S. Monnerat*a (Ms), C. Atilaa (Dr), S. Urwylera (Dr), J. Refardta (Dr), B. Winzelera (Dr), M. Christ-Craina (Prof)

a University Hospital Basel, Basel, SWITZERLAND

* sophie.monnerat@usb.ch

INTRODUCTION Non-osmotic tests such as glucagon, arginine or macimorelin stimulations were recently assessed for their ability to evaluate posterior pituitary function. Glucagon and arginine, but not macimorelin, stimulate copeptin secretion (a surrogate marker of vasopressin) and, therefore, represent novel tests to assess the posterior pituitary. The exact mechanism behind their stimulatory effect remains elusive.
MATERIAL AND METHODS This analysis combined data from three diagnostic studies conducted at the University Hospital Basel, Switzerland. In total, 80 healthy adults underwent the glucagon (n=22), arginine (n=30), and macimorelin (n= 28) stimulation tests. The primary objective was to investigate glucose
dynamics upon glucagon, arginine, and macimorelin stimulation tests and their relation to plasma copeptin change.
RESULTS Upon glucagon stimulation, the median [IQR] glucose level at baseline was 5.0 [4.6, 5.2] mmol/l, peaked at 8.1 [7.2, 9.4] mmol/l at 30 minutes and decreased to a minimum of 3.8 [3.5, 4.5] mmol/l at 120 minutes. The median copeptin increase upon glucagon stimulation was 7.6 [2.4, 28.0] pmol/l. Upon arginine, the median glucose level at baseline was 4.9 [4.8, 5.5] mmol/l, peaked at 6.0 [5.2, 6.4] mmol/l at 30 minutes and decreased to a minimum of 4.3 [3.8, 4.8] mmol/l at 60 minutes. The median copeptin increase upon arginine stimulation was 4.5 [2.9, 7.5] pmol/l. Upon macimorelin, glucose levels showed no notable dynamics over the 120 minutes, and no major change in copeptin was observed. In the pooled dataset, a decrease in glucose levels was significantly correlated with an increase in copeptin (ρ=0.49, p<0.001).
DISCUSSION A similar change in plasma glucose could be observed after glucagon and arginine stimulation, whereas macimorelin had no effect on glucose levels. There was a strong correlation between the decrease in glucose and the increase in copeptin. These findings suggest that a drop in glucose levels might be a possible cause for the increase in copeptin levels upon glucagon and arginine stimulation. Whether the drop in glucose levels itself leads to copeptin secretion, or whether it mirrors other stimuli such as hypoglycemia-induced stress cannot be answered with our analysis and should be further investigated.

The author has declared no conflict of interest.