Insulin: "Mission Improbable"

 

 
Persons with diabetes who use insulin crave a sense of certainty or predictability when it comes to the action of their shots or boluses and the effects that follow. Unfortunately there are many reasons why an insulin dose can seem fickle in how it affects your blood sugar levels.


Injected insulin (whether by syringe or a pump) enters the body through the tissues under the skin surface. While we know this method of delivery ultimately works to lower sugar levels, it's nevertheless an unnatural route. In the subcutaneous tissues, insulin begins its journey to reach its intended target: the insulin receptors on the surface of insulin response tissues (muscle, liver, fat) throughout the body. Pearl: the brain does not require insulin for its tissues to use sugar.

 

 

Insulin is introduced into the body like a commando team dropped deep into enemy territory on a near suicide mission. Never mind potential insulin loss from back-leakage at the injection site through oozing or bleeding. Insulin faces a more immediate degradation by destructive enzymes known as insulinases, located throughout the subcutaneous tissues.  As the injected insulin crystals dissolve into their smallest units, known as monomers or dimers, it's these agents which travel through the injection site tissues and hitch a ride in a tiny nearby blood capillary, first penetrating the vessel wall, and next getting swept into the larger bloodstream.


The reason why analog insulins like lispro (Humalog), aspart (Novolog), and glulisine (Apidra) are absorbed faster than injected Regular human insulin is that their crystals are designed to dissolve faster than the Regular insulin crystals. But the dissolving does take time either way.


Once blood borne, insulin molecules are taken in by the venous system will stream directly towards the heart and lungs. After a quick trip through the lungs for more oxygen and to get rid of carbon dioxide, the blood is pumped out into the arterial blood stream towards the body tissues. As blood first reaches the liver (an early stop after leaving the heart), another substantial quantity of its insulin is destroyed by liver cells (hepatocytes). The kidneys also act to degrade and remove insulin as fresh blood courses through them.

 

 


After passing through this "gauntlet of subtraction", insulin finally arrives at its intended targets: insulin responsive cells. Insulin molecules attach to a multitude of receptors on each cell, which next sets in motion a rapid cascade of biochemical events which result in the movement of blood sugar transporter molecules located within each cell, to the cell surface. These glucose transporters are what actually import sugar into the cells. Once in cells, imported sugar serves as a source of chemical energy for cells through a variety of chemical pathways.


This process, from injection to the first significant movement of sugar (glucose) into cells, takes about 20 minutes to start occurring after injecting a rapid acting insulin injection. Long acting insulin’s are more gradual in their dissolving or distribution process but meet the same hurdles after that.


It's for these reasons that proper timing of insulin before a meal can blunt the rise in blood sugar after a meal. This is because most (not all) foods are faster at raising blood sugar than insulin is in lowering it. Synchronization counts. It's a core principle to any Sugar Surfer to know the relative speeds of their insulin doses compared to the foods being eaten.

 

"It's a core principle of Sugar Surfing to know the relative speeds of one's meal time insulin doses compared to the foods being eaten."

Also, it's because of this insulin odyssey that the average type 1 diabetic requires approximately ten times the amount of insulin (injected) to effectively control blood sugar levels, compared to a non-diabetic person. Why the huge difference? That's because insulin is normally released from the inside of the body (the pancreas) and travels straight to the liver, bypassing many of the sources of destruction or inactivation outlined above.


But you might ask, "Why doesn't the liver destroy the insulin coming from the pancreas"? The reason is that insulin produced internally travels in a different circulatory system to start with. It's called the portal circulation. It's a circulatory system within the circulatory system. Insulin coming into the liver from the pancreas in the portal circulation is less degraded and performs its intended action on the liver more efficiently. That effect is to turn the liver into an organ of sugar uptake and storage. Lack of insulin reverses this process.


Since insulin by injection also possesses the properties of peaking (or plateauing) as well as duration of effect, even these properties are altered by amount injected and to a smaller extent, where they are injected. And I've totally ignored any discussion of the quality of the insulin itself, how it was handled or stored before injection; or whether the right dose was taken...or not at all.

 

 

What I've tried to explain here are many of the reasons for the day to day variability in how injected insulin works (or doesn't) to influence sugar levels in persons with type 1 diabetes. For those of us who see more insulin predictability than normal, what they're often really witnessing is the contribution of whatever internal insulin production might still remain. And of course some days, insulin effect can balance just right with food and exercise, and create a tightly controlled blood sugar profile.

 

 

For these reasons I explain to my patients that injected insulin is not a precision instrument. These are just some of the reasons why. It’s why I watch my sugar patterns and trends closely (glance) and aim to keep my fast acting insulin on a “short leash”, so to speak.


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