Type 2 Diabetes Mellitus Clinical Trial
Official title:
Incretin Physiology and Beta-Cell Function Before and After Treatment With Steroid Hormone in Healthy Individuals
The purpose of this study is to evaluate whether the reduced incretin effect and the paradoxical glucagon responses during oral glucose ingestion and isoglycaemic iv glucose infusion observed in patients with type 2 diabetes are causes (non-inducible in lean healthy subjects without family history of diabetes) or consequences (inducible) of the diabetic state.
The incretin effect is severely reduced in patients with type 2 diabetes. This
pathophysiological trait is accompanied by an almost abolished insulinotropic effect of the
incretin hormone glucose-dependent insulinotropic polypeptide (GIP) and a reduced
insulinotropic potency of the other incretin hormone glucagon-like peptide-1 (GLP-1).
Furthermore, recent studies suggest that hypersecretion of glucagon during oral glucose
ingestion, as opposed to a normal suppression of glucagon during isoglycaemic intravenous
(iv) administered glucose, further attenuates the incretin effect in patients with type 2
diabetes.
However, it remains unclear whether the severely reduced incretin effect and its
accompanying pathophysiological traits characterizing patients with type 2 diabetes can be
induced temporarily in healthy subjects by a short period of glucose homeostatic
dysregulation.
In this study the incretin effect will be measured using 50-g oral glucose tolerance test
and isoglycaemic iv glucose infusion and meal test in 10 healthy Caucasian subjects without
family history of diabetes before and after dysregulation of glucose homeostasis using high
calorie diet, physical inactivity and administration of adrenocortical steroids
;
Allocation: Non-Randomized, Endpoint Classification: Efficacy Study, Intervention Model: Single Group Assignment, Masking: Open Label
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