Insulin
Insulin is a hormone produced by the pancreas (a gland that releases a digestive juice into the intestine). The pancreas is composed of acinar cells, which produce digestive enzymes, and the islet cells of Langerhans, which produce hormones.
What Insulin Does
Four hormones are produced by the Langerhans islet cells. Insulin is produced in the B cells, glucagon in the A cells, somatostatin in the D cells, and pancreatic polypeptide in the F cells. Insulin promotes anabolism (building up of tissues) and inhibits catabolism (breaking down of tissues) in muscle, liver, and fat cells. It increases the rate of synthesis (blending) of glycogen, fatty acids, and proteins. Lack of insulin causes diabetes mellitus (a disease characterized by excess sugar in the blood and other body fluids).
Insulin's most important feature is its ability to increase the rate of glucose (a crystalline sugar) absorption by cells. Glucose is the most efficient fuel used by and found in almost all cells. Insulin causes a decreased concentration of glucose in the blood and causes the cells to store glycogen (a starchlike substance), mostly in the liver. It also promotes the entry of other sugars and amino acids into the muscle and fat cells. Insulin is therefore responsible for promoting fat storage in fat cells and for the total quantity of protein in the body.
Insulin Production
Insulin production is stimulated by high levels of glucose and inhibited (limited) by lower levels of glucose. Insulin regulates glucose with glucagon. Glucagon catabolizes (changes into a product of simpler composition) glycogen to glucose and also raises the blood sugar. Glucagon can be given to increase the blood sugar when intravenous (by needle) glucose cannot be given. Glucagon takes about twenty minutes to raise the blood sugar. Intravenous glucose raises it instantaneously, which is why it is preferred in treatment. Together insulin and glucagon ensure that the body stores and maintains the proper level of glucose for its energy needs.
Diabetes
Diabetes is from the Greek word meaning "siphon," and "mellitus" comes from melliferous, meaning "of or relating to honey." Diabetes has been recognized for centuries and was originally diagnosed by tasting the urine and finding it sweet (melliferous). The high sugar also causes the kidneys to excrete (or siphon) large amounts of water. In 1815, French chemist Michel Eugene Chevreul discovered that the sweetness came from grape sugar or glucose. Later discoveries showed how the body makes, stores, and uses glucose.
Injury to the pancreas was linked to diabetes beginning in the seventeenth century and confirmed by animal experiments, particularly those of the German physiologist Joseph von Mehring (1849-1908) and a Russian pathologist, Oscar Minkowski (1858-1931). The acinus cells were found in the seventeenth century by the Dutch anatomist Regnier de Graaf and the islet cells in 1869 by a German pathologist Paul Langerhans (1847-1888).
Hormones
In 1905 English physiologists Ernest Starling and William Bayliss discovered hormones. Hormones are substances secreted (released) by glands and carried in the blood to control cell activity elsewhere. In 1916 an English physiologist named Edward Sharpey-Schafer proposed that a hormone produced by the pancreas lowered the level of glucose in the blood. He called the hormone "insuline," the Latin word for "island," because he believed it came from the islet cells of the pancreas.
Credit for discovering insulin is given to Canadian surgeon Frederick Grant Banting (1891-1941) and Canadian physiologist Charles Herbert Best (1899-1978). Banting and Scottish physiologist and professor John James Rikard Macleod (1876-1935) were jointly awarded the Nobel Prize for medicine in 1923. Banting gave half of his share to Best, and Macleod gave half of his share to James Bertram Collip, because of the men had contributed to the discovery.
The First Insulin Patient
Collip, a professor at the University of Alberta, had experience in the chemistry of hormones. Prior to January 1922, he had prepared an insulin pure enough to be used on human patients. The first patient to receive insulin was 14-year-old Leonard Thompson. Thompson was admitted to Toronto General Hospital with a high blood glucose level; he also was urinating between three and five liters of fluid per day. Despite his rigid diet of only 450 calories (the only known treatment at this time was a diet low in carbohydrates), Thompson continued to excrete (get rid of through bodily waste) large amounts of glucose. On January 11, 1922, he was given insulin. Within a fairly short time, his blood sugar level came down and he stopped urinating large amounts of liquid.
Humulin
In 1982 insulin became available as a genetically-engineered product called Humulin. Humulin's structure is identical with human insulin. The A and B chains are produced separately in different strains of E. coli bacteria. The E. coli have been genetically encoded to produce each of these strains. The strains are separated from the bacteria and purified. The purified chains are combined chemically and repurified.
Insulin binds to cells at specific protein sites called receptors. The insulin receptor consists of two alpha subunits and two beta subunits. The alpha subunits occupy the outer surface of the cell, whereas the beta subunits span the cell membrane and cell interior. The portion of the beta subunits occupying the cell interior are enzymes called protein tyrosine kinases. Isolation of the genetic material, deoxyribonucleic acid (DNA), that codes for the insulin receptor, has been useful in understanding the function and control of these protein tyrosine kinases. When insulin binds to the receptor, it activates the protein tyrosine kinase, which then adds phosphate groups to specific sites on the receptor, the tyrosine residues. This phosphorylation reaction may trigger the various actions of insulin on glucose metabolism. Although tyrosine kinase appears to be essential for insulin action, the mechanisms linking tyrosine kinase phosphorylation of the receptor to insulin effects remain unclear. Insulin receptor DNA has also been useful in identifying insulin receptors of other species such as the fruit fly. Future studies will focus on determining the substances controlled by the tyrosine kinases of the insulin receptor.
When your cells are exposed to insulin at all, they get a little bit more resistant to it. So the pancreas just puts out more insulin. Cells become insulin resistant because they are trying to protect themselves from the toxic effects of high insulin. They down-regulate their receptor activity and number of receptors so that they don't have to be subjected to all that stimuli all the time. When your cells are exposed to insulin at all, they get a little bit more resistant to it. So the pancreas just puts out more insulin. Cells become insulin resistant because they are trying to protect themselves from the toxic effects of high insulin. They down-regulate their receptor activity and number of receptors so that they don't have to be subjected to all that stimuli all the time. Different cells respond to insulin differently. Some cells are more resistant than others, as some cells are incapable of becoming very resistant. The liver becomes resistant first, followed by the muscle tissue and lastly the fats. As all these major tissues, become insulin resistant your pancreas is putting out more insulin to compensate. Any time your cell is exposed to insulin it is going to become more insulin resistant. That is inevitable, we cannot stop this process, but the rate we can control.
But the pancreas can't always keep up that high level of insulin production forever. Once the production of insulin starts slowing down, or the resistance goes up, then blood sugar goes up and the person becomes a diabetic.
"Insulin resistance syndrome" refers to a combination of risk factors for type 2 diabetes, including chronically elevated insulin levels, low HDL ("good") cholesterol, abdominal obesity and high blood pressure.
Excessive intake of all carbohydrates, especially the high-glycemic type, is the primary culprit in the development of insulin resistance.
Type 2 diabetes occurs when the body no longer responds to insulin. As a result, levels of insulin in the blood become elevated and over time, can raise the risk for kidney failure and blindness, as well as heart disease.
A recent study(4) has found that insulin resistance syndrome, or "syndrome X," is found in families with a history of early heart disease - a heart attack or blood vessel blockage before age 55 in men and before age 65 in women.
Please can you give me some advise. My GP wants me to start insulin. My medication at this time is AVANDAMET 2000mg/2mg per day GLIMEPRIDE 4mg
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sara
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