Insulin (part 1): Insulin’s secret life
A lot of people I see in my clinic present with some concern regarding their blood sugar level. Most people have heard of diabetes or know someone who has been diagnosed with the condition. Some members of the public are even acquainted with the technical term insulin resistance. These three—blood sugar level, diabetes, and insulin resistance—are closely related but not interchangeable, as you will see. We generally know that sugar is used for energy, and that diabetes is a serious problem with our ‘sugar energy’, but what about insulin resistance? What does it mean to be resistant to insulin? Or the better question: What exactly is insulin?
To understand insulin, let’s look at where it is produced, why, and what its uses are. Insulin is a hormone; that means we are able to make it ourselves, and it is used to influence our internal biology. We make insulin in our pancreas when our body detects a rise in glucose, most commonly from our food intake. As insulin emerges from the Beta cells of the pancreas, even at its lowest physiological concentration, it signals the pancreas to stop making the counter-hormone glucagon. At this point, it will not have any effect on the blood sugar rise we have just had from a meal. It is still very local, at the site where it was produced—the pancreas—and already it has an important role in our body’s signaling. As per insulin’s instruction, the pancreas needs to stop making glucagon, as the latter hormone would otherwise travel to the liver and dictate that the liver makes more glucose for the body.
This is the perfect time to transition to the liver, as insulin, like glucagon, travels to the liver as its physiological concentration increases. In the liver, insulin signaling stops the liver from responding to any glucagon that might have made it to its vicinity. When the liver makes glucose under glucagon’s direction, it uses its sugar stores—also called glycogen—for this to happen. In the absence of glucagon’s signaling, the liver can still make glucose from other sources without having to use glycogen, but insulin renders this impossible too. Essentially, these three initial insulin signaling effects guarantee that the body does not have to deal with more sugar than it already has postprandially (after a meal).
The last stop before body-wide effects begin is the liver, which changes the whole game. As insulin concentration rises, it gains more influence over the liver. The liver is an astute sensory organ for the body’s handling of energy or metabolism. Under insulin’s direction, the liver then suppresses fat cell breakdown throughout the entire body. So, the first body-wide message insulin communicates after we eat is: "It’s not time to lose weight." If you don’t like the sound of this, wait until you hear its next message: the liver then tells all of the fat cells to actively store weight.
Before you panic, this is truly and fundamentally why we actually eat. If we only ate for the energy to see us to the next meal, we would need to eat every two hours, around the clock, including in our sleep. Fat cells storing weight simply means that when our metabolism is perfect, we have a good handle on energy to last us to the next meal, which might or might not happen the next day.
As the pancreas makes more insulin and its concentration in the liver increases, a new message is sent out to the body—this time focusing on the muscles. The message is one that sounds much like what we have seen with fats: "It’s not time to lose muscle mass," and later: "It’s time to build muscle mass." If you understand the order of how things happen downstream from insulin signaling, you cannot escape building up fats if you want to build muscles. It doesn't mean, however, that muscular people are also fat. It simply is a demonstration of normal physiology and our body's order of priority. When our metabolism is healthy and not broken, these fats are self-burning to a point. Their role is to maintain energy availability in the rest of the body, including the muscle fibers.
Finally, when these are all well underway, the next increase in insulin concentration is ready to take on another big role, the only role we normally talk about: blood sugar regulation. It pushes glucose out of the bloodstream into various cells, including fat, muscle, and nerve cells, as well as cardiac cells, and in the case of the liver itself, by turning it into glycogen—the storage form of glucose.
If we go back to the start and count how many actions insulin has in order, we’ll end up with the following list:
Suppresses pancreatic secretion of glucagon
Suppresses hepatic glucose production from glycogen
Suppresses hepatic glucose production from other materials
Suppresses fat cell breakdown
Promotes fat cell storage
Suppresses protein breakdown
Promotes protein uptake
Promotes glucose uptake into cells
Promotes glucose uptake into the liver
Notice that the fasting glucose test provides us with information regarding the eighth and ninth functions of insulin. When the fasting sugar level comes back high, we call it insulin resistance because our body is resisting the action of insulin.
If insulin is so vital to our physiology, what precisely causes this resistance to occur? Is there a way to screen for insulin resistance before we see the failure of its final functions in a standard fasting glucose test? And what happens to the liver—the orchestrator of our metabolism—when it no longer responds to insulin's crucial instructions? Let's peel at these slowly as we talk more about this fundamental hormone in our body.