Postprandial incretin and islet hormone responses and dipeptidyl-peptidase 4 enzymatic activity in patients with maturity onset diabetes of the young

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Postprandial incretin and islet hormone responses and dipeptidyl-peptidase 4 enzymatic activity in patients with maturity onset diabetes of the young. / Østoft, Signe Harring; Bagger, Jonatan Ising; Hansen, Torben; Hartmann, Bolette; Pedersen, Oluf; Holst, Jens Juul; Knop, Filip Krag; Vilsbøll, Tina.

In: European Journal of Endocrinology, Vol. 173, No. 2, 01.08.2015, p. 205-215.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Østoft, SH, Bagger, JI, Hansen, T, Hartmann, B, Pedersen, O, Holst, JJ, Knop, FK & Vilsbøll, T 2015, 'Postprandial incretin and islet hormone responses and dipeptidyl-peptidase 4 enzymatic activity in patients with maturity onset diabetes of the young', European Journal of Endocrinology, vol. 173, no. 2, pp. 205-215. https://doi.org/10.1530/EJE-15-0070

APA

Østoft, S. H., Bagger, J. I., Hansen, T., Hartmann, B., Pedersen, O., Holst, J. J., ... Vilsbøll, T. (2015). Postprandial incretin and islet hormone responses and dipeptidyl-peptidase 4 enzymatic activity in patients with maturity onset diabetes of the young. European Journal of Endocrinology, 173(2), 205-215. https://doi.org/10.1530/EJE-15-0070

Vancouver

Østoft SH, Bagger JI, Hansen T, Hartmann B, Pedersen O, Holst JJ et al. Postprandial incretin and islet hormone responses and dipeptidyl-peptidase 4 enzymatic activity in patients with maturity onset diabetes of the young. European Journal of Endocrinology. 2015 Aug 1;173(2):205-215. https://doi.org/10.1530/EJE-15-0070

Author

Østoft, Signe Harring ; Bagger, Jonatan Ising ; Hansen, Torben ; Hartmann, Bolette ; Pedersen, Oluf ; Holst, Jens Juul ; Knop, Filip Krag ; Vilsbøll, Tina. / Postprandial incretin and islet hormone responses and dipeptidyl-peptidase 4 enzymatic activity in patients with maturity onset diabetes of the young. In: European Journal of Endocrinology. 2015 ; Vol. 173, No. 2. pp. 205-215.

Bibtex

@article{42bdf2eff3e9465aa995fa12696b7ba3,
title = "Postprandial incretin and islet hormone responses and dipeptidyl-peptidase 4 enzymatic activity in patients with maturity onset diabetes of the young",
abstract = "Objective: The role of the incretin hormones in the pathophysiology of maturity onset diabetes of the young (MODY) is unclear. Design: We studied the postprandial plasma responses of glucagon, incretin hormones (glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP)), and dipeptidyl-peptidase 4 (DPP-4) enzymatic activity in patients with glucokinase (GCK)-diabetes (MODY2), hepatocyte nuclear factor 1α (HNF1A)-diabetes (MODY3), and in matched healthy individuals (CTRLs). Subjects and methods: Ten patients with GCK-diabetes (age: 43±5 years; BMI: 24±2 kg/m2; FPG: 7.1±0.3 mmol/l: HbA1c: 6.6±0.2{\%}), 10 patients with HNF1A-diabetes (age: 31±3 years (mean ± SEM); body mass index (BMI): 24±1 kg/m2; fasting plasma glucose (FPG): 8.9±0.8 mmol/l; haemoglobin A1c (HbA1c): 7.0±0.3{\%}), and 10 CTRLs (age: 40±5 years; BMI: 24±1 kg/m2; FPG: 5.1±0.1 mmol/l; HbA1c: 5.3±0.1{\%}) were examined with a liquid test meal. Results: All groups exhibited similar baseline values of glucagon (7±1 (GCK-diabetes), 6±1 pmol/l (HNF1A-diabetes), 8±2 (CTRLs), P=0.787), but patients with HNF1A-diabetes exhibited postprandial hyperglucagonaemia (area under curve (AUC): 838±108 min×pmol/l) compared to CTRLs (182±176 min×pmol/l, P=0.005) and tended to have a greater response than patients with GCK-diabetes (410±154 min×pmol/l, P=0.063). Similar peak concentrations and AUCs for plasma GIP and plasma GLP-1 were observed across the groups. Increased fasting DPP-4-activity was seen in patients with HNF1A-diabetes (17.7±1.2 mU/ml) vs. CTRLs (13.6±0.8, P=0.011), but was similar to patients with GCK-diabetes (15.0±0.7 mU/ml, P=0.133). Conclusions: The pathophysiology of HNF1A-diabetes includes exaggerated postprandial glucagon responses and increased fasting DPP-4 enzymatic activity, but normal postprandial incretin responses in both patients with GCK-diabetes and HNF1A-diabetes.",
author = "{\O}stoft, {Signe Harring} and Bagger, {Jonatan Ising} and Torben Hansen and Bolette Hartmann and Oluf Pedersen and Holst, {Jens Juul} and Knop, {Filip Krag} and Tina Vilsb{\o}ll",
year = "2015",
month = "8",
day = "1",
doi = "10.1530/EJE-15-0070",
language = "English",
volume = "173",
pages = "205--215",
journal = "European Journal of Endocrinology",
issn = "0804-4643",
publisher = "BioScientifica Ltd.",
number = "2",

