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Additional Online Content AvailableGastric Bypass Increases Energy Expenditure in Rats

Marco BueterCorresponding Author Informationemail address, Christian Löwenstein§, Torsten Olbers, Maggie Wang, Nina L. Cluny, Stephen R. Bloom, Keith A. Sharkey, Thomas A. Lutz§, Carel W. Le Roux

Received 29 May 2009; accepted 6 November 2009. published online 19 November 2009.
Corrected Proof

Background & Aims

Mechanisms underlying weight loss maintenance after gastric bypass are poorly understood. Our aim was to examine the effects of gastric bypass on energy expenditure in rats.

Methods

Thirty diet-induced obese male Wistar rats underwent either gastric bypass (n = 14), sham-operation ad libitum fed (n = 8), or sham-operation body weight-matched (n = 8). Energy expenditure was measured in an open circuit calorimetry system.

Results

Twenty-four-hour energy expenditure was increased after gastric bypass (4.50 ± 0.04 kcal/kg/h) compared with sham-operated, ad libitum fed (4.29 ± 0.08 kcal/kg/h) and sham-operated, body weight-matched controls (3.98 ± 0.10 kcal/kg/h, P < .001). Gastric bypass rats showed higher energy expenditure during the light phase than sham-operated control groups (sham-operated, ad libitum fed: 3.63 ± 0.04 kcal/kg/h vs sham-operated, body weight-matched: 3.42 ± 0.05 kcal/kg/h vs bypass: 4.12 ± 0.03 kcal/kg/h, P < .001). Diet-induced thermogenesis was elevated after gastric bypass compared with sham-operated, body weight-matched controls 3 hours after a test meal (0.41% ± 1.9% vs 10.5% ± 2.0%, respectively, P < .05). The small bowel of gastric bypass rats was 72.1% heavier because of hypertrophy compared with sham-operated, ad libitum fed rats (P < .0001).

Conclusions

Gastric bypass in rats prevented the decrease in energy expenditure after weight loss. Diet-induced thermogenesis was higher after gastric bypass compared with body weight-matched controls. Raised energy expenditure may be a mechanism explaining the physiologic basis of weight loss after gastric bypass.

Abbreviations used in this paperARC, arcuate nucleus, NPY, neuropeptide Y, POMC, pro-opiomelanocortin, PYY, peptide YY

 Department of Investigative Medicine, Hammersmith Hospital, Imperial College London, London, United Kingdom

 Department of Surgery, University of Würzburg, Würzburg, Germany

§ Institute of Veterinary Physiology and Zürich Centre for Integrative Human Physiology, Vetsuisse Faculty University of Zurich, Zurich, Switzerland

 Snyder Institute of Infection, Immunity and Inflammation, Hotchkiss Brain Institute and Department of Physiology and Pharmacology, University of Calgary, Calgary, Alberta, Canada

Corresponding Author InformationReprint requests Address requests for reprints to: Carel le Roux, MD, PhD, Imperial Weight Centre, Imperial College London, W6 8RF, United Kingdom. fax: (44) 0 20 83838320

 Conflicts of interest The authors disclose no conflicts.

 Funding Supported by the Deutsche Forschungsgemeinschaft (DFG; to M.B.); by the Swiss National Research Foundation (to T.L., C.L.); by a Department of Health Clinician scientist award (to S.B. and C.le R.); support from the NIHR Biomedical Research Centre funding scheme to Imperial College London; by the Markin Undergraduate Student Research Program (to M.W.); and from Canadian Institutes of Health Research (to K.A.S.).

PII: S0016-5085(09)02002-2

doi:10.1053/j.gastro.2009.11.012

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