How To Regulate Blood Glucose
How To Regulate Blood Glucose – Good blood glucose control is an important factor in overall health and longevity. High blood glucose levels, either after eating or continuously, can increase oxidative stress in the body, leading to long-term health problems.
Genetics play a big role in blood sugar control. Some people may be able to get away with junk food and not exercise properly. But for some, a genetic predisposition combines with poor food choices to raise blood glucose levels. Members will see their genotype report below, and additional solutions in the Lifehacks section. Join today.
How To Regulate Blood Glucose
Before we get into the genes involved in controlling blood glucose levels, let’s cover the basics of how the body regulates blood sugar. (Skip once you understand all of this.)
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Your body regulates the amount of glucose in your blood through a complex negative feedback system.
Insulin is released by beta cells in the pancreas in response to high blood glucose levels. Although a constant, low insulin level is usually achieved, when glucose levels rise, insulin is released in large enough amounts to combat the rise in blood glucose.
In response to insulin, skeletal muscle cells, adipose tissue (adipose) and red blood cells increase glucose absorption.
In addition to insulin, the beta cells of the pancreas also release amylin, which delays emptying and tells your brain that you are full. This slowing of digestion prevents glucose levels from rising too quickly after a meal.
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Another hormone involved here is glucagon. The alpha cells of the pancreas produce glucagon. But it works opposite to insulin – when blood glucose levels are low, glucagon is produced.
Glucagon signals the liver to convert glycogen into sugar and release it into the bloodstream. If needed, glucagon can also stimulate the liver and muscle cells to make glucose from amino acids in a process called gluconeogenesis.
Blood sugar level is usually defined as somewhere between 65 and 100 mg/dl when you have not eaten for a long time – the fasting state. (This range varies slightly, depending on who defines normal). Within two to three hours after a meal, a blood sugar level of less than 180 mg/dl is considered normal.
The release of insulin and glucagon is a negative feedback loop: when blood glucose is high, insulin is released, preventing the release of glucagon. When blood sugar levels drop, glucagon is released and insulin is inhibited.
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This system is hard on sugar. People with diabetes may have trouble making enough insulin because glucagon still causes the liver to release some glucose. This increases the level of glucose in the blood.
While the obvious solution to high blood glucose is to cut back on carbohydrates, it’s not always easy—and it’s not the right answer for everyone.
Glucose is tightly controlled by the body because it is toxic at high levels. You have to have it, but you don’t want too much. (Yes, you can burn fatty acids for fuel, but the brain needs glucose.)
Doctors start talking about diabetes when fasting glucose levels are above 125 mg/dL and an oral glucose tolerance test result above 200 mg/dL.[ref]
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If your fasting glucose is 100-125 mg/dL on several tests, you will likely be diagnosed with prediabetes.
But what if your blood sugar rises from time to time after eating sweets? Or what if your fasting glucose stays around 99 mg/dL, just below the pre-diabetic range? As you can see, there are a lot of gray areas here.
Therefore, persistent blood sugar levels, even if not in the prediabetic/diabetic range, can increase oxidative stress and the formation of advanced glycation end products.
Another important point here – after the COVID-19 pandemic – is that insulin sensitivity and insulin sensitivity are required for T-cells of the immune system to fight this virus. People with problems with insulin secretion (such as diabetes) or insulin sensitivity (insulin resistance, prediabetes) do not have a strong T-cell response to viruses.[ref]
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Let’s dive deeper into the blood sugar control system and look at some of the genes involved and the solution to those genes.
By looking for genetic variants that significantly affect blood sugar or insulin levels, we can better understand the regulatory mechanisms involved in this complex feedback loop.
Understanding your genetic predisposition to sugar problems can help you come up with a targeted plan to keep your glucose levels stable.
First, we’ll look at the science to understand how genes work, and then you can test your genes in the Genetic Variants section below (some Lifehacks included).
