J C Espinós1, R Turró1, G Moragas2, A Bronstone3, J N Buchwald3, F Mearin1, A Mata1, H Uchima1, J Turró1, S Delgado-Aros4. 1. Unidad de Endoscopia, Centro Médico Teknon, Barcelona, Catalonia, Spain. 2. CETIR Grup Médic Barcelona, Barcelona, Catalonia, Spain. 3. Division of Scientific Research Writing, Medwrite Medical Communications, Maiden Rock, WI, USA. 4. Neuro-Enteric Translational Science (NETS) Research Group, Institut Hospital del Mar d'Investigacions Mèdiques. IMIM-Parc de Salut Mar. PRBB, c/ Dr. Aiguader, 88, 08003, Barcelona, Catalonia, Spain. delgadoaross@gmail.com.
Abstract
BACKGROUND: Primary Obesity Surgery Endolumenal (POSE) is a novel bariatric endoscopic procedure that has been shown to reduce weight safely through 12 months. The study investigated potential mechanisms of weight loss following POSE. METHODS: Patients with class I-II obesity received transmural plications in the gastric fundus and distal gastric body. Patients were evaluated at baseline and at 2- and 6-month follow-up with gastric-emptying (GE) scintigraphy, a validated test of intake capacity (kcal) and plasma glucose homeostasis hormones/gastrointestinal peptides. Weight was recorded through 15 months. Mean data and 95% CIs are reported. Regression modeling assessed variables that influenced total weight loss (%TWL) and excess weight loss (%EWL). RESULTS: POSE was performed on 18 patients (14 F/4 M); mean age 39 years (34-44), body mass index (BMI, kg/m(2)) 36 (95% CI, 35; 37). At 15 months (n = 15), mean TWL was 19.1 ± 6.6% (15.5; 22.8) and EWL was 63.7 ± 25.1% (49.8; 77.6). At 2 and 6 months (n = 18), intake capacity decreased significantly from 901 (685; 1117) to 473 (345; 600) and 574 kcal (418; 730), respectively (p < 0.001). At 2 months, GE was delayed but returned to baseline levels at 6 months (n = 18). Glucose/insulin ratio improved (p < 0.05). Postprandial decrease in ghrelin was enhanced (p = 0.03) as well as postprandial increase in PYY (p = 0.001). The best model for EWL prediction 15 months after POSE (R (2): 66%, p = 0.006) included pre-POSE BMI, post-POSE GE, and postprandial PYY increase. CONCLUSIONS: The POSE procedure was followed by significant sustained weight loss and improved glucose homeostasis and satiation peptide responses. Weight loss following POSE may be mediated through changes in gastrointestinal neuro-endocrine physiology.
BACKGROUND: Primary Obesity Surgery Endolumenal (POSE) is a novel bariatric endoscopic procedure that has been shown to reduce weight safely through 12 months. The study investigated potential mechanisms of weight loss following POSE. METHODS:Patients with class I-II obesity received transmural plications in the gastric fundus and distal gastric body. Patients were evaluated at baseline and at 2- and 6-month follow-up with gastric-emptying (GE) scintigraphy, a validated test of intake capacity (kcal) and plasma glucose homeostasis hormones/gastrointestinal peptides. Weight was recorded through 15 months. Mean data and 95% CIs are reported. Regression modeling assessed variables that influenced total weight loss (%TWL) and excess weight loss (%EWL). RESULTS: POSE was performed on 18 patients (14 F/4 M); mean age 39 years (34-44), body mass index (BMI, kg/m(2)) 36 (95% CI, 35; 37). At 15 months (n = 15), mean TWL was 19.1 ± 6.6% (15.5; 22.8) and EWL was 63.7 ± 25.1% (49.8; 77.6). At 2 and 6 months (n = 18), intake capacity decreased significantly from 901 (685; 1117) to 473 (345; 600) and 574 kcal (418; 730), respectively (p < 0.001). At 2 months, GE was delayed but returned to baseline levels at 6 months (n = 18). Glucose/insulin ratio improved (p < 0.05). Postprandial decrease in ghrelin was enhanced (p = 0.03) as well as postprandial increase in PYY (p = 0.001). The best model for EWL prediction 15 months after POSE (R (2): 66%, p = 0.006) included pre-POSE BMI, post-POSE GE, and postprandial PYY increase. CONCLUSIONS: The POSE procedure was followed by significant sustained weight loss and improved glucose homeostasis and satiation peptide responses. Weight loss following POSE may be mediated through changes in gastrointestinal neuro-endocrine physiology.
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