Emma C E Meessen1, Guido J Bakker2, Max Nieuwdorp2, Geesje M Dallinga-Thie2, E Marleen Kemper3, Steven W Olde Damink4, Johannes A Romijn5, Bolette Hartmann6, Jens J Holst6, Filip K Knop7, Albert K Groen2, Frank G Schaap4, Maarten R Soeters8. 1. Department of Endocrinology and Metabolism, Amsterdam Gastroenterology Endocrinology Metabolism, Amsterdam University Medical Centers - Location AMC, University of Amsterdam, Amsterdam, the Netherlands. 2. Department of Vascular Medicine, Amsterdam University Medical Centers - Location AMC, University of Amsterdam, Amsterdam, the Netherlands. 3. Department of Hospital Pharmacy, Amsterdam University Medical Centers - Location AMC, University of Amsterdam, Amsterdam, the Netherlands. 4. Department of Surgery, NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University, the Netherlands; Department of General, Visceral and Transplantation Surgery, RWTH University Hospital Aachen, Germany. 5. Department of Internal Medicine, Amsterdam University Medical Centers - Location AMC, University of Amsterdam, Amsterdam, the Netherlands. 6. Department of Biomedical Sciences and NNF Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark; Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark. 7. Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark; Center for Clinical Metabolic Research, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark; Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark; Steno Diabetes Center Copenhagen, Gentofte, Denmark. 8. Department of Endocrinology and Metabolism, Amsterdam Gastroenterology Endocrinology Metabolism, Amsterdam University Medical Centers - Location AMC, University of Amsterdam, Amsterdam, the Netherlands. Electronic address: m.r.soeters@amsterdamumc.nl.
Abstract
BACKGROUND & AIMS: To investigate the acute effects of intravenous vs enteral meal administration on circulating bile acid and gut hormone responses. METHODS: In a randomized crossover design, we compared the effects of duodenal (via a nasoduodenal tube) vs parenteral (intravenous) administration over 180 min of identical mixed meals on circulating bile acid and gut hormone concentrations in eight healthy lean men. We analysed the bile acid and gut hormone responses in two periods: the intraprandial period from time point (T) 0 until T180 during meal administration and the postprandial period from T180 until T360, after discontinuation of meal administration. RESULTS: Intravenous meal administration decreased the intraprandial (AUC (μmol/L∗min) duodenal 1469 ± 284 vs intravenous 240 ± 39, p < 0.01) and postprandial bile acid response (985 ± 240 vs 223 ± 5, p < 0.05) and was accompanied by decreased gut hormone responses including glucose-dependent insulinotropic polypeptide, glucagon-like peptide 1, glucagon-like peptide 2 and fibroblast growth factor 19. Furthermore, intravenous meal administration elicited greater glucose concentrations, but similar insulin concentrations compared to enteral administration. CONCLUSIONS: Compared to enteral administration, parenteral nutrition results in lower postprandial bile acid and gut hormone responses in healthy lean men. This was accompanied by higher glucose concentrations in the face of similar insulin concentrations exposing a clear incretin effect of enteral mixed meal administration. The alterations in bile acid homeostasis were apparent after only one intravenous meal.
RCT Entities:
BACKGROUND & AIMS: To investigate the acute effects of intravenous vs enteral meal administration on circulating bile acid and gut hormone responses. METHODS: In a randomized crossover design, we compared the effects of duodenal (via a nasoduodenal tube) vs parenteral (intravenous) administration over 180 min of identical mixed meals on circulating bile acid and gut hormone concentrations in eight healthy lean men. We analysed the bile acid and gut hormone responses in two periods: the intraprandial period from time point (T) 0 until T180 during meal administration and the postprandial period from T180 until T360, after discontinuation of meal administration. RESULTS: Intravenous meal administration decreased the intraprandial (AUC (μmol/L∗min) duodenal 1469 ± 284 vs intravenous 240 ± 39, p < 0.01) and postprandial bile acid response (985 ± 240 vs 223 ± 5, p < 0.05) and was accompanied by decreased gut hormone responses including glucose-dependent insulinotropic polypeptide, glucagon-like peptide 1, glucagon-like peptide 2 and fibroblast growth factor 19. Furthermore, intravenous meal administration elicited greater glucose concentrations, but similar insulin concentrations compared to enteral administration. CONCLUSIONS: Compared to enteral administration, parenteral nutrition results in lower postprandial bile acid and gut hormone responses in healthy lean men. This was accompanied by higher glucose concentrations in the face of similar insulin concentrations exposing a clear incretin effect of enteral mixed meal administration. The alterations in bile acid homeostasis were apparent after only one intravenous meal.
Authors: Jennifer L LaBarre; Emily Hirschfeld; Tanu Soni; Maureen Kachman; Janis Wigginton; William Duren; Johanna Y Fleischman; Alla Karnovsky; Charles F Burant; Joyce M Lee Journal: Nutrients Date: 2021-09-25 Impact factor: 5.717
Authors: Rob J J van Gassel; Marcel C G van de Poll; Frank G Schaap; Mark Plummer; Adam Deane; Steven W M Olde Damink Journal: JPEN J Parenter Enteral Nutr Date: 2021-05-06 Impact factor: 3.896