OBJECTIVES:The relationships between the adipokines tumor necrosis factor (TNF)-α and adiponectin and the parameters of glucose homeostasis and severity of liver disease were assessed in nonobese nondiabetic subjects with nonalcoholic steatohepatitis (NASH). METHODS:A frequently sampled intravenous glucose tolerance test, serum cytokine measurement, and 7-day alimentary record were performed in 20 biopsy-proven NASH patients and 45 age-, sex-, and BMI-matched controls (30 insulin sensitive and 15 insulin resistant). RESULTS:Patients with NASH had impaired pancreatic β-cell function compared with both insulin-sensitive (adaptation index, AI: 97.7 ± 17.7 vs 307.4 ± 24.1 min -2 mmol -1 L; p = 0.00001) and insulin-resistant (adaptation index, AI: 97.7 ± 17.7 vs 201.4 ± 41.1 min -2 mmol -1 L; p = 0.001) controls. Serum adiponectin levels were also significantly lower in the NASH group than in the two control groups and correlated with adaptation index and with the severity of hepatic steatosis, necroinflammation, and fibrosis. When NASH patients were grouped according to the severity of histological liver damage, adiponectin was the only variable discriminating patients with higher necroinflammatory grade and fibrosis score from those with milder lesions.CONCLUSIONS: β-cell secretory impairment is present in nonobese patients with NASH before glucose intolerance appears and may contribute to their increased risk for developing diabetes. Hypoadiponectinemia is a feature of NASH and may have a pathogenetic role in β-cell dysfunction and in hepatic necroinflammation and fibrosis, independently of insulin resistance, visceral fat accumulation, TNF-α axis activity, and dietary habits. Our findings provide further rationale for therapeutic approaches aimed at increasing adiponectin levels together with restoring β-cell function and insulin sensitivity.(Am J Gastroenterol 2005;100:2438-2446)

Propofol deep sedation administered by an anesthesiologist with appropriate monitorings seems to be a safe procedure during colonoscopy or ERCP in cirrhotic patients.

Postprandial intestinal VLDL1 accumulation is associated with a pro-oxidant imbalance in normolipidemic non-diabetic NASH, and both correlate with the severity of liver disease. Modulating postprandial lipoprotein metabolism may be beneficial in NASH, even if normolipidemic.

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