Influence of gastrointestinal factors on glucose metabolism in patients with cirrhosis

Background and AimThe impaired glucose tolerance in cirrhosis is poorly understood. We evaluated the influence of gastrointestinal-mediated glucose disposal and incretin effect in patients with cirrhosis. MethodsNon-diabetic patients with Child-Pugh A or B cirrhosis (n=10) and matched healthy controls (n=10) underwent a 50-g oral glucose tolerance test (OGTT) and an isoglycemic intravenous glucose infusion. We presented data as medianinterquartile range and compared groups using non-parametric analysis of variance. ResultsPatients with cirrhosis were glucose intolerant compared with healthy controls (4-h OGTT(AUC): 609 +/- 458 vs 180 +/- 155minxmmol/L; P=0.005), insulin resistant (homeostatic model assessment for insulin resistance: 3.7 +/- 4.9 vs 2.6 +/- 1.4; P=0.014) and had fasting hyperglucagonemia (8 +/- 3 vs 3 +/- 4pmol/L; P=0.027). Isoglycemia was achieved using 35 +/- 12g of intravenous glucose in patients with cirrhosis compared with 24 +/- 10g in healthy controls (P=0.003). The gastrointestinal-mediated glucose disposal was markedly lower in patients with cirrhosis (30 +/- 23 vs 52 +/- 20%; P=0.003). Despite higher levels of the incretin hormones glucagon-like peptide-1 and glucose-dependent insulinotropic peptide patients with cirrhosis had reduced incretin effect (35 +/- 44 vs 55 +/- 30%; P=0.008). ConclusionImpaired gastrointestinal-mediated glucose disposal and reduced incretin effect may contribute to the glucose intolerance seen in patients with cirrhosis.