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The role of central reward and satiety centers in the etiology of obesity: genetic and environmental influences

The role of central reward and satiety centers in the etiology of obesity: genetic and environmental influences - Obesity and Brain: Genes and Environment

Status
Active, not recruiting
Phases
Unknown
Study type
Observational
Source
NL-OMON
Registry ID
NL-OMON40336
Enrollment
90
Registered
2013-10-28
Start date
2014-01-04
Completion date
Unknown
Last updated
2024-04-29

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

obestas Obesity overweight

Interventions

None listed

Sponsors

Vrije Universiteit Medisch Centrum
Lead Sponsor

Eligibility

Age
18 Years to 99 Years

Inclusion criteria

Inclusion criteria: For all participants (study 1 and study 2): - Age 18-65 years - Male or female - Stable bodyweight ( 3kg/m2 between cotwins);For participants in study 2 (60 subjects): - Available information on genetic material as well as body weight - 15 Subjects with calculated low genetic predisposition risk for obesity and low BMI - 15 Subjects with calculated low genetic predisposition risk for obesity and high BMI - 15 Subjects with calculated high genetic predisposition risk for obesity and low BMI - 15 Subjects with calculated high genetic predisposition risk for obesity and high BMI

Exclusion criteria

Exclusion criteria: - Self reported type 2 diabetes mellitus - Irregularity of menstruation in premenopausal females defined as: cycle lengths shorter than 21 or longer than 35 days and/or menses periods shorter than 2 or longer than 8 days - Neurological illness - Psychiatric illness including eating disorders and depression - Malignancy - Pregnancy or breast feeding - Alcohol abuse defined as: for men > 21 units/week, for women > 14 units/week - History of claustrophobia or presence of metal objects/implants (because of MRI protocol) - Current or chronic use of the following medication: weight lowering agents (within 3 months before screening); antihyperglycemic agents (within 3 months before screening); glucocorticoids, centrally acting drugs, cytostatic drugs or immunomodulatory agents (alle of these within 2 weeks immediately prior to screening, because of the possible effects on cerebral functioning); opiates, narcotics, tranquilizers, and other potentially addictive medications - Visual disability, not correctable with glasses or contact lenses - Inability to understand the study protocol and/or inability to give informed consent

Design outcomes

Primary

MeasureTime frame
Study 1: The difference in neuronal activity in CNS reward and satiety circuits (including striatum, amygdala, orbitofrontal cortex, insula, hypothalamus) as represented by BOLD fMRI signal change from baseline (%) in response to food-related stimuli within 15 obesity discordant MZ twin pairs. Study 2: a. The difference in neuronal activity in CNS reward and satiety circuits (including striatum, amygdala, orbitofrontal cortex, insula, hypothalamus) as represented by BOLD fMRI signal change from baseline (%) in response to food-related stimuli between individuals at high verses those at low genetic obesity risk based on measured risk alleles from genome wide association studies. b. The difference in neuronal activity in CNS reward and satiety circuits (including striatum, amygdala, orbitofrontal cortex, insula, hypothalamus) as represented by BOLD fMRI signal change from baseline (%) in response to food-related stimuli between lean and obese subjects with either high or low genetic obesity risk.

Secondary

MeasureTime frame
Secondary study parameters (study 1 and study 2): We will investigate the influence of environment and genetics on the following potential underlying mechanisms by performing additional tests in study 1 and study 2 respectively: 1. eating behavior measured as quantitative (kcal) and qualitative (energy density, macronutrient composition) dietary intake using a choice lunch buffet on the visit day and assessing dietary habits at home using the 24 hours recall method on two week days and one weekend day at home; 2. physical activity measured as metabolic equivalent of task (METs)-hours per week using seven-day ActiGraph triaxial accelerometry at home and using available longitudinal data from NTR surveys; 3. basal metabolic rate measured in kcal/day using oxygen consumption and carbon dioxide production measured with indirect calorimetry; 4. fasting plasma biomarkers (glucose, insulin, glucagon) measured in a fasting blood sample; 5. autonomic nervous system balance assessment based on measurements of heart rate variability (HRV), respiratory rate (RR) and respiratory sinus arrhythmia (RSA) using a portable electro- and impedance cardiogram (VU University Ambulatory Monitoring System, VU-AMS). Exploratory study parameters (study 1 and study 2): Conditional to available budget we will investigate the influence of environment and genetics on the following potential underlying mechanisms by performing additional tests in study 1 and study 2 respectively: 1. gut microbiota composition assessed by identifying microbial phylotypes using 16S rRNA molecule-based approaches of diagnostic analysis on collected fecal samples; 2. epigenetic changes by measuring DNA methylation in a blood sample; 3. exploratory fasting plasma biomarkers (leptin, GLP-1, PYY and ghrelin) will be determined in a fasting blood sample; 4. white matter tract integrity, functional connectivity of the brain and metabolic changes in the hypothalamus will be investigated using

Countries

Netherlands

Outcome results

None listed

Source: NL-OMON (via WHO ICTRP)