1 TRNS1 GBA CACNA1S INSR GJB3 SDHD CTLA4 NPM1 IL6 RPS20 BRCA1 XRCC2 KCNJ18 GALT H19 MPL HAVCR2 TRIM28 BRCA2 GDNF FAS COL1A1 WT1 HLA-DRB1 TLR4 PTPN22 HSPG2 COX1 STAT4 IKZF1 CNTNAP1 ATRX ABCC8 STAR DAXX MRAP CCND1 TET2 POLG EWSR1 CDC73 GJA1 EDN3 ND1 CENPJ NAB2 IGH LPIN2 FANCL SLC52A2 HLA-DRB1 TRNW HLA-DRB1 COX3 GIGYF2 SDHD PIK3R1 B2M EPCAM TCF4 PLAGL1 TGFB1 PRNP KLRC4 PLK4 KIF1B TGFBR2 SEMA4A SCNN1B UBAC2 BTK HLA-B COX2 CFTR SDHB ATR TTR GNPTAB PLA2G6 C4A RET SMAD4 SCNN1A ERCC2 UNC80 BTNL2 FANCC PTEN MALT1 SCNN1G PALB2 BRIP1 RB1 EIF4G1 MEFV GABRA3 CUL4B PTEN ZBTB16 KCNJ11 VPS35 COL6A1 PRTN3 RAD51C UBE2T RRM2B STAT5B SLC6A8 JAK2 MLX
Insulin resistance
Genes 122
LIPC KCNJ11 HNF1A GCGR STAT3 BSCL2 HSD3B2 ABCC8 AGPAT2 INS LMNA LMNB2 LMNA PDX1 ABCC8 ABCC8 INS CAV1 FOS ZMPSTE24 LMNA HYMAI LIPE BSCL2 CIDEC PLIN1 PPARG HYMAI CAV1 XRCC4 ADCY3 SLC2A2 CEP19 IGFALS LMNA MAPK8IP1 TCF7L2 DBH NEUROD1 NSMCE2 AKT2 PPARG XRCC4 IGF1 GATA6 NEUROD1 GCK AKT2 POLD1 PAX4 BSCL2 ALMS1 LMNA PDX1 PMM2 KCNJ11 HNF1A PTF1A HYMAI PLAGL1 HNF1B KLF11 NSMCE2 PIK3R1 BLK LIPE KCNJ11 GPD2 HMGA1 CEL INSR INSR ZFP57 CAV1 LEP ABCC8 SLC12A3 SLC30A8 EIF2AK3 LMNA GCK PDX1 RETN PDX1 CAVIN1 HNF4A IRS1 PIK3R1 ZFP57 PLAGL1 LEPR KCNJ11 ZMPSTE24 GCK MFN2 WFS1 ALMS1 APPL1 DCAF17 ABCC8 PAX4 ZMPSTE24 HSD11B1 AGPAT2 ENPP1 IRS2 HNF4A WRN PTPN1 PPP1R3A LMNA PAX4 PPARG IGF2BP2 KCNJ11 LMNA MTNR1B CLCNKB PPARG CAVIN1 EIF2AK3 CYP19A1
Type I diabetes mellitus
Genes 51
COX1 EDA2R TRNF SLC12A3 TRNH CFTR CORIN EIF2AK3 ND1 SLC16A2 MMP2 TRNE NEUROG3 DNAJC21 CNOT1 ND4 STOX1 TRNW COX3 FOXP3 TRNL1 EDA MMP14 PRSS1 TCF4 HNF1A EFL1 KCTD1 COX2 SRP54 TRNQ TRNS2 STUB1 DNAJC3 MST1 TTC7A ND6 PSTPIP1 FLT1 TRNS1 INS CLCNKB ND5 CTRC ITCH SBDS FOXP3 AIRE SPINK1 GPR35 STAT1