Type 2 Diabetes Mellitus Clinical Trial
Official title:
The Role of GIP, GLP-1 and GLP-2 in Type 2 Diabetic Hyperglucagonemia
In order to investigate the mechanisms underlying the hyperglucagonemia characterizing patients with type 2 diabetes mellitus (T2DM) we wish to test the following hypothesis: Do pancreatic alpha-cells exhibit inappropriate glucagon responses to substances released from the small intestine (GIP, GLP-2 and GLP-2) in patients with T2DM?
Patients with T2DM are not able to suppress their secretion of glucagon after a meal or
after oral ingestion of glucose. Patients actually respond with pathological high
plasmaglucagon concentrations to these stimuli. Previous studies have shown that
postprandial hyperglucagonemia results in increased hepatic glucose production and therefore
contributes significantly to the hyperglycemia characterizing these patients.
Recently we have shown that patients with T2DM exhibit a normal suppression of glucagon
secretion following an adjustable intravenous (iv) glucose challenge mimicking the glucose
excursion following a 50-g oral glucose tolerance test (OGTT) with the latter resulting in
lack of glucagon suppression. Why this difference? A possible explanation could be that the
oral administration stimulates intestinal factors resulting in a differentially glucagon
response to the two similar glucose excursions. We wish to establish whether GIP, GLP-1
and/or GLP-2 are responsible for the inappropriate glucagon suppression following OGTT and
meals in patients with T2DM.
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Observational Model: Case-Only, Time Perspective: Cross-Sectional
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