Charlotte de Jonge1,2, Sander S Rensen3, Froukje J Verdam4, Royce P Vincent5, Steve R Bloom6, Wim A Buurman7, Carel W le Roux8,9, Nicole D Bouvy10, Jan Willem M Greve11,12. 1. Department of General Surgery and NUTRIM School for Nutrition, Toxicology and Metabolism, Maastricht University Medical Center, P. Debyelaan 25, 6229 HX, Maastricht, The Netherlands. c.dejonge@maastrichtuniversity.nl. 2. Department of General Surgery, Atrium Medical Center Parkstad, Henri Dunantstraat 5, 6419 PC, Heerlen, The Netherlands. c.dejonge@maastrichtuniversity.nl. 3. Department of General Surgery and NUTRIM School for Nutrition, Toxicology and Metabolism, Maastricht University Medical Center, P. Debyelaan 25, 6229 HX, Maastricht, The Netherlands. s.rensen@maastrichtuniversity.nl. 4. Department of General Surgery and NUTRIM School for Nutrition, Toxicology and Metabolism, Maastricht University Medical Center, P. Debyelaan 25, 6229 HX, Maastricht, The Netherlands. F.J.Verdam@umcutrecht.nl. 5. Department of Clinical Biochemistry, King's College Hospital NHS Foundation Trust, Denmark Hill, SE5 9RS, London, UK. royce.vincent@nhs.net. 6. Department of Medicine, Imperial College London, Du Cane Road, W12 0NN, London, UK. s.bloom@imperial.ac.uk. 7. School for Mental Health and Neuroscience, Maastricht University Medical Center, P. Debyelaan 25, 6229 HX, Maastricht, The Netherlands. w.buurman@maastrichtuniversity.nl. 8. Department of Medicine, Imperial College London, Du Cane Road, W12 0NN, London, UK. carel.leroux@ucd.ie. 9. Department of Experimental Pathology, UCD Conway Institute, School of Medicine and Medical Science, University College Dublin, Belfield Dublin 4, Dublin, Ireland. carel.leroux@ucd.ie. 10. Department of General Surgery and NUTRIM School for Nutrition, Toxicology and Metabolism, Maastricht University Medical Center, P. Debyelaan 25, 6229 HX, Maastricht, The Netherlands. n.bouvy@maastrichtuniversity.nl. 11. Department of General Surgery, Atrium Medical Center Parkstad, Henri Dunantstraat 5, 6419 PC, Heerlen, The Netherlands. j.greve@atriummc.nl. 12. Department of General Surgery, Atrium Medical Center Parkstad, PO box 4446, 6401 CX, Heerlen, The Netherlands. j.greve@atriummc.nl.
Abstract
OBJECTIVE: Bariatric procedures that exclude the proximal small intestine lead to significant weight loss which is probably mediated by changes in hormones that alter appetite, such as peptide YY (PYY), ghrelin, cholecystokinin (CCK), and leptin. Here, the effect of the non-surgical duodenal-jejunal bypass liner (DJBL) on concentrations of hormones implicated in appetite control was investigated. SUBJECTS: A two-center prospective study was conducted between January and December 2010. Seventeen obese subjects with type 2 diabetes were treated with the DJBL for 24 weeks. Fasting concentrations of leptin and meal responses of plasma PYY, CCK, and ghrelin were determined prior to and after implantation of the DJBL. RESULTS: At baseline, subjects had an average body weight of 116.0 ± 5.8 kg. One week after implantation, subjects had lost 4.3 ± 0.6 kg (p < 0.01), which progressed to 12.7 ± 1.3 kg at week 24 (p < 0.01). Postprandial concentrations of PYY and ghrelin increased (baseline vs. week 1 vs. week 24 PYY: 2.6 ± 0.2 vs. 4.1 ± 0.4 vs. 4.1 ± 0.7 nmol/L/min and ghrelin: 7.8 ± 1.8 vs. 11.0 ± 1.8 vs. 10.6 ± 1.8 ng/mL/min, all p < 0.05). In parallel, the CCK response decreased (baseline vs. week 1 vs. week 24: 434 ± 51 vs. 229 ± 52 vs. 256 ± 51 pmol/L/min, p < 0.01). Fasting leptin concentrations also decreased (baseline vs. week 24: 98 ± 17 vs. 53 ± 10 ng/mL, p < 0.01). CONCLUSIONS: DJBL treatment induces weight loss paralleled by changes in concentrations of hormones involved in appetite control.
OBJECTIVE: Bariatric procedures that exclude the proximal small intestine lead to significant weight loss which is probably mediated by changes in hormones that alter appetite, such as peptide YY (PYY), ghrelin, cholecystokinin (CCK), and leptin. Here, the effect of the non-surgical duodenal-jejunal bypass liner (DJBL) on concentrations of hormones implicated in appetite control was investigated. SUBJECTS: A two-center prospective study was conducted between January and December 2010. Seventeen obese subjects with type 2 diabetes were treated with the DJBL for 24 weeks. Fasting concentrations of leptin and meal responses of plasma PYY, CCK, and ghrelin were determined prior to and after implantation of the DJBL. RESULTS: At baseline, subjects had an average body weight of 116.0 ± 5.8 kg. One week after implantation, subjects had lost 4.3 ± 0.6 kg (p < 0.01), which progressed to 12.7 ± 1.3 kg at week 24 (p < 0.01). Postprandial concentrations of PYY and ghrelin increased (baseline vs. week 1 vs. week 24 PYY: 2.6 ± 0.2 vs. 4.1 ± 0.4 vs. 4.1 ± 0.7 nmol/L/min and ghrelin: 7.8 ± 1.8 vs. 11.0 ± 1.8 vs. 10.6 ± 1.8 ng/mL/min, all p < 0.05). In parallel, the CCK response decreased (baseline vs. week 1 vs. week 24: 434 ± 51 vs. 229 ± 52 vs. 256 ± 51 pmol/L/min, p < 0.01). Fasting leptin concentrations also decreased (baseline vs. week 24: 98 ± 17 vs. 53 ± 10 ng/mL, p < 0.01). CONCLUSIONS: DJBL treatment induces weight loss paralleled by changes in concentrations of hormones involved in appetite control.
Entities:
Keywords:
Bariatric surgery; Gut hormones; Obesity; Satiety
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