Clinical Trials Directory

Trials / Completed

CompletedNCT02792400

The Role of Glucagon in the Effects of Dipeptidyl Peptidase-4 Inhibitors and Sodium-glucose Co-transporter-2 Inhibitors

Status
Completed
Phase
N/A
Study type
Interventional
Enrollment
24 (actual)
Sponsor
University Hospital, Gentofte, Copenhagen · Academic / Other
Sex
All
Age
30 Years – 75 Years
Healthy volunteers
Not accepted

Summary

In normal physiology, glucagon from pancreatic alpha cells plays an important role in maintaining glucose homeostasis via its regulatory effect on hepatic glucose production. Patients with type 2 diabetes exhibit elevated plasma glucagon levels in the fasting state, and in response to ingestion of glucose or a mixed meal.glucagon, glucagon concentrations fail to decrease appropriately and may even increase. This diabetic hyperglucagonaemia may therefore contribute importantly to the hyperglycaemia of the patients. Several glucose-lowering treatment modalities have been shown to affect glucagon levels in patients with type 2 diabetes, but the role of glucagon in the glucose-lowering effects of these treatment modalities has been difficult to discern. By using a glucagon receptor antagonist (GRA) the investigators will exploit glucagon receptor antagonism to delineate the role of glucagon during treatment with sodium-glucose co-transporter 2 (SGLT2) inhibitors and dipeptidyl peptidase 4 (DPP-4) inhibitors, which have been shown to increase and decrease plasma glucagon levels, respectively.

Conditions

Interventions

TypeNameDescription
DRUGLY2403021Glucagon receptor antagonist
DRUGLY2403021 placebo
PROCEDUREStandardised liquid meal
DRUGLinagliptinDPP-4-inhibitor
DRUGLinagliptin placebo
DRUGEmpagliflozinSGLT2-inhibitor
DRUGEmpagliflozin placebo

Timeline

Start date
2016-05-01
Primary completion
2016-08-01
Completion
2018-07-01
First posted
2016-06-07
Last updated
2020-04-08

Locations

1 site across 1 country: Denmark

Source: ClinicalTrials.gov record NCT02792400. Inclusion in this directory is not an endorsement.