Effects of Sleep Restriction on BAT Activation in Humans



Status:Recruiting
Conditions:Insomnia Sleep Studies, Obesity Weight Loss
Therapuetic Areas:Endocrinology, Psychiatry / Psychology
Healthy:No
Age Range:20 - 49
Updated:2/1/2017
Start Date:January 2016
End Date:December 2017
Contact:Marie-Pierre St-Onge, Ph.D
Email:ms2554@cumc.columbia.edu
Phone:212-851-5578

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The goal of this proposed research is to test the hypothesis that long-term mild sleep
restriction (SR), as occurs frequently in adults and adolescents, leads to a positive energy
balance and weight gain.

Aim 1. To determine the effects of SR, relative to habitual sleep (HS), on food choice and
energy intake (EI) in adults at risk of obesity.

- Hypothesis 1a. EI, assessed by multiple weekly 24-hour recalls, will be greater during
a period of SR relative to HS. This will be mostly due to increased fat and
carbohydrate intakes.

- Hypothesis 1b. Neuronal responses to food stimuli, assessed by functional MRI (fMRI)
after 6 weeks of SR or HS, will indicate increased activity in networks associated with
reward and food valuation (insula, orbitofrontal cortex) during a period of SR relative
to HS. These responses will be correlated with intakes of high carbohydrate and high
fat foods (hypothesis 1a) and neuropeptide Y (NPY). Moreover, activation of the default
mode network (DMN) will be suppressed to a lesser extent after SR compared to HS.

Aim 2. To determine the effects of SR, relative to HS, on energy expenditure (EE) via
independent and complementary approaches.

- Hypothesis 2a. EE, assessed by doubly-labeled water (DLW), and physical activity level,
monitored daily by actigraphy, will be lower during SR relative to HS.

- Hypothesis 2b. Brown adipose tissue (BAT), assessed by positron emission tomography and
magnetic resonance combined scanner (PET/MR) using 18F-fluorodeoxyglucose (18FDG-PET)
and fat fraction (FF) measurement under cold stimulation, will be greater after SR
relative to HS. This would suggest higher adaptive thermogenesis after SR compared to
HS. BAT activation will also be correlated with NPY.

Aim 3. To determine whether SR alters body weight and adiposity relative to HS.

- Hypothesis 3a. SR will lead to weight gain and increased total adiposity, as assessed
using magnetic resonance imaging (MRI), relative to HS.

- Hypothesis 3b. Increased adiposity after SR will be correlated to an adverse
cardio-metabolic risk profile (increased glucose, insulin, triglycerides, leptin,
reduced high-density lipoprotein cholesterol and adiponectin) and neuronal responses to
food stimuli (Hypothesis 1b), and EE (Hypothesis 2a & 2b). Failure to stimulate BAT
with SR will be associated with greater gain in adiposity.

There is an association between short sleep duration (SSD) and obesity. Moreover, short
sleepers (<7 hours sleep/night) gain more weight over time than normal sleepers (7-8 hours
sleep/night). These relationships are increasingly supported by clinical data showing that
restricting sleep duration in healthy, normal weight adults, increases energy intake (EI).

Inclusion Criteria:

- Normal scores on:

- Pittsburgh Quality of Sleep Questionnaire

- Epworth Sleepiness Scale

- Berlin Questionnaire

- Sleep Disorders Inventory Questionnaire

- Beck Depression Inventory

- Composite Scale of Morningness/Eveningness

- Three Factor Eating Questionnaire

- Sleep 7-9 hours in bed/night with no daytime nap

- Age 20-49 years, premenopausal women

- All racial/ethnic groups

- Body mass index 25-29.9 kg/m2

Exclusion Criteria:

- Smokers (any cigarettes or ex-smoker <3 years)

- Neurological, medical or psychiatric disorder, diabetics

- Eating and/or sleep disorders

- Contraindications for MRI scanning

- Travel across time zones within 4 weeks

- History of drug and alcohol abuse

- Shift worker (or rotating shift worker)

- Caffeine intake >300 mg/d

- Pregnancy or within 1 y post-partum

- Heavy equipment operators Commercial long-distance drivers
We found this trial at
1
site
New York, New York 10032
Principal Investigator: Marie-Pierre St-Onge, Ph. D.
Phone: 212-851-5578
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New York, NY
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