Glucagon – The Forgotten Hormone in the Pathogenesis of Type
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Type 2 Diabetes is almost always thought of as a disease of simple blood sugar management. In reality there is nothing simple about diabetes. There are multiple factors involved on many levels. Glucagon is secreted into the bloodstream by the Alpha cells, insulin is secreted by the Beta cells. When insulin is produced, glucagon is suppressed (after a meal). When glucagon is released it suppresses insulin.

In case of many diabetics, there are always reports of crazy blood sugar swings when the person claims that they have not had any carbs or sugar. Many report high blood sugar either at wake up or after wake up before eating. It is not uncommon to see a rise in blood sugar after exercising, gardening, or fasting. An argument or bad news can raise blood sugar. What’s going on here?

It isn’t the most recognized hormone insulin that is the culprit behind these issues. Insulin is the hormone that is supposed to lower blood sugar. People often say “The blood sugar went up due to an adrenaline response or a cortisol response”. But why and how?

There is the forgotten hormone Glucagon. It seems that nobody talks about it.

Glucagon is a major player in diabetes and blood sugar control. One of the problems is that no one is able to figure out how to manage it.

The opposite effects of insulin and glucagon in fuel homeostasis, the paracrine/endocrine inhibitory effects of insulin on glucagon secretion and the hyperglucagonemia in the pathogenesis of type 2 diabetes (T2D) have long been recognized. Inappropriately increased alpha-cell function importantly contributes to hyperglycaemia and reflects the loss of tonic restraint normally exerted by high local concentrations of insulin on alpha-cells, possibly as a result of beta-cell failure and alpha-cell insulin resistance, but additional mechanisms, such as the participation of incretin hormones in this response, have also been suggested. Three classes of drugs already available for clinical use address the abnormalities of glucagon secretion in T2D, namely, the GLP-1 receptor agonists (GLP-1RA), the inhibitors of dipeptidyl peptidase-4 (DPP-4i) and the amylin agonist pramlintide; it has been proposed that the glucagonostatic and insulinotropic effects of GLP-1RA equally contribute to their hypoglycaemic efficacy.

It has been found that islet cell function is the primary regulator of glucose metabolism in humans. Insulin secretion and signalling is an important contributor to the pathogenesis of type 2 diabetes. Abnormal glucagon suppression is an early change in the pathogenesis of type 2 diabetes. When measuring beta cell function, it is also important to consider the effect of alpha cell function on the response to oral glucose.