Incretin Hormones in Type-1 Diabetes Mellitus Glycemic Response in Type-1 Diabetes Mellitus

This study has been completed.
Sponsor:
Information provided by:
Hvidovre University Hospital
ClinicalTrials.gov Identifier:
NCT00832741
First received: January 29, 2009
Last updated: NA
Last verified: January 2009
History: No changes posted

January 29, 2009
January 29, 2009
May 2008
October 2008   (final data collection date for primary outcome measure)
blood glucose [ Time Frame: 4 hours ] [ Designated as safety issue: No ]
Same as current
No Changes Posted
  • GLP-1 and GIP response during a meal [ Time Frame: 4 hours ] [ Designated as safety issue: No ]
  • betacell function (incremental area under the c-peptide concentration curve) [ Time Frame: 4 hours ] [ Designated as safety issue: No ]
  • alfa cell function (plasma glucagon) [ Time Frame: 4 hours ] [ Designated as safety issue: No ]
  • gastric emptying [ Time Frame: 4 hours ] [ Designated as safety issue: No ]
Same as current
Not Provided
Not Provided
 
Incretin Hormones in Type-1 Diabetes Mellitus Glycemic Response in Type-1 Diabetes Mellitus
Secretion and Significance of the Incretin Hormones on the Postprandial Glycemic Response in Type-1 Diabetes Mellitus

The purpose of this study is to investigate whether secretion of incretin hormones is intact and to what extent endogenous as well as exogenous GLP-1 controls postprandial glucose excursions in patients with type-1 diabetes mellitus.

GLP-1 and GIP are incretin hormones secreted from specific endocrine celles in the gut. Stimulus for secretion is prescence of carbohydrates, fat and protein in the gut. The incretin hormones controls postprandial glucose excursions through stimulation of insulinsecretion as well as inhibition of glucagon and gastric emptying.The effects of GLP-1 on insulin secretion and glucagon inhibition are glucose dependent and the risc of hypoglycemia is therefore negligible when the hormone is administered in supra physiological concentrations.Furthermore, some animal studies suggest that GLP-1 has a trofic effect on the betacells and the hormone has been shown to replenish intracellular stores of insulin. Because the main bloodglucose lowering effect of GLP-1 has been thought to be due to increased insulin secretion, analouges of the hormone has been developed for the treatment of type-2 diabetes. So far, relatively little is known about the effect of GLP-1 in type-1 diabetes.It possible, that GLP-1 in combination with insulin (possibly mainly through its effect on glucagon inhibition and gastric emptying) could reduce the need for exogenous insulin with a concomitant reduced risc of hypoglycemia. Without compromising the target glucemic control. This study focuses of the postprandial bloodglucose lowering effects of endogenous as well as exogenous GLP-1 in patients with type-1 diabetes according to residual betacell function and glycemic control.Furthermore, the endogenous secretion of incretin hormones in patients with type-1 diabetes mellitus will be compared to that of matched normal controls.

Observational
Not Provided
Not Provided
Retention:   Samples With DNA
Description:

whole blood, plasma

Non-Probability Sample

primary care clinic patients and community population(control subjects)

Type 1 Diabetes
Not Provided
Not Provided
Not Provided

*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Completed
30
October 2008
October 2008   (final data collection date for primary outcome measure)

Inclusion Criteria:

  • type-1 diabetes mellitus
  • diagnosis between 5-40 years.
  • age 18-60 year
  • normal weight at time of diagnosis
  • insulintreatment from diagnosis
  • HbA1c < 7.6 %

Exclusion Criteria:

  • diabetic complications
  • disease other than type-1 diabetes
Both
18 Years to 60 Years
Yes
Contact information is only displayed when the study is recruiting subjects
Denmark
 
NCT00832741
H-C-2007-0080, 2008-41-1811
No
Urd Kielgast, MD, Hvidovre University Hospital
Hvidovre University Hospital
Not Provided
Study Director: Urd Kielgast, MD unafilliated
Principal Investigator: Sten Madsbad, MD, DMSc Unafilliated
Hvidovre University Hospital
January 2009

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP