Influence of Glucagon Inhibition in Relation to the Anti-... | NCT00655603

Status Module

Record Verification Date

Apr 2009

Overall Recruitment Status or Expanded Access Status

Unknown status

Last Known Status

Enrolling by invitation

Delayed Posting

Not provided

Why Stopped

Not provided

Expanded Access Info

Start Date

Mar 2008

Primary Completion Date

May 2009Estimated

Completion Date

Sep 2009Estimated

First Submitted Date

Apr 4, 2008

First Submission Date that Met QC Criteria

Apr 4, 2008

First Posted Date

Apr 10, 2008Estimated

Results Waived

Not provided

Results First Submitted Date

Not provided

Results First Submitted that Met QC Criteria

Not provided

Results First Posted Date

Not provided

Certification/Extension (aka Delayed Results) First Submitted Date

Not provided

Certification/Extension First Submitted that Passed QC Review

Not provided

Certification/Extension First Posted Date

Not provided

Last Update Submitted Date

Apr 3, 2009

Last Update Posted Date

Apr 6, 2009Estimated

Sponsor/Collaborators Module

Responsible Party, by Official Title

Not provided

Lead Sponsor

University Hospital, Gentofte, CopenhagenOTHER

Collaborators

Name	Class
University of Copenhagen	OTHER
Hvidovre University Hospital	OTHER
Glostrup University Hospital, Copenhagen	OTHER

Oversight Module

Has Data Monitoring Committee (DMC)

Is FDA Regulated Drug

Not provided

Is FDA Regulated Device

Not provided

Is Unapproved Device

Not provided

Pediatric Postmarket Surveillance of a Device Product

Not provided

Product Exported from US

Not provided

FDAAA801 Violation

Not provided

Description Module

Brief Summary

Incretinbased treatment of patients with type 2 diabetes mellitus (T2DM) has increasing interest. The incretin glucagon-like peptide-1 (GLP-1) stimulates beta-cells to increased secretion and production of insulin. Glucose sensitivity is enhanced, apoptosis inhibited - progression in disease is potentially stopped. The alpha-cell is also influenced by GLP-1 as infusion lowers plasmaglucose (PG) levels in patients with type 1 diabetes mellitus (T1DM) (C-peptide negative) by inhibition of glucagon and thereby decreased hepatic glucoseproduction (HGP). Further Vilsboll et al has proved normalization of the glacgonostatic effect of glucose in patients with T2DM. As an attempt to elucidate glucose-intolerance in patients with T2DM further Knop et al investigated the glucagonresponse to both oral glucose tolerance test (OGTT) and a following iso-glycemic clamp. He saw a sufficient suppression of glucagon when glucose was introduced intravenously but the suppression of glucagon was attenuated and delayed when glucose was given orally.

The aim of this study is to elucidate the glucose intolerance further. Due to the complex interactions and mutual feed-back regulation between the pancreatic hormones and the PG level this protocol includes five days. All days include a euglycemic-clamp, patients with T2DM (n=10) are clamped at their fasting PG as are healthy control subjects (n=10). During the clamp either GLP-1 alone; GLP-1 in combination with somatostatin, insulin and glucagon; or somatostatin, insulin and glucagon are infused and blood samples are drawn.

The design of the study makes it possible to isolate the effect of each hormone. Further the investigators will be able to enlighten the effect of GLP-1 on the increase in glucose turn-over it induces.

The essential part in this design will be hormone concentrations and the response parameter the amount of glucose (AUC) it takes to create the euglycemic-clamp.

Detailed Description

Not provided

Design Module

Study Type

Interventional

Number of References to an Expanded Access Study

Not provided

Expanded Access Types

Not provided

Patient Registry

Not provided

Target Follow-Up Duration

Not provided

Phases

Not Applicable

Interventional Study Design

Allocation

Biospecimen

No data available

No data is available for this block.

Enrollment

20Estimated

Arms/Interventions Module

Arm Groups

Label	Type	Description	Intervention Names
1	Experimental	10 patients with Type 2 Diabetes Mellitus	Other: Infusion of native hormones from the pancreas and gut (GLP-1)
2	Experimental	10 healthy, matched control participants	Other: Infusion of native hormones from the pancreas and gut (GLP-1)

Interventions

Name	Type	Description	Arm Group Labels	Other Names
Infusion of native hormones from the pancreas and gut (GLP-1)	Other	Glucose-clamps at fasting levels during infusion of hormones in different combinations.	1 2

Outcomes Module

Primary Outcomes

Measure	Description	Time Frame
Glucose turn-over		12 months

Secondary Outcomes

Measure	Description	Time Frame
The inhibitory effect of GLP-1 on glucagon, and the role of this in its anti-diabetic potential, measured by looking at glucose turn-over.		12 months

Other Outcomes

Not provided

Eligibility Module

Eligibility Criteria

Inclusion Criteria:

Type 2 Diabetes Mellitus according to criteria from WHO
Normal hepatic and kidney function
No overt diabetic complications
Treatment with insulin or glitazones
Informed consent

Exclusion Criteria:

BMI < 23
BMI > 35
HbA1c > 10%
Pregnancy

Accepts Healthy Volunteers

Yes

Sex

All

Sex/Gender Based

Not provided

Sex/Gender Description

Not provided

Minimum Age

18 Years

Maximum Age

70 Years

Standard Ages

AdultOlder Adult

Study Population

Not provided

Sampling Method

Not provided

Derived Section

Miscellaneous Info Module

Version Holder

Jul 10, 2026

Removed Countries

Not provided

Submission Tracking

No data available

No data is available for this block.

Condition Browse Module

MeSH Terms

Intervention Browse Module

MeSH Terms

ID	Term
D003924	Diabetes Mellitus, Type 2

Ancestor Terms

ID	Term
D003920	Diabetes Mellitus
D044882	Glucose Metabolism Disorders
D008659	Metabolic Diseases
D009750	Nutritional and Metabolic Diseases
D004700	Endocrine System Diseases

ID	Term
D052216	Glucagon-Like Peptide 1

Ancestor Terms

ID	Term
D004763	Glucagon-Like Peptides
D052336	Proglucagon
D005768	Gastrointestinal Hormones
D006728	Hormones
D006730	Hormones, Hormone Substitutes, and Hormone Antagonists