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Cited by 63Gut microbiota and healthDiet, Metabolism, and DiseaseLiver Disease Diagnosis and Treatment

Dietary fructose causes defective insulin signalling and ceramide accumulation in the liver that can be reversed by gut microbiota modulation

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Crescenzo, Raffaella, Mazzoli, Arianna, Di Luccia, Blanda, Bianco, Francesca, Cancelliere, Rosa, Cigliano, Luisa, Liverini, Giovanna, Baccigalupi, Loredana +1 more·2017·Food & Nutrition Research
DOI 10.1080/16546628.2017.1331657PMC PMC5475320
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Abstract

Objective : The link between metabolic derangement of the gut–2013liver–visceral white adipose tissue (v-WAT) axis and gut microbiota was investigated. Methods : Rats were fed a fructose-rich diet and treated with an antibiotic mix. Inflammation was measured in portal plasma, ileum, liver, and v-WAT, while insulin signalling was analysed by measuring levels of phosphorylated kinase Akt. The function and oxidative status of hepatic mitochondria and caecal microbiota composition were also evaluated. Results : Ileal inflammation, increase in plasma transaminases, plasma peroxidised lipids, portal concentrations of tumour necrosis factor alpha, lipopolysaccharide, and non-esterified fatty acids, were induced by fructose and were reversed by antibiotic. The increased hepatic ceramide content, inflammation and decreased insulin signaling in liver and v-WAT induced by fructose was reversed by antibiotic. Antibiotic also blunted the increase in hepatic mitochondrial efficiency and oxidative damage of rats fed fructose-rich diet. Three genera, Coprococcus, Ruminococcus, and Clostridium, significantly increased, while the Clostridiaceae family significantly decreased in rats fed a fructose-rich diet, and antibiotic abolished these variations Conclusions : When gut microbiota modulation by fructose is prevented by antibiotic, inflammatory flow from the gut to the liver and v-WAT are reversed.

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  • Mice fed a fructose-rich diet demonstrate significant increases in Coprococcus, Ruminococcus and Clostridium, and a reduction in Clostridiaceae family.

    “Mice fed a fructose-rich diet demonstrated significant increases in Coprococcus, Ruminococcus and Clostridium, and a reduction in Clostridiaceae family (Crescenzo et al., 2017).”

    From The Microbiota-Gut-Brain Axis (2019) · cites this paper as Crescenzo et al., 2017

    The Results (Caecal microbiota) report increased Coprococcus and Ruminococcus in fructose-fed rats, but the opposite of the claimed directions for the other groups: Clostridium decreased and Clostridiaceae increased. The Methods (Animals and treatments) identify the animals as rats, not mice. (LLM, conf=0.90)

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Authors
Crescenzo, R., Mazzoli, A., Di Luccia, B., Bianco, F., Cancelliere, R., Cigliano, L., Liverini, G., Baccigalupi, L., & Iossa, S.
Affiliations
  • University of Naples Federico II (IT)
  • Department of Biology, Federico II University of Naples, Naples, Italy
Corresponding author
Iossa, Susanna
ORCID
Venue
Food & Nutrition Research
Publisher
SNF Swedish Nutrition Foundation
Published
2017-01
Volume
61
Issue
1
Pages
1331657
ISSN
  • 1654-661X (ISSN-L)
  • 1654-6628
DOI
10.1080/16546628.2017.1331657
PMC
PMC5475320
OpenAlex
W2622697709
Cited by
63
References
1
Citations by year
2026: 1 · 2025: 6 · 2024: 5 · 2023: 3 · 2022: 11 · 2021: 9 · 2020: 9 · 2019: 8 · 2018: 9 · 2017: 2
FWCI
3.13
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Food & Nutrition Research (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diet, Metabolism, and Disease
  • Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
Keywords
dietary fructose, gut-liver axis, visceral white adipose tissue, gut microbiota, antibiotic-induced dysbiosis, insulin signaling, Akt phosphorylation, liver inflammation, mitochondrial oxidative damage, ileal inflammation, Clostridiaceae, Ruminococcus, Coprococcus, lipopolysaccharide, TNF-α, free fatty acids

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