Abstract
PurposeInulin-type fructans (ITF) are prebiotic dietary fibre (DF) that may confer beneficial health effects, by interacting with the gut microbiota. We have tested the hypothesis that a dietary intervention promoting inulin intake versus placebo influences fecal microbial-derived metabolites and markers related to gut integrity and inflammation in obese patients.MethodsMicrobiota (16S rRNA sequencing), long- and short-chain fatty acids (LCFA, SCFA), bile acids, zonulin, and calprotectin were analyzed in fecal samples obtained from obese patients included in a randomized, placebo-controlled trial. Participants received either 16 g/d native inulin (prebiotic n = 12) versus maltodextrin (placebo n = 12), coupled to dietary advice to consume inulin-rich versus inulin-poor vegetables for 3 months, in addition to dietary caloric restriction.ResultsBoth placebo and prebiotic interventions lowered energy and protein intake. A substantial increase in Bifidobacterium was detected after ITF treatment (q = 0.049) supporting our recent data obtained in a larger cohort. Interestingly, fecal calprotectin, a marker of gut inflammation, was reduced upon ITF treatment. Both prebiotic and placebo interventions increased the ratio of tauro-conjugated/free bile acids in feces. Prebiotic treatment did not significantly modify fecal SCFA content but it increased fecal rumenic acid, a conjugated linoleic acid (cis-9, trans-11 CLA) with immunomodulatory properties, that correlated notably to the expansion of Bifidobacterium (p = 0.031; r = 0.052).ConclusionsOur study demonstrates that ITF-prebiotic intake during 3 months decreases a fecal marker of intestinal inflammation in obese patients. Our data point to a potential contribution of microbial lipid-derived metabolites in gastro-intestinal dysfunction related to obesity.ClinicalTrials.gov IdentifierNCT03852069 (February 22, 2019 retrospectively, registered).
Highlights
Recent studies have highlighted the role of gut dysbiosis in the etiology and pathogenesis of obesity-related metabolic disorders [1]
We explored a FOOD4GUT subcohort to study the link between prebiotic intake, gut microbial signature in terms of bacterial composition, the profile of key gut-derived metabolites, and fecal biomarkers related to gut barrier function and gut inflammation such as fecal zonulin and fecal calprotectin, respectively [24, 25]
We have previously shown that improvement of anthropometric and cardiometabolic risk parameters of obese patients after prebiotic intervention may be related to specific changes in gut bacteria in the whole FOOD4GUT cohort [22]
Summary
Recent studies have highlighted the role of gut dysbiosis in the etiology and pathogenesis of obesity-related metabolic disorders [1]. Despite the controversial role of gut dysbiosis as a cause of obesity in humans, numerous animal Extended author information available on the last page of the article human) studies suggest beneficial metabolic effects of gut-derived microbial metabolites that could be used in the prevention and treatment of obesity and related metabolic disorders. Acetate, propionate, and butyrate, produced upon microbial fermentation of carbohydrates and fibre, may influence the production of gut hormones (like glucagon-like peptide 1) by enteroendocrine L cells, thereby having a beneficial impact on metabolic functions, intestinal epithelial integrity, appetite and glucose homeostasis [4,5,6,7].
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