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Article: Adipocyte fatty acid binding protein levels relate to inflammation and fibrosis in nonalcoholic fatty liver disease

TitleAdipocyte fatty acid binding protein levels relate to inflammation and fibrosis in nonalcoholic fatty liver disease
Authors
Issue Date2009
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/
Citation
Hepatology, 2009, v. 49 n. 6, p. 1926-1934 How to Cite?
AbstractSeveral circulating cytokines are increased with obesity and may combine with the influence of visceral fat to generate insulin resistance, inflammation, and fibrosis in nonalcoholic fatty liver disease (NAFLD). Little information exists in NAFLD about three recently recognized tissue-derived cytokines that are all lipid-binding and involved in inflammation, namely adipocyte fatty acid-binding protein (AFABP), lipocalin-2, and retinol-binding protein 4 (RBP4). We examined the association of these three peptides with hepatic steatosis, inflammation, and fibrosis plus indices of adiposity, insulin resistance, and dyslipidaemia in 100 subjects with NAFLD and 129 matched controls. Levels of AFABP and lipocalin-2, but not RBP4, were significantly elevated in NAFLD versus control (AFABP, 33.5 ± 14.4 versus 23.1 ± 12.1 ng/mL [P < 0.001]; lipocalin-2, 63.2 ± 26 versus 48.6 ± 20 ng/mL [P < 0.001]) and correlated with indices of adiposity. AFABP correlated with indices of subcutaneous rather than visceral fat. AFABP alone distinguished steatohepatitis from simple steatosis (P = 0.02). Elevated AFABP independently predicted increasing inflammation and fibrosis, even when insulin resistance and visceral fat were considered; this applied to lobular inflammation and ballooning (odds ratio 1.4, confidence interval 1.0-1.8) and fibrosis stage (odds ratio 1.3, confidence interval 1.0-1.7) (P < 0.05 for all). None of the cytokines correlated with steatosis grade. AFABP levels correlated with insulin resistance (homeostasis model assessment of insulin resistance) in controls and NAFLD, whereas lipocalin-2 and RBP4 only correlated positively with insulin resistance in controls. Conclusion: Circulating AFABP, produced by adipocytes and macrophages, and lipocalin-2, produced by multiple tissues, are elevated and may contribute to the metabolic syndrome in NAFLD. AFABP levels, which correlate with subcutaneous, but not visceral fat, independently predict inflammation and fibrosis in NAFLD and may have a direct pathogenic link to disease progression. Copyright © 2009 by the American Association for the Study of Liver Diseases.
Persistent Identifierhttp://hdl.handle.net/10722/59232
ISSN
2015 Impact Factor: 11.711
2015 SCImago Journal Rankings: 4.752
ISI Accession Number ID
Funding AgencyGrant Number
Hong Kong Research Council CRFHKU 2/07C
National Health and Medical Research Council of Australia358398
GESA postgraduate medical research scholarship
Robert W. Storr Bequest
University of Sydney
Funding Information:

Supported in part by Hong Kong Research Council CRF Grant HKU 2/07C (to A. X), National Health and Medical Research Council of Australia Grant 358398, a GESA postgraduate medical research scholarship, a Robert W. Storr Bequest to the University of Sydney, and a University of Sydney Grant.

