How Does Insulin Regulate Blood Glucose Levels – As part of homeostasis, the body must control the amount of glucose in the blood. Glucose enters the body from food, is stored as glycogen, and is broken down during respiration. Hormones control blood glucose concentrations in a negative feedback loop. People with diabetes have difficulty regulating their blood glucose levels, so they need medication or access to controlled foods.
Glucose enters the body as part of dietary carbohydrates, digests individual glucose molecules, and is absorbed into the bloodstream. It is then stored as glycogen in the liver and muscles or used for respiration and other metabolic reactions. When a person exercises, it takes more energy and more glucose is removed from the blood to breathe.
Insulin moves glucose out of the blood and into the surrounding tissues. It also converts glucose into glycogen in the liver and muscle cells where it can be stored until more glucose is needed.
When blood glucose levels are too low, the pancreas releases the hormone glucagon. Glucagon converts liver glycogen back into glucose. Glucose is then released into the blood and the blood glucose concentration rises again.
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Genetics play an important role in blood glucose regulation. Some people may be able to get away with eating junk food and not exercising as much as they should. But for others, genetic predisposition adds to poor food choices to raise blood glucose levels. Members will see their genotype report below and additional solutions in the Lifehacks section. Join today
Before we get into the genes involved in regulating blood glucose levels, let’s cover the basics of how the body regulates blood sugar. (Skip ahead if you already understand all of this.)
Your body regulates the amount of glucose in your blood through a complex negative feedback mechanism.
Insulin is released by the beta cells of the pancreas in response to blood glucose levels. Although most of the time, insulin levels are low, when glucose levels rise, insulin is released at higher levels to prevent high blood glucose.
In response to insulin, skeletal muscle cells, adipose (fat) tissue, and red blood cells increase glucose uptake.
In addition to insulin, the beta cells of the pancreas also release amylin, which delays the emptying of the stomach and tells the brain that it is full. This slow digestion prevents blood glucose levels from rising too quickly after eating.
Another hormone involved here is glucagon. The alpha cells of the pancreas release glucagon. But it works in the opposite direction to insulin: when blood glucose levels are low, glucagon is released.
Glucagon tells the liver to convert glycogen into glucose and release it into the blood. If needed, glucagon can also stimulate the liver and muscle cells to create glucose from amino acids through a process called gluconeogenesis.
The blood glucose range is usually defined as between 65 and 100 mg/dl when you have not eaten for a while: the fasting state. (This section varies slightly, depending on who normally defines it). Within two to three hours after a meal, blood glucose levels below 180 mg/dl are considered OK.
The release of insulin and glucagon is a negative feedback loop: when blood glucose is high, insulin is released, which inhibits the release of glucagon. When blood glucose levels drop, glucagon is released and insulin is suppressed.
This system becomes dysregulated in diabetes. People with diabetes may have trouble making enough insulin because glucagon still causes the liver to release some glucose. Blood glucose levels then rise.
While the obvious solution to high blood glucose levels is to reduce your carbohydrate intake, it’s not always easy, and it’s not the right answer for everyone.
Glucose is difficult for the body to handle because it is toxic at high levels. You should have it, but you don’t want much. (Yes, you can also burn fatty acids for fuel, but the brain needs some glucose.)
Doctors start talking about diabetes when fasting blood glucose levels are above 125 mg/dL and an oral glucose tolerance test result is above 200 mg/dL.[ref]
If your fasting blood glucose is 100 to 125 mg/dL on multiple tests, you are likely to be labeled prediabetic.
But what if, from time to time, blood sugar rises after eating sweets? Or what if your fasting glucose is always around 99 mg/dL, below the threshold for prediabetes? As you can see, there are a lot of gray areas here.
Therefore, persistent blood glucose levels, even if not within the pre-diabetes/diabetes range, can increase oxidative stress and the formation of advanced glycation end products.
Another important point here, after the COVID-19 crisis, is that insulin and insulin sensitivity are essential for the immune system’s T cells to fight viruses. People with insulin secretion problems (such as diabetes) or insulin sensitivity (insulin resistance, prediabetes) do not have a strong T-cell response to the virus.
Let’s dig a little deeper into the blood glucose regulatory system and look at some of the genes involved and the solution to those genes.
By looking at the types of genes that significantly affect blood glucose or insulin levels, we can better understand the control mechanisms that exist in this complex feedback loop.
Understanding your exact genetic susceptibility to blood sugar problems can help you figure out a specific plan to keep your glucose levels under control.
First we’ll look at the science of how genes work, and then you can check your genes in the Genetic Differences section below (including exclusive Lifehacks).
KCNJ11 gene: The KCNJ11 gene encodes a potassium channel subunit found in pancreatic beta cells. The ATP-sensitive channel opens and closes in response to blood glucose levels. When glucose is present, ATP levels increase (cells use glucose to make more ATP). When ATP increases, ATP-sensitive potassium channels in pancreatic beta cells close, triggering the release of insulin.
ABCC8 gene: The KCNJ11 gene (above) encodes a subunit of an ATP-sensitive potassium channel. Another component, called SUR1, is encoded by the ABCC8 gene.
A class of diabetes drugs called sulfonylureas bind to SUR1 and thereby increase the release of insulin. Variations in the ABCC8 gene can affect blood glucose levels.
Glucokinase (GCK gene) is important in the regulation of glucose metabolism in the liver and beta cells. In beta cells, glucose can enter the GLUT2 receptor (which does not require insulin). Glucokinase in the pancreas can increase the signal for increased glucose levels, increasing insulin secretion. Genetic variation in the GCK gene is a risk factor for diabetes.
CDKAL1 (cyclin-dependent kinase 5 regulatory subunit associated with protein 1-like 1) is part of the signaling pathway that causes insulin release. Genetic variations in this gene can cause reduced insulin secretion, which in turn leads to higher blood glucose levels when carbohydrates/sugars are consumed.[ref][ref]
Glucose molecules are too large to cross the cell membrane unaided. Therefore, for glucose to enter a cell, it must be transported. There are actually several different glucose transport systems, depending on the type of cell.
Muscles use a lot of energy, and delivering glucose to muscles is the body’s way of controlling blood glucose levels.
In muscle cells, GLUT4 (glucose transporter 4) transports glucose into cells. The GLUT4 transporter is intracellular and requires
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