}

RIS

TY - JOUR

T1 - Postprandial incretin and islet hormone responses and dipeptidyl-peptidase 4 enzymatic activity in patients with maturity onset diabetes of the young

AU - Østoft, Signe Harring

AU - Bagger, Jonatan Ising

AU - Hansen, Torben

AU - Hartmann, Bolette

AU - Pedersen, Oluf

AU - Holst, Jens Juul

AU - Knop, Filip Krag

AU - Vilsbøll, Tina

PY - 2015/8/1

Y1 - 2015/8/1

N2 - Objective: The role of the incretin hormones in the pathophysiology of maturity onset diabetes of the young (MODY) is unclear. Design: We studied the postprandial plasma responses of glucagon, incretin hormones (glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP)), and dipeptidyl-peptidase 4 (DPP-4) enzymatic activity in patients with glucokinase (GCK)-diabetes (MODY2), hepatocyte nuclear factor 1α (HNF1A)-diabetes (MODY3), and in matched healthy individuals (CTRLs). Subjects and methods: Ten patients with GCK-diabetes (age: 43±5 years; BMI: 24±2 kg/m2; FPG: 7.1±0.3 mmol/l: HbA1c: 6.6±0.2%), 10 patients with HNF1A-diabetes (age: 31±3 years (mean ± SEM); body mass index (BMI): 24±1 kg/m2; fasting plasma glucose (FPG): 8.9±0.8 mmol/l; haemoglobin A1c (HbA1c): 7.0±0.3%), and 10 CTRLs (age: 40±5 years; BMI: 24±1 kg/m2; FPG: 5.1±0.1 mmol/l; HbA1c: 5.3±0.1%) were examined with a liquid test meal. Results: All groups exhibited similar baseline values of glucagon (7±1 (GCK-diabetes), 6±1 pmol/l (HNF1A-diabetes), 8±2 (CTRLs), P=0.787), but patients with HNF1A-diabetes exhibited postprandial hyperglucagonaemia (area under curve (AUC): 838±108 min×pmol/l) compared to CTRLs (182±176 min×pmol/l, P=0.005) and tended to have a greater response than patients with GCK-diabetes (410±154 min×pmol/l, P=0.063). Similar peak concentrations and AUCs for plasma GIP and plasma GLP-1 were observed across the groups. Increased fasting DPP-4-activity was seen in patients with HNF1A-diabetes (17.7±1.2 mU/ml) vs. CTRLs (13.6±0.8, P=0.011), but was similar to patients with GCK-diabetes (15.0±0.7 mU/ml, P=0.133). Conclusions: The pathophysiology of HNF1A-diabetes includes exaggerated postprandial glucagon responses and increased fasting DPP-4 enzymatic activity, but normal postprandial incretin responses in both patients with GCK-diabetes and HNF1A-diabetes.

AB - Objective: The role of the incretin hormones in the pathophysiology of maturity onset diabetes of the young (MODY) is unclear. Design: We studied the postprandial plasma responses of glucagon, incretin hormones (glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP)), and dipeptidyl-peptidase 4 (DPP-4) enzymatic activity in patients with glucokinase (GCK)-diabetes (MODY2), hepatocyte nuclear factor 1α (HNF1A)-diabetes (MODY3), and in matched healthy individuals (CTRLs). Subjects and methods: Ten patients with GCK-diabetes (age: 43±5 years; BMI: 24±2 kg/m2; FPG: 7.1±0.3 mmol/l: HbA1c: 6.6±0.2%), 10 patients with HNF1A-diabetes (age: 31±3 years (mean ± SEM); body mass index (BMI): 24±1 kg/m2; fasting plasma glucose (FPG): 8.9±0.8 mmol/l; haemoglobin A1c (HbA1c): 7.0±0.3%), and 10 CTRLs (age: 40±5 years; BMI: 24±1 kg/m2; FPG: 5.1±0.1 mmol/l; HbA1c: 5.3±0.1%) were examined with a liquid test meal. Results: All groups exhibited similar baseline values of glucagon (7±1 (GCK-diabetes), 6±1 pmol/l (HNF1A-diabetes), 8±2 (CTRLs), P=0.787), but patients with HNF1A-diabetes exhibited postprandial hyperglucagonaemia (area under curve (AUC): 838±108 min×pmol/l) compared to CTRLs (182±176 min×pmol/l, P=0.005) and tended to have a greater response than patients with GCK-diabetes (410±154 min×pmol/l, P=0.063). Similar peak concentrations and AUCs for plasma GIP and plasma GLP-1 were observed across the groups. Increased fasting DPP-4-activity was seen in patients with HNF1A-diabetes (17.7±1.2 mU/ml) vs. CTRLs (13.6±0.8, P=0.011), but was similar to patients with GCK-diabetes (15.0±0.7 mU/ml, P=0.133). Conclusions: The pathophysiology of HNF1A-diabetes includes exaggerated postprandial glucagon responses and increased fasting DPP-4 enzymatic activity, but normal postprandial incretin responses in both patients with GCK-diabetes and HNF1A-diabetes.

U2 - 10.1530/EJE-15-0070

DO - 10.1530/EJE-15-0070

M3 - Journal article

C2 - 25953829

VL - 173

SP - 205

EP - 215

JO - European Journal of Endocrinology

JF - European Journal of Endocrinology

SN - 0804-4643

IS - 2

ER -

ID: 137418800