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Cited by 930

The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.

Probiotics and antibodies to TNF inhibit inflammatory activity and improve nonalcoholic fatty liver disease

Li, Zhiping, Yang, Shiqi, Lin, Huizhi, Huang, Jiawen, Watkins, Paul A., Moser, Ann B., DeSimone, Claudio, Song, Xiao-yu, Diehl, Anna Mae·2003·Hepatology
DOI 10.1053/jhep.2003.50048
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Abstract

Ob/ob mice, a model for nonalcoholic fatty liver disease (NAFLD), develop intestinal bacterial overgrowth and overexpress tumor necrosis factor α (TNF-α). In animal models for alcoholic fatty liver disease (AFLD), decontaminating the intestine or inhibiting TNF-α improves AFLD. Because AFLD and NAFLD may have a similar pathogenesis, treatment with a probiotic (to modify the intestinal flora) or anti-TNF antibodies (to inhibit TNF-α activity) may improve NAFLD in ob/ob mice. To evaluate this hypothesis, 48 ob/ob mice were given either a high-fat diet alone (ob/ob controls) or the same diet + VSL#3 probiotic or anti-TNF antibodies for 4 weeks. Twelve lean littermates fed a high-fat diet served as controls. Treatment with VSL#3 or anti-TNF antibodies improved liver histology, reduced hepatic total fatty acid content, and decreased serum alanine aminotransferase (ALT) levels. These benefits were associated with decreased hepatic expression of TNF-α messenger RNA (mRNA) in mice treated with anti-TNF antibodies but not in mice treated with VSL#3. Nevertheless, both treatments reduced activity of Jun N-terminal kinase (JNK), a TNF-regulated kinase that promotes insulin resistance, and decreased the DNA binding activity of nuclear factor κB (NF-κB), the target of IKKβ, another TNF-regulated enzyme that causes insulin resistance. Consistent with treatment-related improvements in hepatic insulin resistance, fatty acid β-oxidation and uncoupling protein (UCP)-2 expression decreased after treatment with VSL#3 or anti-TNF antibodies. In conclusion, these results support the concept that intestinal bacteria induce endogenous signals that play a pathogenic role in hepatic insulin resistance and NAFLD and suggest novel therapies for these common conditions.

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Metadata

Authors
Li, Z., Yang, S., Lin, H., Huang, J., Watkins, P. A., Moser, A. B., DeSimone, C., Song, X.-Y., & Diehl, A. M.
Venue
Hepatology
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2003-02
Volume
37
Issue
2
Pages
343-350
ISSN
0270-9139 (ISSN-L)
DOI
10.1053/jhep.2003.50048
OpenAlex
W2088366586
Cited by
930
References
6
FWCI
27.35
Type
journal article
Language
en
Open access
closed

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