Diabetes is one of the important threats to the health of the global population. There are 422 million diabetic patients worldwide.
In ancient times, ordinary people did not have enough material life, so most aristocrats and upper-class society suffered from diabetes.
Human understanding of diabetes, as the name suggests, comes from the sweet urine of patients. Even early Western doctors used their mouths to diagnose.In ancient times, if a person had diabetes, it was a terminal illness and there was no way to treat it.As a result, many people quickly die from complications of diabetes.It was not until the middle of the last century that people knew the essence of diabetes and the true role of insufficient insulin secretion in the onset of diabetes.
This article will introduce in detail how people's insulin gets insufficient or exhausted.
Insulin secretion mechanism
The production of insulin is completed by the secretion of islet β cells of the pancreas.Of course, the pancreas is also a multifunctional organ. It can not only secrete insulin but also secrete pancreatic juice, glucagon, and other substances.Among them, pancreatic juice contains the protease with the strongest activity in human digestion and degradation of proteins, and so-called pancreatitis refers to diseases caused by inflammation and other reactions caused by the degradation of own tissues after the leakage of pancreatic juice, which can cause death.Glucagon and insulin are antagonistic hormones, insulin is a hypoglycemic hormone, and glucagon is a blood glucose-increasing hormone.
However, it is interesting that the human body has only one blood sugar-lowering hormone-insulin, but many hormones can raise blood sugar.This results in the "rare" properties of insulin, and when insulin secretion has problems, the body's blood sugar cannot be lowered.
The surface of pancreatic β-cells, like other normal human tissue cells, has a protein channel dedicated to transporting glucose.When the blood sugar (glucose) in the blood vessel passes through the channel,
the glucose will undergo a complex biochemical reaction in the β cell, and finally produce the energy substance ATP.
ATP is the most important "currency" for cells to use energy materials. Cells can use ATP to complete a series of energy-consuming physiological processes.
And if there is too much blood sugar in the blood vessels, glucose molecules will continuously enter the β cells.At this time, enough ATP is produced in the pancreatic β cells, and part of the ATP will be combined with the ATP-sensitive potassium ion channel on the surface of the pancreatic β cell membrane, resulting in the closure of the potassium ion channel on the cell membrane.
The potassium ion channel on the cell membrane is closed, which means that the potassium ion concentration in the cell is rising, and the potassium ion itself is positively charged, so the potential on the cell membrane begins to change, which is medically called "Depolarization".
The depolarization process on the cell membrane can be coupled to the calcium ion channel on the β cell membrane, and the calcium ion channel is opened.
Furthermore, calcium ions continuously enter the cell from outside the cell membrane.
The calcium ions that enter the cell will be combined with the filtering of the insulin wrapped in the β cell, and finally drag it to the cell membrane, and then discharge to the outside of the cell.
Insulin hypoglycemic mechanism
Simply,when the glucose concentration in the plasma is too high, it will inevitably cause too much glucose to enter the pancreatic β-cells.
Then, there is a special reaction mechanism in β cells, which eventually causes insulin to be secreted from the cells, and finally enter the blood vessels and flow to the whole body.
It is worth mentioning that some friends may be curious, where will the glucose that is transported to skeletal muscle and fat cells go? In fact, they will be used directly or converted into fat, glycogen, and other substances for storage.
Insulin causes inflammation
Under normal circumstances, the excessively high blood glucose concentration in blood vessels can be reduced by this mechanism of insulin.However, if the blood glucose concentration in the blood vessels remains high for a long time, the pancreatic beta cells will have to increase horsepower to produce more insulin.
In this way, the function of the pancreatic β-cells is overloaded, and the blood sugar concentration is too high, and the "no cold" starts.As a result, some of the blood sugar is like "garbage" that accumulates near the beta cells of the pancreatic islets.This is a foreign body, so white blood cells, one of the human immune cells, are enriched here, trying to "clean up".
The white blood cells that come here are "indiscriminately" and directly release very oxidizing free radicals.The released free radicals then bind to the special structure of the sentinel protein, causing the protein to be bound.The 6 activated sentinel proteins form a "circle" with each other to form a more active complex.Subsequently, a single aptamer protein in the cell is not active, but when a ring complex appears in the cell, they continue to move closer.
Every two aptamer proteins bind to each other on the circular complex, and finally form a more active aptamer integral protein.Once the adapter proteins are activated, they are "released" by the ring complex.As a result, they are constantly being produced and released, reaching an alarming number.The released adaptor proteins will obviously not be idle, and they also have their own mission: to activate smaller signaling proteins.The signal protein is an important protein that mediates inflammation.
A steady stream of inflammatory signal proteins are enriched near pancreatic islet cells, and eventually inflammatory reactions occur at this site.
The apoptosis and death mechanism of islet cells
When white blood cells “sweep” the battlefield through inflammation, they inevitably damage the surrounding islet cells, especially the pancreatic β cells.In the end, pancreatic β cells gradually die in the "killing action" of white blood cells, and the number of pancreatic β cells turns out to be less until the surviving pancreatic β cells cannot produce enough insulin.
Thus, diabetes occurred!
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