Journal
MOLECULAR NUTRITION & FOOD RESEARCH
Volume 67, Issue 14, Pages -Publisher
WILEY
DOI: 10.1002/mnfr.202200389
Keywords
cyclic oligosaccharide; glucose metabolism; gut bacteria; high-fat diet; immunoglobulin A
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This study evaluates the effect of a dietary fiber called cyclic nigerosylnigerose (CNN) on high-fat diet-induced gut dysbiosis, inflammation, and insulin resistance. The results show that CNN reduces fat deposition, inflammation, and endotoxin levels, and improves abnormal glucose metabolism. Additionally, CNN promotes IgA secretion and alters IgA reactivity to specific gut bacteria.
ScopeHigh-fat diet (HFD) intake induces gut dysbiosis, inflammation in the peripheral tissues, and a reduction in immunoglobulin A (IgA) coating of gut bacteria, which is related to HFD-induced insulin resistance (IR). This study evaluates the effect of cyclic nigerosylnigerose (CNN), a dietary fiber that prevents gut inflammation and promotes IgA coating of gut bacteria, on the above-mentioned HFD-induced disorders. Methods and resultsBalb/c mice are fed an HFD and administered CNN for 20 weeks. CNN administration reduces mesenteric adipose tissue weight, colonic tumor necrosis factor & alpha; (TNF & alpha;) mRNA expression, and serum endotoxin levels and ameliorates HFD-induced abnormal glucose metabolism. Additionally, CNN administration promotes gut bacteria-specific IgA secretion and alters IgA reactivity to gut bacteria. The alterations of IgA reactivity to specific bacteria such as Erysipelatoclostridium, Escherichia, Faecalibaculum, Lachnospiraceae genera, and Stenotrophomonas are correlated with mesenteric adipose tissue weight, colonic TNF & alpha; mRNA expression, serum endotoxin levels, and a homeostasis model assessment for IR. ConclusionCNN-induced alterations in IgA reactivity to gut bacteria may be related to the suppression of HFD-induced fat deposition, colonic inflammation, endotoxemia, and IR. These observations indicate that dietary fiber that modulates IgA reactivity to gut bacteria may be useful in preventing HFD-induced disorders.
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