Glucagon, Goldilocks, and the Three Bears
To understand the role of the medication, Glucagon, one must understand how it figures in the grand scheme of things, and it all starts with eating. In healthy people, eating causes1
- the intestines release two chemicals (peptides), GLP-1 (glucagon-like peptide-1) and GIP (glucose-dependent insulinotropic polypeptide)—thank goodness for abbreviations!
- the pancreas to release insulin and amylin.
The GLP-1 from the intestines and the amylin from the pancreas work together to:
- inhibit stomach emptying, delaying food’s passing on into the intestines where sugar (glucose) is absorbed;
- inhibit glucagon release (glucagon raises blood sugar);4
- inhibit appetite (the “fed” signal to the brain).
The GLP-1 and the GIP from the intestines stimulate the secretion of insulin from the pancreas (called “the incretin effect”).
Therefore, a short summary would be:
Eating causes secretion of chemicals from the intestines and pancreas that promotes the actions and secretion of insulin, decreases appetite, delays stomach emptying into the intestines, and causes insulin to lower the blood sugar, while inhibiting the sugar-raising hormone, glucagon.
This insulin vs. glucagon battle is a checks-and-balances system to mantain a situation where the sugar is not too high nor is it too low, but just right, in a Goldilocks motif.
And in people with diabetes?
In people with diabetes…forgettaboutit.
Forget all the above, because the whole sequence of steps is mucked up. In diabetes, insulin just can’t do its job. There is either not enough (or none) of it, as in diabetes mellitus—diabetes type 1, or the body isn’t sensitive to insulin’s actions, resulting in its underachieving—insulin-resistance, or diabetes type 2. Either way, the result is too much sugar in the blood.
Too much sugar—bad!
When a diabetic leaves the Goldilocks zone—into the high range, high sugar (hyperglycemia) can do both macrovascular damage to blood vessels (as in atherosclerosis and coronary heart disease) and microvascular damage (to the retina, kidneys, and brain).2 The longer the sugars are high, the more irreversible damage is done. Damage to the circulation can cause blindness, kidney failure requiring dialysis, and lead to the need for amputation of limbs. It also can lead to heart attacks and strokes. Add to the mix obesity and its associated high blood pressure, and the perfect storm will be moving in.
Goldilocks and the three bears
Glucose, insulin, and glucagon are the three main actors in sugar levels. Glucose is the sugar itself; insulin signals muscle, fat, and liver cells to absorb glucose from the bloodstream;3 glucagon makes sure the insulin doesn’t overshoot and raises blood sugar by stimulating the liver to release stored glucose (glycogen)—called glycogenolysis.4
How to unmuck the mucked-up works
Since diabetes is a higher than normal sugar level, the goal of medications to treat it involves one or more of the following:
- Direct insulin administration (i.e., actually giving a person insulin itself)
- Stimulate insulin secretion
- Improve sensitivity to the insulin one already has
- Delay the absorption of carbohydrates (sugars) from the stomach and intestines
- Increase the elimination of sugar through the urine, bringing the blood levels down
Where are the Isles of Langerhans? Dora?
This is not a nonsensical geography segue, but the Isles of Langerhans are nowhere near Bora Bora. They are groups of cells in the pancreas and they have cells that come in two varieties: the alpha and the beta. The alpha cells make glucagon, the beta cells make insulin. It makes sense these two cell types would be close together, since insulin brings sugar down and glucagon raises it. This arrangement is typical of the many balancing acts and rheostats the human body has to maintain homeostasis.
Where does Glucagon fit in?
Glucagon, given as a medication, does the same thing that glucagon the hormone from the pancreas does. It stimulates the release of stored glucose when the sugar is too low. This can happen in diabetics who have difficulty balancing their insulin needs with their dietary intake, which can result in their sugars plunging too low. An initial mild hypoglycemia can progress into something called insulin shock:5
- Rapid pulse
Progressing on to:
This is why the American Diabetes Association recommends having a Glucagon Kit available.6,7
Non-diabetics also can have hypoglycemia. This can occur with alcohol abuse; kidney, liver, or cardiac failure; sepsis; glucagon hormone deficiencies; and pancreatic tumors.8
How is Glucagon administered?
By injection. Such injections can be administered from a prepared kit.
How often is it used?
Obviously, if Glucagon is needed frequently, there is a definite problem with either the diagnosis or the correct management of the diagnosis, and more evaluation is needed to study the subtle differences in the causes for repeated bouts of hypoglycemia.
Sugar is sweet, but it is bittersweet when it comes to the human body. Anyone who is at risk for hypoglycemia should have some glucagon available for emergencies.
- Cryer PE, Axelrod L, Grossman AB, et al. Evaluation and management of adult hypoglycemic disorders: an Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab 2009; 94:709.
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