Atropin and Glucose Stimulated Insulinsecretion and the Cephalic Insulin Response

The Significances of Atropin Administration for the GLP-1 Potentiation of Glucose Induced Insulin Secretion and the Cephalic Insulin Response

The aim of this study is to investigate the role of transmission of vagal cholinerg for the GLP-1 potentiation of the glucose stimulated insulin secretion and the cephalic insulin response by using atropin administration.

The hypothesis is that a great deal of the effects of GLP-1 is mediated via the nervous system and for this reason the investigators will research individuals with an intact nervous supply with and without atropin administration.

GLP-1 is a importent enterogastron and incretin hormone. Rapid degradation of GLP-1 by dipeptidyl peptidase 4 (DPP-4) suggests that GLP-1 may act locally (through vagal afferents) before being degraded. We aimed to clarify the role of vagal innervation on the incretin effect.

Inclusion Criteria:

• age between 18 and 45 years
• normal fasting plasma glucose
• normal hemoglobin
• informed consent

Exclusion Criteria:

• diabetes mellitus
• body mass index above 30
• inflamatoric bowel disease
• intestinal surgery
• serum creatinine above 250 microM
• ALAT above to times normal value
• treatment with medicine wich cannot be paused for 12 hours
• contraindication for treatment with atropin