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The influence of the glucagon agonist on myopia development was much more pronounced.
There is still the possibility that the amount of glucagon precursor protein, which is most likely not detected by the radioimmunoassay, changes diurnally.
No diurnal variation in the retinal amount of glucagon was detected.
Neither glucagon nor serotonin increased in any patient.
In the present study, it was tested whether these changes are reflected in different amounts of glucagon peptide in hyperopic and myopic eyes.
The level of somatostatin and glucagon was high in this patient.
No effect of the glucagon antagonist on hyperopia development was visible at the lower and the higher dose.
Retinal glucagon content was about two-fold higher than choroidal content.
In their experiments, about 18% of the total glucagon could be released by high potassium stimulation.
The glucagon antagonist inhibited hyperopia development, albeit only in a narrow concentration range, and at most by 50%, but not myopia development.
Therefore, a considerable number of glucagon antagonists and agonists have been designed as potential treatments for diabetes.
Phosphatidylinositol-3-kinase is involved in the glucagon-induced translocation of aquaporin-8 to hepatocyte plasma membrane.
Moreover, higher doses may trigger a feedback mechanism, perhaps through regulation of glucagon receptor expression.
The level of glucagon was the highest in this patient at 171 pg/ml.
However, glucagon may act through other signal pathways.
