Title : Glucagon a plausible contributor, hiding in plain sight
Abstract:
We have been taught to believe that type 2 diabetes is result of insulin resistance. We know that glucose haemostasis is controlled by a variety of hormones The two most spoken of are insulin and glucagon, the former more so than the latter. Our talk will focus on these two hormones. Insulin functions in the removal of glucose from the blood stream. Glucagon on the other hand functions in increasing the amount of glucose in the blood stream. Simply put these hormones act antagonistically to each other.
In our presentation we will present scientific evidence which indicates a higher-than-normal circulating level of glucagon in the diabetic patient. This to us suggests that glucagon in some way may be involved in the pathogenesis of diabetes. We see the almost immediate impact of bariatric surgery on the need for hypoglycaemic preparations, we recognise that there is a spike in glucagon levels following oral intake in a diabetic. Interestingly, that same spike is not seen in the same individual who is provided with a parenteral source of glucose which leads us to the singular conclusion that there is an additional source of glucagon which is not activated by glucose stimulation outside of the gut.
Conclusion: We have come to realise, therefore, that in our guts is an extra pancreatic source of glucagon in the diabetic. Are we saying that this source of glucagon develops in the individual predisposed to developing diabetes? No, we think this is the result of dysfunction in specialised receptors in the GUT, the GLP-1 receptors.
