Probiotics and antibodies to TNF inhibit inflammatory activity and improve nonalcoholic fatty liver disease. Li, Z., Yang, S., Lin, H., Huang, J., Watkins, P. A, Moser, A. B, Desimone, C., Song, X., & Diehl, A. M. Hepatology, 37(2):343–350, 2003. Place: United States ISBN: 0270-9139doi abstract bibtex Ob/ob mice, a model for nonalcoholic fatty liver disease (NAFLD), develop intestinal bacterial overgrowth and overexpress tumor necrosis factor alpha (TNF-alpha). In animal models for alcoholic fatty liver disease (AFLD), decontaminating the intestine or inhibiting TNF-alpha 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-alpha 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-alpha 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 kappaB (NF-kappaB), the target of IKKbeta, another TNF-regulated enzyme that causes insulin resistance. Consistent with treatment-related improvements in hepatic insulin resistance, fatty acid beta-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.
@article{li_probiotics_2003,
title = {Probiotics and antibodies to {TNF} inhibit inflammatory activity and improve nonalcoholic fatty liver disease.},
volume = {37},
doi = {10.1053/jhep.2003.50048},
abstract = {Ob/ob mice, a model for nonalcoholic fatty liver disease (NAFLD), develop intestinal bacterial overgrowth and overexpress tumor necrosis factor alpha (TNF-alpha). In animal models for alcoholic fatty liver disease (AFLD), decontaminating the intestine or inhibiting TNF-alpha 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-alpha 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-alpha 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 kappaB (NF-kappaB), the target of IKKbeta, another TNF-regulated enzyme that causes insulin resistance. Consistent with treatment-related improvements in hepatic insulin resistance, fatty acid beta-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.},
language = {eng},
number = {2},
journal = {Hepatology},
author = {Li, Zhiping and Yang, Shiqi and Lin, Huizhi and Huang, Jiawen and Watkins, Paul A and Moser, Ann B and Desimone, Claudio and Song, Xiao-yu and Diehl, Anna Mae},
year = {2003},
pmid = {12540784},
note = {Place: United States
ISBN: 0270-9139},
keywords = {Alanine Transaminase, Animals, Antibodies, DNA, Dietary Fats, Fatty Acids, Fatty Liver, Hepatitis, Insulin Resistance, Ion Channels, JNK Mitogen-Activated Protein Kinases, Liver, Male, Membrane Transport Proteins, Mice, Mice, Inbred C57BL, Mitochondrial Proteins, Mitogen-Activated Protein Kinases, NF-kappa B, Obesity, Oxidation-Reduction, Probiotics, Proteins, RNA, Messenger, Tumor Necrosis Factor-alpha, research support, u.s. gov't, p.h.s.},
pages = {343--350},
}
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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-alpha 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-alpha 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 kappaB (NF-kappaB), the target of IKKbeta, another TNF-regulated enzyme that causes insulin resistance. Consistent with treatment-related improvements in hepatic insulin resistance, fatty acid beta-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.","language":"eng","number":"2","journal":"Hepatology","author":[{"propositions":[],"lastnames":["Li"],"firstnames":["Zhiping"],"suffixes":[]},{"propositions":[],"lastnames":["Yang"],"firstnames":["Shiqi"],"suffixes":[]},{"propositions":[],"lastnames":["Lin"],"firstnames":["Huizhi"],"suffixes":[]},{"propositions":[],"lastnames":["Huang"],"firstnames":["Jiawen"],"suffixes":[]},{"propositions":[],"lastnames":["Watkins"],"firstnames":["Paul","A"],"suffixes":[]},{"propositions":[],"lastnames":["Moser"],"firstnames":["Ann","B"],"suffixes":[]},{"propositions":[],"lastnames":["Desimone"],"firstnames":["Claudio"],"suffixes":[]},{"propositions":[],"lastnames":["Song"],"firstnames":["Xiao-yu"],"suffixes":[]},{"propositions":[],"lastnames":["Diehl"],"firstnames":["Anna","Mae"],"suffixes":[]}],"year":"2003","pmid":"12540784","note":"Place: United States ISBN: 0270-9139","keywords":"Alanine Transaminase, Animals, Antibodies, DNA, Dietary Fats, Fatty Acids, Fatty Liver, Hepatitis, Insulin Resistance, Ion Channels, JNK Mitogen-Activated Protein Kinases, Liver, Male, Membrane Transport Proteins, Mice, Mice, Inbred C57BL, Mitochondrial Proteins, Mitogen-Activated Protein Kinases, NF-kappa B, Obesity, Oxidation-Reduction, Probiotics, Proteins, RNA, Messenger, Tumor Necrosis Factor-alpha, research support, u.s. gov't, p.h.s.","pages":"343–350","bibtex":"@article{li_probiotics_2003,\n\ttitle = {Probiotics and antibodies to {TNF} inhibit inflammatory activity and improve nonalcoholic fatty liver disease.},\n\tvolume = {37},\n\tdoi = {10.1053/jhep.2003.50048},\n\tabstract = {Ob/ob mice, a model for nonalcoholic fatty liver disease (NAFLD), develop intestinal bacterial overgrowth and overexpress tumor necrosis factor alpha (TNF-alpha). In animal models for alcoholic fatty liver disease (AFLD), decontaminating the intestine or inhibiting TNF-alpha 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-alpha 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-alpha 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 kappaB (NF-kappaB), the target of IKKbeta, another TNF-regulated enzyme that causes insulin resistance. Consistent with treatment-related improvements in hepatic insulin resistance, fatty acid beta-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.},\n\tlanguage = {eng},\n\tnumber = {2},\n\tjournal = {Hepatology},\n\tauthor = {Li, Zhiping and Yang, Shiqi and Lin, Huizhi and Huang, Jiawen and Watkins, Paul A and Moser, Ann B and Desimone, Claudio and Song, Xiao-yu and Diehl, Anna Mae},\n\tyear = {2003},\n\tpmid = {12540784},\n\tnote = {Place: United States\nISBN: 0270-9139},\n\tkeywords = {Alanine Transaminase, Animals, Antibodies, DNA, Dietary Fats, Fatty Acids, Fatty Liver, Hepatitis, Insulin Resistance, Ion Channels, JNK Mitogen-Activated Protein Kinases, Liver, Male, Membrane Transport Proteins, Mice, Mice, Inbred C57BL, Mitochondrial Proteins, Mitogen-Activated Protein Kinases, NF-kappa B, Obesity, Oxidation-Reduction, Probiotics, Proteins, RNA, Messenger, Tumor Necrosis Factor-alpha, research support, u.s. gov't, p.h.s.},\n\tpages = {343--350},\n}\n\n","author_short":["Li, Z.","Yang, S.","Lin, H.","Huang, J.","Watkins, P. 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