Adipokines in NASH: postprandial lipid metabolism as a link between adiponectin and liver disease (Articolo in rivista)

Type
Label
  • Adipokines in NASH: postprandial lipid metabolism as a link between adiponectin and liver disease (Articolo in rivista) (literal)
Anno
  • 2005-01-01T00:00:00+01:00 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
  • 10.1002/hep.20896 (literal)
Alternative label
  • Musso G.; Gambino R.; Durazzo M.; Biroli G.; Carello M.; Fagà E.; Pacini G.; De Michieli F.; Cassader M.; Rabbione L.; Premoli A.; and Pagano G. (2005)
    Adipokines in NASH: postprandial lipid metabolism as a link between adiponectin and liver disease
    in Hepatology (Baltim. Md.); Wiley, New York (Stati Uniti d'America)
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Musso G.; Gambino R.; Durazzo M.; Biroli G.; Carello M.; Fagà E.; Pacini G.; De Michieli F.; Cassader M.; Rabbione L.; Premoli A.; and Pagano G. (literal)
Pagina inizio
  • 1175 (literal)
Pagina fine
  • 1183 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#url
  • http://onlinelibrary.wiley.com/doi/10.1002/hep.20896/pdf (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 42 (literal)
Rivista
Note
  • ISI Web of Science (WOS) (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • 1, 2, 3, 4, 5, 6, 8, 9, 10, 11, 12: Department of Internal Medicine, University of Turin, Turin, Italy 7: Metabolic Unit, Institute of Biomedical Engineering (ISIB), National Research Council, Padova, Italy. (literal)
Titolo
  • Adipokines in NASH: postprandial lipid metabolism as a link between adiponectin and liver disease (literal)
Abstract
  • Circulating levels of four adipokines (adiponectin, TNF-?, leptin, and resistin) and the postprandial lipid and adiponectin responses to an oral fat load were assessed in 25 nonobese, non-diabetic patients with biopsy-proven nonalcoholic steatohepatitis (NASH) and correlated with metabolic indices and liver histology. Circulating adiponectin was lower in NASH compared with controls (5,476 ? 344 vs. 11,548 ? 836 ng/mL; P ? .00001) and on multiple regression analysis correlated negatively with liver steatosis, necroinflammation (OR ? 5.0; P ? .009), and fibrosis (OR ? 8.0; P ? .003).The magnitude of postprandial lipemia was significantly higher in NASH than in controls and was related to fasting adiponectin (? ? ?0.78; P ? .00003). Controls showed a significant increase in serum adiponectin in response to the fat load, whereas patients with NASH showed a slight decrease. Postprandial free fatty acids response correlated inversely with adiponectin response in both groups and independently predicted the severity of liver steatosis in NASH (? ? 0.51; P ? .031). In conclusion, hypoadiponectinemia is present before overt diabetes and obesity appear and correlates with the severity of liver histology in NASH. Impaired postprandial lipid metabolism may be an additional mechanism linking hypoadiponectinemia and NASH and posing a higher cardiovascular risk to these subjects. The mechanism(s) underlying these differences are unknown, but the type of dietary fat seems to play a role. These findings may have important pathogenetic and therapeutic implications in both liver and metabolic disease. (HEPATOLOGY 2005;42:1175-1183.) (literal)
Editore
Prodotto di
Autore CNR

Incoming links:


Prodotto
Autore CNR di
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#rivistaDi
Editore di
data.CNR.it