Impact of PPAR-gamma agonists on adipose-tissue insulin resistance in patients with IGT or T2DM and non-alcoholic steatohepatitis (NASH) (Abstract/Poster in atti di convegno)

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  • Impact of PPAR-gamma agonists on adipose-tissue insulin resistance in patients with IGT or T2DM and non-alcoholic steatohepatitis (NASH) (Abstract/Poster in atti di convegno) (literal)
Anno
  • 2007-01-01T00:00:00+01:00 (literal)
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  • Gastaldelli A.; Balas B.; Hardies J.; Harrison S.; Belfort R.; Brown K.; Schenker S.; Defronzo R. A.; Cusi K. (2007)
    Impact of PPAR-gamma agonists on adipose-tissue insulin resistance in patients with IGT or T2DM and non-alcoholic steatohepatitis (NASH)
    in 43rd EASD Annual Meeting, Amsterdam
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Gastaldelli A.; Balas B.; Hardies J.; Harrison S.; Belfort R.; Brown K.; Schenker S.; Defronzo R. A.; Cusi K. (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#note
  • In: 43rd EASD Annual Meeting (Amsterdam, 17-21 September 2007). Proceedings, pp. S36 - S36. EASD (ed.). EASD, 2007. (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#descrizioneSinteticaDelProdotto
  • Background and Aims: Hepatocellular lipids (Hep-L) accumulation is frequently observed in insulin-resistant states including type 2 diabetes mellitus. We have recently reported that pioglitazone (PIO) treatment improved glucose metabolism, steatosis and necro-inflammation in IGT/T2DM patients and biopsy-proven non-alcoholic steatohepatitis (NASH). Because abnormal lipid metabolism/elevated plasma FFA are believed to play an important role in the development of hepatic steatosis (i.e., fat overflow to the liver) we examined the role of adipose tissue IR and impact of PIO therapy in this cohort of NASH pts. Materials and Methods: Patients received a hypocaloric diet (-500 kcal/d) and were randomized (double-blind) to PIO (45mg/d) or placebo (Pbo) for 6 months. Before and after treatment pts underwent: 1) liver biopsy; 2) liver fat measurement by magnetic resonance (Hep-L); 3) double-tracer 75g OGTT to assess glucose tolerance, glucose production (EGP) and clearance, and to estimate indexes of IR at the level of adipose tissue (Adip-IR=fasting plasma FFA x insulin conc [FPI]) and liver (Hep-IR=EGP x FPI). 15 control subjects (CT) were also studied in the same way (except for liver biopsy). Results: Compared to CT, NASH had increased FFA (739±34 vs. CT 596±44 umol/l; p0.001), impaired FFA suppression during OGTT (360±18 vs 240±19 umol/l; p0.001), severe Adip-IR (12.1±1.3 vs. 2.7±0.6 mmol/l\"mU/l, p0.0003) and low adiponectin (7.0±1.6 vs. 13.2±2.1 mg/l p0.001). Hep-L was ~3-fold higher in NASH (p0.001) and correlated positively with Adip-IR (r (literal)
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  • Impact of PPAR-gamma agonists on adipose-tissue insulin resistance in patients with IGT or T2DM and non-alcoholic steatohepatitis (NASH) (literal)
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