BACKGROUND AND AIMS: The impaired glucose tolerance in cirrhosis is poorly understood. We evaluated the influence of gastrointestinal-mediated glucose disposal and incretin effect in patients with cirrhosis.

METHODS: Non-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 (IIGI). We presented data as median ± interquartile range and compared groups using non-parametric analysis of variance.

RESULTS: Patients with cirrhosis were glucose intolerant compared to healthy controls (4 hour OGTTAUC : 609 ± 458 vs. 180 ± 155 min x mmol/L; P = 0.005), insulin resistant (homeostatic model assessment (HOMAIR ): 3.7 ± 4.9 vs. 2.6 ± 1.4; P = 0.014) and had fasting hyperglucagonemia (8 ± 3 vs. 3 ± 4 pmol/L; P = 0.027). Isoglycemia was achieved using 35 ± 12 g of intravenous glucose in patients with cirrhosis compared to 24 ± 10 g 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 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) patients with cirrhosis had reduced incretin effect (35 ± 44 vs. 55 ± 30%; P = 0.008).

CONCLUSIONS: Impaired gastrointestinal-mediated glucose disposal and reduced incretin effect may contribute to the glucose intolerance seen in patients with cirrhosis.