The impact of liraglutide on glucose tolerance and the risk of type 2 diabetes in women with previous gestational diabetes mellitus

Status

Active, not recruiting

Phases

Phase 4

Study type

Interventional

Source

EU CTR

Registry ID

EUCTR2012-001371-37-DK

Enrollment

160

Registered

2012-07-09

Start date

2012-07-10

Completion date

Unknown

Last updated

2019-12-10

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Gestational diabetes mellitus Non-alcoholic fatty liver disease MedDRA version: 20.0 Level: LLT Classification code 10018210 Term: Gestational diabetes mellitus System Organ Class: 100000004868 MedDRA version: 20.1 Level: PT Classification code 10029530 Term: Non-alcoholic fatty liver System Organ Class: 10019805 - Hepat

Interventions

Trade Name: Victoza Pharmaceutical Form: Suspension for injection in pre-filled pen INN or Proposed INN: LIRAGLUTIDE CAS Number: 204656-20-2

Eligibility

Sex/Gender

All

Inclusion criteria

Inclusion criteria: Women with previous GDM: • Informed oral and written consent • Previous diagnosis of GDM according to current Danish guidelines (plasma glucose concentration at 120 min after 75 g oral glucose tolerance test =9.0 mM) during pregnancy within the last 10 years • Age >18 years • 25 kg/m2 18 years • 25 kg/m2 18 years • 25 kg/m2 18 years • At least one prior pregnancy Are the trial subjects under 18? no Number of subjects for this age range: F.1.2 Adults (18-64 years) yes F.1.2.1 Number of subjects for this age range 160 F.1.3 Elderly (>=65 years) no F.1.3.1 Number of subjects for this age range

Exclusion criteria

Exclusion criteria: Women with previous GDM • Patients with diabetes • HbA1c =6.5% • Patients with previous pancreatitis or previous neoplasia • Pregnant or breast feeding women • Anaemia (haemoglobin 3 times upper normal limit) • Impaired renal function (se-creatinine >120 µM and/or albuminuria) • Uncontrolled hypertension (systolic blood pressure >180 mmHg, diastolic blood pressure >100 mmHg) • Any condition that the investigator feels would interfere with trial participation • Receiving any investigational drug within the last 3 months Women without previous GDM • Pregnant or breast feeding women • Anaemia (haemoglobin 120 µM and/or albuminuria) • Uncontrolled hypertension (systolic blood pressure >180 mmHg, diastolic blood pressure >100 mmHg) • Any condition that the investigator feels would interfere with trial participation

Design outcomes

Primary

Measure	Time frame
Main Objective: To investigate the effect of the glucagon-like peptide-1 receptor agonist liraglutide on patophysiological characteristics and the risk of type 2 diabetes mellitus in women with previous gestational diabetes mellitus (GDM).; Secondary Objective: To investigate if liraglutide has an effect on appetite which is different during OGTT and IIGI, if liraglutide improves the subjects' quality of life and bone mineral density. To investigate if the quality of life in women with prior GDM and non-alcoholic fatty liver (NAFLD) is better or worse than women with prior GDM without NAFLD, women without prior GDM and without NAFLD and women with NAFLD who attend an outpatient clinic due to their liver disease. ;Timepoint(s) of evaluation of this end point: After 52, 53, 260, and 261 weeks;Primary end point(s): Primary endpoint is the change in glucose tolerance from baseline to week 52 as measured by area under the curve (AUC) for the PG excursion following a 4-hour 75 g-oral glucose tolerance test (OGTT). Additional endpoints regarding glucose tolerance includes changes from baseline to week 53 (after trial medication wash-out) and at end of the study (260 weeks and 261 weeks (liraglutide-treated).	—

Measure

Time frame

Main Objective: To investigate the effect of the glucagon-like peptide-1 receptor agonist liraglutide on patophysiological characteristics and the risk of type 2 diabetes mellitus in women with previous gestational diabetes mellitus (GDM).; Secondary Objective: To investigate if liraglutide has an effect on appetite which is different during OGTT and IIGI, if liraglutide improves the subjects' quality of life and bone mineral density. To investigate if the quality of life in women with prior GDM and non-alcoholic fatty liver (NAFLD) is better or worse than women with prior GDM without NAFLD, women without prior GDM and without NAFLD and women with NAFLD who attend an outpatient clinic due to their liver disease. ;Timepoint(s) of evaluation of this end point: After 52, 53, 260, and 261 weeks;Primary end point(s): Primary endpoint is the change in glucose tolerance from baseline to week 52 as measured by area under the curve (AUC) for the PG excursion following a 4-hour 75 g-oral glucose tolerance test (OGTT). Additional endpoints regarding glucose tolerance includes changes from baseline to week 53 (after trial medication wash-out) and at end of the study (260 weeks and 261 weeks (liraglutide-treated).

