Sympathetic support of energy expenditure and sympathetic nervous system activity after gastric bypass surgery

Objective: This study was designed to determine how gastric bypass affects the sympathetically‐mediated component of resting energy expenditure (REE) and muscle sympathetic nerve activity (MSNA). Design and Methods: We measured REE before and after beta‐blockade in seventeen female subjects approxim...

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Published in:Obesity (Silver Spring, Md.) Md.), 2013-03, Vol.21 (3), p.480-485
Main Authors: Curry, Timothy B., Somaraju, Madhuri, Hines, Casey N., Groenewald, Cornelius B., Miles, John M., Joyner, Michael J., Charkoudian, Nisha
Format: Article
Language:English
Subjects:
Abdomen
Adolescent
Adult
Age
Aldosterone - blood
Basal Metabolism - physiology
Behavior
Blood Glucose - analysis
Body Composition
Body Mass Index
Catheters
Cholesterol - blood
Energy Metabolism - physiology
Epinephrine - blood
Fasting
Female
Gastric Bypass - methods
Gastrointestinal surgery
Heart surgery
Humans
Insulin Resistance
Leptin - blood
Linear Models
Metabolism
Muscle, Skeletal - metabolism
Nervous system
Norepinephrine - blood
Obesity
Obesity - surgery
Overweight - surgery
Studies
Sympathetic Nervous System - physiology
Triglycerides - blood
Weight control
Weight Loss
Young Adult
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Summary:Objective: This study was designed to determine how gastric bypass affects the sympathetically‐mediated component of resting energy expenditure (REE) and muscle sympathetic nerve activity (MSNA). Design and Methods: We measured REE before and after beta‐blockade in seventeen female subjects approximately three years post‐gastric bypass surgery and in nineteen female obese individuals for comparison. We also measured MSNA in a subset of these subjects. Results: The gastric bypass subjects had no change in REE after systemic beta‐blockade, reflecting a lack of sympathetic support of REE, in contrast to obese subjects where REE was reduced by beta‐blockade by approximately 5% (P < 0.05). The gastric bypass subjects, while still overweight (BMI = 29.3 vs 38.0 kg·m−2 for obese subjects, P < 0.05), also had significantly lower MSNA compared to obese subjects (10.9 ± 2.3 vs. 21.9 ± 4.1 bursts·min−1, P < 0.05). The reasons for low MSNA and a lack of sympathetically mediated support of REE after gastric bypass are likely multifactorial and may be related to changes in insulin sensitivity, body composition, and leptin, among other factors. Conclusions: These findings may have important consequences for the maintenance of weight loss after gastric bypass. Longitudinal studies are needed to further explore the changes in sympathetic support of REE and if changes in MSNA or tissue responsiveness are related to the sympathetic support of REE.
ISSN:1930-7381
1930-739X
DOI:10.1002/oby.20106