Impact of oral vancomycin on gut microbiota, bile acid metabolism, and insulin sensitivity
Obesity has been associated with changes in the composition and function of the intestinal microbiota. Modulation of the microbiota by antibiotics also alters bile acid and glucose metabolism in mice. Hence, we hypothesized that short term administration of oral antibiotics in humans would affect fe...
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| Published in | Journal of hepatology Vol. 60; no. 4; pp. 824 - 831 |
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| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Netherlands
Elsevier B.V
01.04.2014
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| Subjects | |
| Online Access | Get full text |
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| Abstract | Obesity has been associated with changes in the composition and function of the intestinal microbiota. Modulation of the microbiota by antibiotics also alters bile acid and glucose metabolism in mice. Hence, we hypothesized that short term administration of oral antibiotics in humans would affect fecal microbiota composition and subsequently bile acid and glucose metabolism.
In this single blinded randomized controlled trial, 20 male obese subjects with metabolic syndrome were randomized to 7days of amoxicillin 500mg t.i.d. or 7days of vancomycin 500mg t.i.d. At baseline and after 1week of therapy, fecal microbiota composition (Human Intestinal Tract Chip phylogenetic microarray), fecal and plasma bile acid concentrations as well as insulin sensitivity (hyperinsulinemic euglycemic clamp using [6,6-2H2]-glucose tracer) were measured.
Vancomycin reduced fecal microbial diversity with a decrease of gram-positive bacteria (mainly Firmicutes) and a compensatory increase in gram-negative bacteria (mainly Proteobacteria). Concomitantly, vancomycin decreased fecal secondary bile acids with a simultaneous postprandial increase in primary bile acids in plasma (p<0.05). Moreover, changes in fecal bile acid concentrations were predominantly associated with altered Firmicutes. Finally, administration of vancomycin decreased peripheral insulin sensitivity (p<0.05). Amoxicillin did not affect any of these parameters.
Oral administration of vancomycin significantly impacts host physiology by decreasing intestinal microbiota diversity, bile acid dehydroxylation and peripheral insulin sensitivity in subjects with metabolic syndrome. These data show that intestinal microbiota, particularly of the Firmicutes phylum contributes to bile acid and glucose metabolism in humans. This trial is registered at the Dutch Trial Register (NTR2566). |
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| AbstractList | BACKGROUND: Obesity has been associated with changes in the composition and function of the intestinal microbiota. Modulation of the microbiota by antibiotics also alters bile acid and glucose metabolism in mice. Hence, we hypothesized that short term administration of oral antibiotics in humans would affect fecal microbiota composition and subsequently bile acid and glucose metabolism. METHODS: In this single blinded randomized controlled trial, 20 male obese subjects with metabolic syndrome were randomized to 7 days of amoxicillin 500mg t.i.d. or 7 days of vancomycin 500mg t.i.d. At baseline and after 1 week of therapy, fecal microbiota composition (Human Intestinal Tract Chip phylogenetic microarray), fecal and plasma bile acid concentrations as well as insulin sensitivity (hyperinsulinemic euglycemic clamp using [6,6-2H2]-glucose tracer) were measured. RESULTS: Vancomycin reduced fecal microbial diversity with a decrease of gram-positive bacteria (mainly Firmicutes) and a compensatory increase in gram-negative bacteria (mainly Proteobacteria). Concomitantly, vancomycin decreased fecal secondary bile acids with a simultaneous postprandial increase in primary bile acids in plasma (p Obesity has been associated with changes in the composition and function of the intestinal microbiota. Modulation of the microbiota by antibiotics also alters bile acid and glucose metabolism in mice. Hence, we hypothesized that short term administration of oral antibiotics in humans would affect fecal microbiota composition and subsequently bile acid and glucose metabolism. In this single blinded randomized controlled trial, 20 male obese subjects with metabolic syndrome were randomized to 7days of amoxicillin 500mg t.i.d. or 7days