Influence of gastrointestinal factors on glucose metabolism in patients with cirrhosis

TY - JOUR

T1 - Influence of gastrointestinal factors on glucose metabolism in patients with cirrhosis

AU - Junker, Anders E

AU - Gluud, Lise L

AU - Holst, Jens Juul

AU - Knop, Filip K

AU - Vilsbøll, Tina

N1 - This article is protected by copyright. All rights reserved.

PY - 2015/10/1

Y1 - 2015/10/1

N2 - Background and Aim: 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. We presented data as median ± interquartile range and compared groups using non-parametric analysis of variance. Results: Patients with cirrhosis were glucose intolerant compared with healthy controls (4-h OGTTAUC: 609 ± 458 vs 180 ± 155 min× mmol/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). Conclusion: Impaired gastrointestinal-mediated glucose disposal and reduced incretin effect may contribute to the glucose intolerance seen in patients with cirrhosis.

AB - Background and Aim: 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. We presented data as median ± interquartile range and compared groups using non-parametric analysis of variance. Results: Patients with cirrhosis were glucose intolerant compared with healthy controls (4-h OGTTAUC: 609 ± 458 vs 180 ± 155 min× mmol/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). Conclusion: Impaired gastrointestinal-mediated glucose disposal and reduced incretin effect may contribute to the glucose intolerance seen in patients with cirrhosis.

U2 - 10.1111/jgh.12981

DO - 10.1111/jgh.12981

M3 - Journal article

C2 - 25867498

SN - 0815-9319

VL - 30

SP - 1522

EP - 1528

JO - Journal of Gastroenterology and Hepatology

JF - Journal of Gastroenterology and Hepatology

IS - 10

ER -