Influence of gastrointestinal factors on glucose metabolism in patients with cirrhosis

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Standard

Influence of gastrointestinal factors on glucose metabolism in patients with cirrhosis. / Junker, Anders E; Gluud, Lise L; Holst, Jens Juul; Knop, Filip K; Vilsbøll, Tina.

I: Journal of Gastroenterology and Hepatology, Bind 30, Nr. 10, 10.2015, s. 1522-8.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Junker, AE, Gluud, LL, Holst, JJ, Knop, FK & Vilsbøll, T 2015, 'Influence of gastrointestinal factors on glucose metabolism in patients with cirrhosis', Journal of Gastroenterology and Hepatology, bind 30, nr. 10, s. 1522-8. https://doi.org/10.1111/jgh.12981

APA

Junker, A. E., Gluud, L. L., Holst, J. J., Knop, F. K., & Vilsbøll, T. (2015). Influence of gastrointestinal factors on glucose metabolism in patients with cirrhosis. Journal of Gastroenterology and Hepatology, 30(10), 1522-8. https://doi.org/10.1111/jgh.12981

Vancouver

Junker AE, Gluud LL, Holst JJ, Knop FK, Vilsbøll T. Influence of gastrointestinal factors on glucose metabolism in patients with cirrhosis. Journal of Gastroenterology and Hepatology. 2015 okt.;30(10):1522-8. https://doi.org/10.1111/jgh.12981

Author

Junker, Anders E ; Gluud, Lise L ; Holst, Jens Juul ; Knop, Filip K ; Vilsbøll, Tina. / Influence of gastrointestinal factors on glucose metabolism in patients with cirrhosis. I: Journal of Gastroenterology and Hepatology. 2015 ; Bind 30, Nr. 10. s. 1522-8.

Bibtex

@article{6945d40a69ca4ef0bc1a1941a5cf8664,
title = "Influence of gastrointestinal factors on glucose metabolism in patients with cirrhosis",
abstract = "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.",
author = "Junker, {Anders E} and Gluud, {Lise L} and Holst, {Jens Juul} and Knop, {Filip K} and Tina Vilsb{\o}ll",
note = "This article is protected by copyright. All rights reserved.",
year = "2015",
month = oct,
doi = "10.1111/jgh.12981",
language = "English",
volume = "30",
pages = "1522--8",
journal = "Journal of Gastroenterology and Hepatology",
issn = "0815-9319",
publisher = "Wiley-Blackwell Publishing Asia",
number = "10",

}

RIS

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

Y1 - 2015/10

N2 - 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.

AB - 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.

U2 - 10.1111/jgh.12981

DO - 10.1111/jgh.12981

M3 - Journal article

C2 - 25867498

VL - 30

SP - 1522

EP - 1528

JO - Journal of Gastroenterology and Hepatology

JF - Journal of Gastroenterology and Hepatology

SN - 0815-9319

IS - 10

ER -

ID: 137418841