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Secondary

Measure	Time frame
Secondary end point(s): 1) Percentage of subjects in each treatment arm with normal glucose tolerance (NGT: FPG = 6.0 mM and 2h PG < 7.8 mM) at inclusion who develop prediabetes (impaired fasting glucose (IFG): (6.1 mM = fasting PG (FPG) < 7.0 mM and 2h PG after 75 g-OGTT < 7.8 mM) and/or impaired glucose tolerance (IGT): (FPG < 6.1 mM and 7.8 mM = 2h PG after 75 g-OGTT = 11.0 mM) or T2DM (FPG= 7mM or 2h PG = 11.1 mM) 2) Improvement in glycaemic status, as percentage of patients in each treatment arm going from: • IFG to normal glucose tolerance (FPG = 6.0 mM and 2h PG < 7.8 mM) • IGT to NGT • Combined IFG and IGT to IFG, IGT, or NGT 3) Progression of isolated IFG or isolated IGT (at inclusion) to combined IFG/IGT or type 2 diabetes mellitus (T2DM), and progression of combined IFG/IGT (at inclusion) to T2DM 4) Changes in glycosylated haemoglobin (HbA1c) as percentage of patients who progress from: • Normoglycaemic to prediabetic (HbA1c <6.0 ? 6.0-6.4) • Normoglycaemic to T2DM (HbA1c <6.0 ? = 6.5) • Prediabetic to T2DM (HbA1c 6.0-6.4 ? = 6.5) or improves from: • Prediabetic to normoglycaemic (HbA1c 6.0-6.4 ? <6.0) 5) Changes in anthropometric measurements (BMI, absolute body weight (kg) and waist:hip ratio) 6) Changes in beta cell secretory responses (AUC for insulin and C-peptide) during OGTT and IIGI, the homeostatic model assessment (HOMA) and pro-insulin to insulin ratio) 7) Changes in insulin sensitivity (assessment of insulin resistance (HOMAIR ) and Matsuda insulin sensitivity index) 8) Changes in incretin hormone secretion (fasting plasma concentrations and plasma responses of GLP-1, GLP-2 and GIP) and plasma glucagon during OGTT 9) Changes in incretin effect (insulin and C-peptide responses after OGTT vs. I	—

Measure

Time frame

Secondary end point(s): 1) Percentage of subjects in each treatment arm with normal glucose tolerance (NGT: FPG = 6.0 mM and 2h PG < 7.8 mM) at inclusion who develop prediabetes (impaired fasting glucose (IFG): (6.1 mM = fasting PG (FPG) < 7.0 mM and 2h PG after 75 g-OGTT < 7.8 mM) and/or impaired glucose tolerance (IGT): (FPG < 6.1 mM and 7.8 mM = 2h PG after 75 g-OGTT = 11.0 mM) or T2DM (FPG= 7mM or 2h PG = 11.1 mM) 2) Improvement in glycaemic status, as percentage of patients in each treatment arm going from: • IFG to normal glucose tolerance (FPG = 6.0 mM and 2h PG < 7.8 mM) • IGT to NGT • Combined IFG and IGT to IFG, IGT, or NGT 3) Progression of isolated IFG or isolated IGT (at inclusion) to combined IFG/IGT or type 2 diabetes mellitus (T2DM), and progression of combined IFG/IGT (at inclusion) to T2DM 4) Changes in glycosylated haemoglobin (HbA1c) as percentage of patients who progress from: • Normoglycaemic to prediabetic (HbA1c <6.0 ? 6.0-6.4) • Normoglycaemic to T2DM (HbA1c <6.0 ? = 6.5) • Prediabetic to T2DM (HbA1c 6.0-6.4 ? = 6.5) or improves from: • Prediabetic to normoglycaemic (HbA1c 6.0-6.4 ? <6.0) 5) Changes in anthropometric measurements (BMI, absolute body weight (kg) and waist:hip ratio) 6) Changes in beta cell secretory responses (AUC for insulin and C-peptide) during OGTT and IIGI, the homeostatic model assessment (HOMA) and pro-insulin to insulin ratio) 7) Changes in insulin sensitivity (assessment of insulin resistance (HOMAIR ) and Matsuda insulin sensitivity index) 8) Changes in incretin hormone secretion (fasting plasma concentrations and plasma responses of GLP-1, GLP-2 and GIP) and plasma glucagon during OGTT 9) Changes in incretin effect (insulin and C-peptide responses after OGTT vs. I

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Countries

Denmark

Contacts

Public ContactCenter for diabetesforskning

Gentofte Hospital, University of Copenhagen

t.vilsboll@dadlnet.dk4538672461

Outcome results

None listed

Source: EU CTR (via WHO ICTRP) · Data processed: Feb 4, 2026