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Insulin
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DRUG CLASS AND MECHANISM: Insulin is a naturally-occurring hormone secreted by the pancreas. Insulin is required by the cells of the body in order for them to remove and use glucose from the blood. From glucose the cells produce the energy that they need to carry out their functions. Researchers first gave an active extract of the pancreas containing insulin to a young diabetic patient in 1922, and the FDA first approved insulin in 1939. Currently, insulin used for treatment is derived from beef and pork pancreas as well as recombinant (human) technology. The first recombinant human insulin was approved by the FDA in 1982.
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Insulin is a hormone that regulates glucose metabolism by muscle, fat, and liver. Diabetes mellitus is a disease in which the body’s metabolism of sugars is greatly impaired due to either faulty secretion of insulin by the pancreas or the body’s insensitivity to the insulin that is produced. The vast majority of diabetics are diagnosed with Type II (adult onset) non-insulin dependent diabetes mellitus (NIDDM). Of the 7.8 million people characterized as diabetic in the U.S. in 1993, over 90 percent have NIDDM and the incidence is rising sharply. Risk factors for NIDDM include older age, family history, African-American ethnicity, and obesity. Insulin insensitivity from Type II diabetes may lead to serious complications including kidney failure, cardiovascular disease, and vision impairment.
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Insulin preparations have been used for the adjunctive treatment of diabetic ketoacidosis, uncomplicated diabetes mellitus and as adjunctive therapy in treating hyperkalemia. Insulin treatment in veterinary species has been primarily in dogs and cats. Experience in using insulin in large animals is rather limited.
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INSULIN SIGNALING — Insulin action begins with the binding of insulin to a heterotrameric receptor on the cell membrane of the target cells. Insulin receptors are membrane glycoproteins composed of separate insulin-binding (alpha-subunit) and signal transduction (beta-subunit) domains. Binding of insulin to the receptor results in activation of a tyrosine kinase in the beta-subunit that autophosphorylates the receptor. The phosphorylated receptor in turn phosphorylates other protein substrates beginning with insulin-receptor substrate (IRS) 1 and 2. The insulin signal is further propagated through a phosphorylation network involving other intracellular substances, leading to the various metabolic actions of insulin (see "Metabolic effects of insulin" below). Through activation of these signaling pathways, insulin acts as a powerful regulator of metabolic function.
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Insulin molecules circulate throughout the blood stream until they bind to their associated (insulin) receptors. The insulin receptors promote the uptake of glucose into various tissues that contain type 4 glucose transporters (GLUT4). Such tissues include skeletal muscles (which burn glucose for energy) and fat tissues (which convert glucose to triglycerides for storage). The initial binding of insulin to its receptor initiates a signal transduction cascade that communicates the message delivered by insulin: remove glucose from blood plasma (see panel 3). Among the wide array of cellular responses resulting from insulin ?activation,? the key step in glucose metabolism is the immediate activation and increased levels of GLUT4 glucose transporters.
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Insulin was first extracted from the pancreatic tissue of dogs in 1921 by the Canadian physiologists Sir Frederick Grant Banting and Charles Herbert Best and the British physiologist John James Rickard Macleod. The Canadian biochemist James Bertram Collip then produced it in sufficiently pure form to be injected into humans. The molecular structure of insulin was determined in 1955 by the British biochemist Frederick Sanger; it was the first protein to be deciphered. Human insulin, the first human protein to be synthesized, was made in 1965. In 1981 insulin made in bacteria by genetic engineering became the first human hormone obtained in this way to be used to treat human disease. For the biochemistry of insulin, see Sugar Metabolism.
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Insulin