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KCNJ11 gene: The KCNJ11 gene encodes a potassium channel subunit found in pancreatic beta cells. This ATP-sensitive channel opens and closes in response to blood glucose levels. When glucose is present, ATP levels rise (cells use glucose to make more ATP). When ATP increases, the ATP-sensitive potassium channel in the beta cells of the pancreas closes, triggering the release of insulin.[ref]
ABCC8 gene: The KCNJ11 gene (top) encodes one subunit of an ATP-sensitive potassium channel. The second subunit, known as SUR1, is encoded by the ABCC8 gene.
A class of diabetes medications called sulfonylureas bind to SUR1 and thereby increase the release of insulin. Genetic variants in ABCC8 can affect blood sugar levels.
Glucokinase (GCK gene) is important in the regulation of glucose metabolism in the liver and beta cells. In beta cells, glucose can enter through the GLUT2 receptor (which does not require insulin). Glucokinase in the pancreas can amplify the signal for increased glucose levels, increasing insulin production. Genetic variants of the GCK gene are one of the risk factors for diabetes.
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CDKAL1 (cyclin-dependent kinase 5 regulatory subunit associated with protein 1-like 1) is part of the signaling pathway that causes insulin release. Genetic variants of this gene can cause reduced insulin secretion, which then keeps blood glucose levels high when you eat carbohydrates/sugar.[ref][ref]
Glucose molecules are too large to cross the cell membrane without help. Therefore, in order for glucose to enter the cell, it needs to be transported. There are actually several different ways to transport glucose, depending on the type of tissue.
Muscles use a lot of energy, and the transport of glucose to muscles is how the body regulates blood glucose levels.
In muscle tissue, GLUT4 (glucose transporter 4) transports glucose into cells. The GLUT4 transporter is found inside cells and needs to be translocated across the cell membrane to transport glucose.
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Insulin, which binds to the insulin receptor on the cell, causes a signal to be sent to the GLUT4 receptor, moving it across the cell membrane. This causes glucose to be taken up by the cell via the GLUT4 receptor.
There are several genes involved in the insulin receptor and the secondary signals sent to GLUT4. The main gene for the insulin receptor, INSR, is essential for health, so a mutation here is rarely associated with health. But variations in the signals produced by insulin binding to the insulin receptor can change the way the signal is sent to the GLUT4 receptor.
The IRS1 (insulin receptor substrate 1) gene encodes a key protein in the insulin-stimulated signaling pathway. After insulin binds to the insulin receptor, IRS1 is one of the molecules activated to send the message. Variants in IRS1 are also associated with an increased risk of type 2 diabetes.[ref]
Another gene that interacts with the insulin receptor is ENPP1 (ectoenzyme nucleotide pyrophosphate phosphodiesterase 1). This enzyme reduces insulin signaling by interacting with one of the insulin receptor subunits. Mutations of this gene are associated with insulin resistance.[ref]
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In addition to signaling insulin to move GLUT4 to the cell membrane, exercise also causes GLUT4 to switch and take up glucose.[ref]
Another part of the picture with glucose control is the signal to the liver to stop converting glycogen into glucose and release it into the bloodstream.
Alpha cells in the pancreas release glucagon when blood sugar levels drop. Glucagon signals the liver to convert glycogen into sugar and release it, which is called glycogenolysis (-lysis = breakdown, thus breaking down glycogen).
A low level of blood glucose in the alpha-cells causes a decrease in the production of ATP, which subsequently changes the separation of certain ion channels. This change in voltage then causes calcium to enter the cells, which causes the release of glucagon.[ref]
Insulin Glucagon Regulate Blood Glucose Levels Stock Vector (royalty Free) 275297069
The KCNH2 gene encodes a potassium ion channel that has several different roles in the body. It is important for the heart in regulating the rhythm, and recently it was found that it plays an important role in the alpha-cells of the pancreas for the release of glucagon. [ref] Gene variants in KCNH2 are associated with a decrease in the production of glucagon. .
GIP (glucose-dependent insulinotropic peptide) and GLP-1 (glucagon-like peptide-1) are released by cells in the intestine due to food.
While glucagon raises blood sugar levels by stimulating the liver to release glucose, glucagon-like peptide-1 (GLP-1) has the opposite effect as it can lower blood sugar by stimulating more insulin to be released by beta cells. in the pancreas.[ref]
GIP (glucose-dependent insulinotropic
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