Disclosure: The authors declared no conflict of interest.
Article first published online: 16 APR 2013
Copyright © 2013 The Obesity Society
Volume 21, Issue 3, pages 480–485, March 2013
How to Cite
Curry, T. B., Somaraju, M., Hines, C. N., Groenewald, C. B., Miles, J. M., Joyner, M. J. and Charkoudian, N. (2013), Sympathetic support of energy expenditure and sympathetic nervous system activity after gastric bypass surgery. Obesity, 21: 480–485. doi: 10.1002/oby.20106
Funding agencies: The project described was supported by the Mayo Foundation for Medical Education and Research and NIH Grant Numbers K23 DK82424, R01 HL67933, R01 HL083947, and UL1 RR024150.
Current address for author Dr. Nisha Charkoudian: Thermal & Mountain Medicine Division, US Army Research Institute of Environmental Medicine, Kansas Street, Bldg 42, Natick, MA 01760-5007.
- Issue published online: 16 APR 2013
- Article first published online: 16 APR 2013
- Accepted manuscript online: 24 OCT 2012 09:13AM EST
- Manuscript Accepted: 24 AUG 2012
- Manuscript Received: 8 FEB 2012
- The Mayo Foundation for Medical Education
- Research and NIH. Grant Numbers: K23 DK82424, R01 HL67933, R01 HL083947, UL1 RR024150
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.
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.
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.