of vancomycin 500mg t.i.d. At baseline and after 1week of therapy, fecal microbiota composition (Human Intestinal Tract Chip phylogenetic microarray), fecal and plasma bile acid concentrations as well as insulin sensitivity (hyperinsulinemic euglycemic clamp using [6,6-2H2]-glucose tracer) were measured. Vancomycin reduced fecal microbial diversity with a decrease of gram-positive bacteria (mainly Firmicutes) and a compensatory increase in gram-negative bacteria (mainly Proteobacteria). Concomitantly, vancomycin decreased fecal secondary bile acids with a simultaneous postprandial increase in primary bile acids in plasma (p<0.05). Moreover, changes in fecal bile acid concentrations were predominantly associated with altered Firmicutes. Finally, administration of vancomycin decreased peripheral insulin sensitivity (p<0.05). Amoxicillin did not affect any of these parameters. Oral administration of vancomycin significantly impacts host physiology by decreasing intestinal microbiota diversity, bile acid dehydroxylation and peripheral insulin sensitivity in subjects with metabolic syndrome. These data show that intestinal microbiota, particularly of the Firmicutes phylum contributes to bile acid and glucose metabolism in humans. This trial is registered at the Dutch Trial Register (NTR2566). Obesity has been associated with changes in the composition and function of the intestinal microbiota. Modulation of the microbiota by antibiotics also alters bile acid and glucose metabolism in mice. Hence, we hypothesized that short term administration of oral antibiotics in humans would affect fecal microbiota composition and subsequently bile acid and glucose metabolism. In this single blinded randomized controlled trial, 20 male obese subjects with metabolic syndrome were randomized to 7 days of amoxicillin 500 mg t.i.d. or 7 days of vancomycin 500 mg t.i.d. At baseline and after 1 week of therapy, fecal microbiota composition (Human Intestinal Tract Chip phylogenetic microarray), fecal and plasma bile acid concentrations as well as insulin sensitivity (hyperinsulinemic euglycemic clamp using [6,6-(2)H2]-glucose tracer) were measured. Vancomycin reduced fecal microbial diversity with a decrease of gram-positive bacteria (mainly Firmicutes) and a compensatory increase in gram-negative bacteria (mainly Proteobacteria). Concomitantly, vancomycin decreased fecal secondary bile acids with a simultaneous postprandial increase in primary bile acids in plasma (p<0.05). Moreover, changes in fecal bile acid concentrations were predominantly associated with altered Firmicutes. Finally, administration of vancomycin decreased peripheral insulin sensitivity (p<0.05). Amoxicillin did not affect any of these parameters. Oral administration of vancomycin significantly impacts host physiology by decreasing intestinal microbiota diversity, bile acid dehydroxylation and peripheral insulin sensitivity in subjects with metabolic syndrome. These data show that intestinal microbiota, particularly of the Firmicutes phylum contributes to bile acid and glucose metabolism in humans. This trial is registered at the Dutch Trial Register (NTR2566). Graphical abstract Obesity has been associated with changes in the composition and function of the intestinal microbiota. Modulation of the microbiota by antibiotics also alters bile acid and glucose metabolism in mice. Hence, we hypothesized that short term administration of oral antibiotics in humans would affect fecal microbiota composition and subsequently bile acid and glucose metabolism.BACKGROUND & AIMSObesity has been associated with changes in the composition and function of the intestinal microbiota. Modulation of the microbiota by antibiotics also alters bile acid and glucose metabolism in mice. Hence, we hypothesized that short term administration of oral antibiotics in humans would affect fecal microbiota composition and subsequently bile acid and glucose metabolism.In this single blinded randomized controlled trial, 20 male obese subjects with metabolic syndrome were randomized to 7 days of amoxicillin 500 mg t.i.d. or 7 days of vancomycin 500 mg t.i.d. At baseline and after 1 week of therapy, fecal microbiota composition (Human Intestinal Tract Chip phylogenetic microarray), fecal and plasma bile acid concentrations as well as insulin sensitivity (hyperinsulinemic euglycemic clamp using [6,6-(2)H2]-glucose tracer) were measured.METHODSIn this single blinded randomized controlled trial, 20 male obese subjects with metabolic syndrome were randomized to 7 days of amoxicillin 500 mg t.i.d. or 7 days of vancomycin 500 mg t.i.d. At baseline and after 1 week of therapy, fecal microbiota composition (Human Intestinal Tract Chip phylogenetic microarray), fecal and plasma bile acid concentrations as well as insulin sensitivity (hyperinsulinemic euglycemic clamp using [6,6-(2)H2]-glucose tracer) were measured.Vancomycin reduced fecal microbial diversity with a decrease of gram-positive bacteria (mainly Firmicutes) and a compensatory increase in gram-negative bacteria (mainly Proteobacteria). Concomitantly, vancomycin decreased fecal secondary bile acids with a simultaneous postprandial increase in primary bile acids in plasma (p<0.05). Moreover, changes in fecal bile acid concentrations were predominantly associated with altered Firmicutes. Finally, administration of vancomycin decreased peripheral insulin sensitivity (p<0.05). Amoxicillin did not affect any of these parameters.RESULTSVancomycin reduced fecal microbial diversity with a decrease of gram-positive bacteria (mainly Firmicutes) and a compensatory increase in gram-negative bacteria (mainly Proteobacteria). Concomitantly, vancomycin decreased fecal secondary bile acids with a simultaneous postprandial increase in primary bile acids in plasma (p<0.05). Moreover, changes in fecal bile acid concentrations were predominantly associated with altered Firmicutes. Finally, administration of vancomycin decreased peripheral insulin sensitivity (p<0.05). Amoxicillin did not affect any of these parameters.Oral administration of vancomycin significantly impacts host physiology by decreasing intestinal microbiota diversity, bile acid dehydroxylation and peripheral insulin sensitivity in subjects with metabolic syndrome. These data show that intestinal microbiota, particularly of the Firmicutes phylum contributes to bile acid and glucose metabolism in humans. This trial is registered at the Dutch Trial Register (NTR2566).CONCLUSIONSOral administration of vancomycin significantly impacts host physiology by decreasing intestinal microbiota diversity, bile acid dehydroxylation and peripheral insulin sensitivity in subjects with metabolic syndrome. These data show that intestinal microbiota, particularly of the Firmicutes phylum contributes to bile acid and glucose metabolism in humans. This trial is registered at the Dutch Trial Register (NTR2566). |
| Author | Romijn, Johannes A. Reijnders, Dorien Zoetendal, Erwin G. Dallinga-Thie, Geesje M. Holst, Jenst J. Holleman, Frits Soeters, Maarten R. Kootte, Ruud S. Nieuwdorp, Max van der Ley, Claude Kema, Ido P. Vrieze, Anne Serlie, Mireille J. Stroes, Erik S. de Vos, Willem M. Hoekstra, Joost B.L. Knaapen, Max Blaak, Ellen E. Ackermans, Mariëtte T. van Nood, Els Out, Carolien Jonker, Lisanne Reuling, Isaie Knop, Filip K. Groen, Albert K. Fuentes, Susana |
| Author_xml | – sequence: 1 givenname: Anne surname: Vrieze fullname: Vrieze, Anne organization: Department of Medicine, Academic Medical Center, Amsterdam, The Netherlands – sequence: 2 givenname: Carolien surname: Out fullname: Out, Carolien organization: Department of Pediatrics, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands – sequence: 3 givenname: Susana surname: Fuentes fullname: Fuentes, Susana organization: Laboratory of Microbiology, Wageningen University, Wageningen, The Netherlands – sequence: 4 givenname: Lisanne surname: Jonker fullname: Jonker, Lisanne organization: Department of Medicine, Academic Medical Center, Amsterdam, The Netherlands – sequence: 5 givenname: Isaie surname: Reuling fullname: Reuling, Isaie organization: Department of Medicine, Academic Medical Center, Amsterdam, The Netherlands – sequence: 6 givenname: Ruud S. surname: Kootte fullname: Kootte, Ruud S. organization: Department of Vascular Medicine and Experimental Vascular Medicine, Academic Medical Center, Amsterdam, The Netherlands – sequence: 7 givenname: Els surname: van Nood fullname: van Nood, Els organization: Department of Medicine, Academic Medical Center, Amsterdam, The Netherlands – sequence: 8 givenname: Frits surname: Holleman fullname: Holleman, Frits organization: Department of Medicine, Academic Medical Center, Amsterdam, The Netherlands – sequence: 9 givenname: Max surname: Knaapen fullname: Knaapen, Max organization: Department of Vascular Medicine and Experimental Vascular Medicine, Academic Medical Center, Amsterdam, The Netherlands – sequence: 