Junker Anders E, Gluud Lise L, Holst Jens J, Knop Filip K, Vilsbøll Tina
Center for Diabetes Research, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark.
NNF Center for Basic Metabolic Research, Department of Biomedical Science, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
J Gastroenterol Hepatol. 2015 Oct;30(10):1522-8. doi: 10.1111/jgh.12981.
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.
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.
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 ± 4 pmol/L; P = 0.027). Isoglycemia was achieved using 35 ± 12 g of intravenous glucose in patients with cirrhosis compared with 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 and glucose-dependent insulinotropic peptide patients with cirrhosis had reduced incretin effect (35 ± 44 vs 55 ± 30%; P = 0.008).
Impaired gastrointestinal-mediated glucose disposal and reduced incretin effect may contribute to the glucose intolerance seen in patients with cirrhosis.
肝硬化患者糖耐量受损的情况目前了解甚少。我们评估了胃肠道介导的葡萄糖处置及肠促胰岛素效应在肝硬化患者中的影响。
Child-Pugh A级或B级肝硬化的非糖尿病患者（n = 10）及相匹配的健康对照者（n = 10）接受了50克口服葡萄糖耐量试验（OGTT）及等血糖静脉葡萄糖输注。我们将数据表示为中位数±四分位间距，并使用非参数方差分析对组间进行比较。
与健康对照者相比，肝硬化患者存在糖耐量受损（4小时OGTT曲线下面积：609±458 vs 180±155分钟×毫摩尔/升；P = 0.005）、胰岛素抵抗（胰岛素抵抗稳态模型评估：3.7±4.9 vs 2.6±1.4；P = 0.014）且有空腹高胰高血糖素血症（8±3 vs 3±4皮摩尔/升；P = 0.027）。肝硬化患者达到等血糖状态需静脉输注葡萄糖35±12克，而健康对照者为24±10克（P = 0.003）。肝硬化患者胃肠道介导的葡萄糖处置明显较低（30±23% vs 52±20%；P = 0.003）。尽管肝硬化患者的肠促胰岛素激素胰高血糖素样肽-1和葡萄糖依赖性促胰岛素多肽水平较高，但其肠促胰岛素效应降低（35±44% vs 55±30%；P = 0.008）。
胃肠道介导的葡萄糖处置受损及肠促胰岛素效应降低可能导致肝硬化患者出现糖耐量受损。
