Incretin Effect Clinical Trial
Official title:
Quantification of the Incretin Effect in Healthy Subjects and Patients With Type 2 Diabetes Using Increasing Amounts of Oral Glucose Challenges
Patients with T2DM lac a sufficient incretin response after oral glucose intake. It has only
been tested using 50g of glucose. We don't know if patients with T2DM are capable of
regulating the incretin effect like healthy people in responds to different amounts of
glucose intake.
The aim of the present study is to quantify the incretin effect in healthy subjects and in
patients with T2DM during increasing amounts of oral glucose challenges. The proposed studies
will answer important questions on the mechanisms underlying T2DM and be of importance in
relation to future preventive- and treatment strategies.
The impaired incretin effect in patients with type 2 diabetes mellitus (T2DM) has previously
only been evaluated using a glucose load of 50 g, and it is uncertain whether patients with
T2DM are capable of regulating their incretin effect equivalent to healthy subjects.
Furthermore, it is of great interest to quantify the secretion of GIP and GLP-1 during
increasing glucose loads in both patients with T2DM and in healthy subjects in order to
evaluate whether an increased secretion of one or both of the two incretin hormones
contributes to the regulation of the incretin effect.
The aim of the present study is to quantify the incretin effect in healthy subjects and in
patients with T2DM during increasing amounts of oral glucose challenges and corresponding
isoglycemic iv glucose challenges. The proposed studies will answer important questions on
the pathophysiology underlying T2DM and be of importance in relation to future preventive-
and treatment strategies.
Eight patients with T2DM and 8 matched healthy subjects will be evaluated with oral glucose
tolerance tests (OGTT) using increasing glucose loads (25, 50 and 100 g glucose) and
isoglycemic iv glucose tolerance tests imitating the glucose concentrations as obtained
during the oral glucose loads. The results will describe the regulation of the incretin
effect in patients with T2DM and, thereby, contribute to the clarification of the
pathophysiology of the postprandial hyperglycemia characterizing these patients.
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