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Excess dietary fructose does not alter gut microbiota or permeability in humans: A pilot randomized controlled study.
Alemán, José O; Henderson, Wendy A; Walker, Jeanne M; Ronning, Andrea; Jones, Drew R; Walter, Peter J; Daniel, Scott G; Bittinger, Kyle; Vaughan, Roger; MacArthur, Robert; Chen, Kun; Breslow, Jan L; Holt, Peter R.
Afiliação
  • Alemán JO; Laboratory of Biochemical Genetics and Metabolism, Rockefeller University, New York, NY, USA.
  • Henderson WA; New York University Langone Health Metabolomics Core Resource Laboratory, New York, NY, USA.
  • Walker JM; Institute for Collaboration on Health, Intervention and Policy, University of Connecticut, Storrs, CT, USA.
  • Ronning A; Clinical Research, The Rockefeller University Hospital, New York, NY, USA.
  • Jones DR; Bionutrition, The Rockefeller University Hospital, New York, NY, USA.
  • Walter PJ; New York University Langone Health Metabolomics Core Resource Laboratory, New York, NY, USA.
  • Daniel SG; NIDDK Clinical Mass Spectrometry Core, National Institutes of Health, Bethesda, MD, USA.
  • Bittinger K; PennCHOP Microbiome Program, Children's Hospital of Philadelphia, Philadelphia, PA, USA.
  • Vaughan R; PennCHOP Microbiome Program, Children's Hospital of Philadelphia, Philadelphia, PA, USA.
  • MacArthur R; Biostatistics, The Rockefeller University, New York, NY, USA.
  • Chen K; Research Pharmacy, The Rockefeller University Hospital, New York, NY, USA.
  • Breslow JL; Institute for Collaboration on Health, Intervention and Policy, University of Connecticut, Storrs, CT, USA.
  • Holt PR; Laboratory of Biochemical Genetics and Metabolism, Rockefeller University, New York, NY, USA.
J Clin Transl Sci ; 5(1): e143, 2021.
Article em En | MEDLINE | ID: mdl-34422323
INTRODUCTION: Non-alcoholic fatty liver disease (NAFLD) is an increasing cause of chronic liver disease that accompanies obesity and the metabolic syndrome. Excess fructose consumption can initiate or exacerbate NAFLD in part due to a consequence of impaired hepatic fructose metabolism. Preclinical data emphasized that fructose-induced altered gut microbiome, increased gut permeability, and endotoxemia play an important role in NAFLD, but human studies are sparse. The present study aimed to determine if two weeks of excess fructose consumption significantly alters gut microbiota or permeability in humans. METHODS: We performed a pilot double-blind, cross-over, metabolic unit study in 10 subjects with obesity (body mass index [BMI] 30-40 mg/kg/m2). Each arm provided 75 grams of either fructose or glucose added to subjects' individual diets for 14 days, substituted isocalorically for complex carbohydrates, with a 19-day wash-out period between arms. Total fructose intake provided in the fructose arm of the study totaled a mean of 20.1% of calories. Outcome measures included fecal microbiota distribution, fecal metabolites, intestinal permeability, markers of endotoxemia, and plasma metabolites. RESULTS: Routine blood, uric acid, liver function, and lipid measurements were unaffected by the fructose intervention. The fecal microbiome (including Akkermansia muciniphilia), fecal metabolites, gut permeability, indices of endotoxemia, gut damage or inflammation, and plasma metabolites were essentially unchanged by either intervention. CONCLUSIONS: In contrast to rodent preclinical findings, excess fructose did not cause changes in the gut microbiome, metabolome, and permeability as well as endotoxemia in humans with obesity fed fructose for 14 days in amounts known to enhance NAFLD.
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Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2021 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2021 Tipo de documento: Article