10 givenname: Johannes A. surname: Romijn fullname: Romijn, Johannes A. organization: Department of Medicine, Academic Medical Center, Amsterdam, The Netherlands – sequence: 11 givenname: Maarten R. surname: Soeters fullname: Soeters, Maarten R. organization: Department of Endocrinology and Metabolism, Academic Medical Center, Amsterdam, The Netherlands – sequence: 12 givenname: Ellen E. surname: Blaak fullname: Blaak, Ellen E. organization: Department of Human Metabolism, NUTRIM, School for Nutrition, Toxicology and Metabolism, Maastricht University, The Netherlands – sequence: 13 givenname: Geesje M. surname: Dallinga-Thie fullname: Dallinga-Thie, Geesje M. organization: Department of Vascular Medicine and Experimental Vascular Medicine, Academic Medical Center, Amsterdam, The Netherlands – sequence: 14 givenname: Dorien surname: Reijnders fullname: Reijnders, Dorien organization: Department of Human Metabolism, NUTRIM, School for Nutrition, Toxicology and Metabolism, Maastricht University, The Netherlands – sequence: 15 givenname: Mariëtte T. surname: Ackermans fullname: Ackermans, Mariëtte T. organization: Department of Clinical Chemistry, Laboratory of Endocrinology, Academic Medical Center, Amsterdam, The Netherlands – sequence: 16 givenname: Mireille J. surname: Serlie fullname: Serlie, Mireille J. organization: Department of Endocrinology and Metabolism, Academic Medical Center, Amsterdam, The Netherlands – sequence: 17 givenname: Filip K. surname: Knop fullname: Knop, Filip K. organization: Department of Internal Medicine, Gentofte Hospital, Hellerup, Denmark – sequence: 18 givenname: Jenst J. surname: Holst fullname: Holst, Jenst J. organization: NNF Center for Basic Metabolic Research, Department of Biomedical Sciences, The Panum Institute, University of Copenhagen, Denmark – sequence: 19 givenname: Claude surname: van der Ley fullname: van der Ley, Claude organization: Department of Laboratory Medicine, University Medical Center Groningen, Groningen, The Netherlands – sequence: 20 givenname: Ido P. surname: Kema fullname: Kema, Ido P. organization: Department of Laboratory Medicine, University Medical Center Groningen, Groningen, The Netherlands – sequence: 21 givenname: Erwin G. surname: Zoetendal fullname: Zoetendal, Erwin G. organization: Laboratory of Microbiology, Wageningen University, Wageningen, The Netherlands – sequence: 22 givenname: Willem M. surname: de Vos fullname: de Vos, Willem M. organization: Laboratory of Microbiology, Wageningen University, Wageningen, The Netherlands – sequence: 23 givenname: Joost B.L. surname: Hoekstra fullname: Hoekstra, Joost B.L. organization: Department of Medicine, Academic Medical Center, Amsterdam, The Netherlands – sequence: 24 givenname: Erik S. surname: Stroes fullname: Stroes, Erik S. organization: Department of Vascular Medicine and Experimental Vascular Medicine, Academic Medical Center, Amsterdam, The Netherlands – sequence: 25 givenname: Albert K. surname: Groen fullname: Groen, Albert K. organization: Department of Pediatrics, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands – sequence: 26 givenname: Max surname: Nieuwdorp fullname: Nieuwdorp, Max email: m.nieuwdorp@amc.uva.nl organization: Department of Medicine, Academic Medical Center, Amsterdam, The Netherlands |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/24316517$$D View this record in MEDLINE/PubMed |
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| SubjectTerms | adiposity Administration, Oral Adult Aged Amoxicillin Animals Anti-Bacterial Agents - administration & dosage Anti-Bacterial Agents - adverse effects Antibiotics Bile acids Bile Acids and Salts - blood Bile Acids and Salts - metabolism capacity diet-induced obesity energy-expenditure Feces - chemistry Feces - microbiology Gastroenterology and Hepatology glucagon Glucose - metabolism Humans Insulin Resistance Intestinal microbiota Intestines - drug effects Intestines - microbiology Male Metabolic syndrome Metabolic Syndrome - complications Metabolic Syndrome - drug therapy Metabolic Syndrome - microbiology Mice Microbiota - drug effects Middle Aged Obesity - complications Obesity - drug therapy Obesity - microbiology resistance salt hydrolase activity Single-Blind Method Vancomycin Vancomycin - administration & dosage Vancomycin - adverse effects |
| Title | Impact of oral vancomycin on gut microbiota, bile acid metabolism, and insulin sensitivity |
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