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DC FieldValueLanguage
dc.contributor.authorMilner, KLen_HK
dc.contributor.authorvan der Poorten, Den_HK
dc.contributor.authorXu, Aen_HK
dc.contributor.authorBugianesi, Een_HK
dc.contributor.authorKench, JGen_HK
dc.contributor.authorLam, KSLen_HK
dc.contributor.authorChisholm, DJen_HK
dc.contributor.authorGeorge, Jen_HK
dc.date.accessioned2010-05-31T03:45:44Z-
dc.date.available2010-05-31T03:45:44Z-
dc.date.issued2009en_HK
dc.identifier.citationHepatology, 2009, v. 49 n. 6, p. 1926-1934en_HK
dc.identifier.issn0270-9139en_HK
dc.identifier.urihttp://hdl.handle.net/10722/59232-
dc.description.abstractSeveral circulating cytokines are increased with obesity and may combine with the influence of visceral fat to generate insulin resistance, inflammation, and fibrosis in nonalcoholic fatty liver disease (NAFLD). Little information exists in NAFLD about three recently recognized tissue-derived cytokines that are all lipid-binding and involved in inflammation, namely adipocyte fatty acid-binding protein (AFABP), lipocalin-2, and retinol-binding protein 4 (RBP4). We examined the association of these three peptides with hepatic steatosis, inflammation, and fibrosis plus indices of adiposity, insulin resistance, and dyslipidaemia in 100 subjects with NAFLD and 129 matched controls. Levels of AFABP and lipocalin-2, but not RBP4, were significantly elevated in NAFLD versus control (AFABP, 33.5 ± 14.4 versus 23.1 ± 12.1 ng/mL [P < 0.001]; lipocalin-2, 63.2 ± 26 versus 48.6 ± 20 ng/mL [P < 0.001]) and correlated with indices of adiposity. AFABP correlated with indices of subcutaneous rather than visceral fat. AFABP alone distinguished steatohepatitis from simple steatosis (P = 0.02). Elevated AFABP independently predicted increasing inflammation and fibrosis, even when insulin resistance and visceral fat were considered; this applied to lobular inflammation and ballooning (odds ratio 1.4, confidence interval 1.0-1.8) and fibrosis stage (odds ratio 1.3, confidence interval 1.0-1.7) (P < 0.05 for all). None of the cytokines correlated with steatosis grade. AFABP levels correlated with insulin resistance (homeostasis model assessment of insulin resistance) in controls and NAFLD, whereas lipocalin-2 and RBP4 only correlated positively with insulin resistance in controls. Conclusion: Circulating AFABP, produced by adipocytes and macrophages, and lipocalin-2, produced by multiple tissues, are elevated and may contribute to the metabolic syndrome in NAFLD. AFABP levels, which correlate with subcutaneous, but not visceral fat, independently predict inflammation and fibrosis in NAFLD and may have a direct pathogenic link to disease progression. Copyright © 2009 by the American Association for the Study of Liver Diseases.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/en_HK
dc.relation.ispartofHepatologyen_HK
dc.rightsHepatology. Copyright © John Wiley & Sons, Inc.en_HK
dc.subject.meshAcute-Phase Proteinsen_HK
dc.subject.meshAdulten_HK
dc.subject.meshFatty Acid-Binding Proteins - blooden_HK
dc.subject.meshFatty Liver - blood - complicationsen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshHepatitis - blood - etiologyen_HK
dc.subject.meshHumansen_HK
dc.subject.meshLipocalins - blooden_HK
dc.subject.meshLiver Cirrhosis - blood - etiologyen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshProto-Oncogene Proteins - blooden_HK
dc.titleAdipocyte fatty acid binding protein levels relate to inflammation and fibrosis in nonalcoholic fatty liver diseaseen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0270-9139&volume=49&spage=1926&epage=34&date=2009&atitle=Adipocyte+fatty+acid+binding+protein+levels+relate+to+inflammation+and+fibrosis+in+nonalcoholic+fatty+liver+disease.en_HK
dc.identifier.emailXu, A:amxu@hkucc.hku.hken_HK
dc.identifier.emailLam, KSL:ksllam@hku.hken_HK
dc.identifier.authorityXu, A=rp00485en_HK
dc.identifier.authorityLam, KSL=rp00343en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/hep.22896en_HK
dc.identifier.pmid19475694-
dc.identifier.scopuseid_2-s2.0-68949111875en_HK
dc.identifier.hkuros157960en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-68949111875&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume49en_HK
dc.identifier.issue6en_HK
dc.identifier.spage1926en_HK
dc.identifier.epage1934en_HK
dc.identifier.isiWOS:000266846400019-
dc.publisher.placeUnited Statesen_HK
dc.relation.projectVascular dysfunction in obesity and diabetes: from risk prediction to therapeutic intervention-
dc.identifier.scopusauthoridMilner, KL=24577068100en_HK
dc.identifier.scopusauthoridvan der Poorten, D=23111746900en_HK
dc.identifier.scopusauthoridXu, A=7202655409en_HK
dc.identifier.scopusauthoridBugianesi, E=6701433364en_HK
dc.identifier.scopusauthoridKench, JG=7006151706en_HK
dc.identifier.scopusauthoridLam, KSL=8082870600en_HK
dc.identifier.scopusauthoridChisholm, DJ=54790548200en_HK
dc.identifier.scopusauthoridGeorge, J=7403558157en_HK

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