Farma tema C virkning

  1. Non-insulin baseret antidiabetika
    • sulfonylureider
    • biguanider
    • glitazoner
    • alpha-glucosidasehæmmere
    • DPP-IV hæmmere
    • GLP1 analoger
  2. Antidiabetic medicin working on insulin
    Sensitizers: Biguanides, glitazones,

    • Secretagogues:
    • - K+ ATP: Sulfonylureas, GLP-1 agonists,DPP-4 inhibitors

    Analogs: fast actin and long acting insulin
  3. sulfonylureider: tolbutamid
    • first generation potassium channel blocker,
    • sulfonylurea oral hypoglycemic drug

    A secretagogues: These are the drugs that increase Insulin output from Pancreas
  4. sulfonylureider:
    second generation potassium channel blocker

    The drug works by binding to and activating the sulfonylurea receptor 1 (SUR1), the regulatory subunit of the ATP-sensitive potassium channels (KATP)[2] in pancreatic beta cells. This inhibition causes cell membrane depolarization opening voltage-dependent calcium channel. This results in an increase in intracellular calcium in the beta cell and subsequent stimulation of insulin release.
  5. glipizid
    potassium channel blocker

    • oral rapid- and short-acting anti-diabetic drug from the sulfonylurea
    • class. It is classified as a second generation sulfonylurea, which
    • means that it undergoes enterohepatic circulation. Second-generation
    • sulfonylureas are both more potent and have shorter half-lives than the
    • first-generation sulfonylureas.
  6. biguanider: metformin
    Metformin decreases hyperglycemia primarily by suppressing glucose production by the liver (hepatic gluconeogenesis)

    In addition to suppressing hepatic glucose production, metformin increases insulin sensitivity, enhances peripheral glucose uptake (by inducing the phosphorylation of GLUT4 enhancer factor), decreases insulin-induced suppression of fatty acid oxidation,[91] and decreases absorption of glucose from the gastrointestinal tract. Increased peripheral utilization of glucose may be due to improved insulin binding to insulin receptors.
  7. glitazoner: pioglitazon
    Pioglitazone selectively stimulates the nuclear receptor peroxisome proliferator-activated receptor gamma (PPAR-γ) and to a lesser extent PPAR-α.[14][15] It modulates the transcription of theinsulin-sensitive genes involved in the control of glucose and lipid metabolism in the muscle,adipose tissue, and the liver. As a result, pioglitazone reduces insulin resistance in the liver and peripheral tissues; increases the expense of insulin-dependent glucose; decreases withdrawal of glucose from the liver; reduces quantity of glucose, insulin and glycated hemoglobin in the bloodstream.
  8. alpha-glucosidasehæmmere: acarbose
    • Acarbose inhibits enzymes (glycoside hydrolases) needed to digest carbohydrates, specifically, alpha-glucosidase enzymes in the brush border of the small intestines and pancreatic alpha-amylase. Pancreatic alpha-amylase hydrolyzes complex starches to oligosaccharides in the lumen of the small intestine, whereas the membrane-bound intestinal alpha-glucosidases hydrolyze oligosaccharides, trisaccharides, and disaccharides to glucose and other monosaccharides in the small intestine. Inhibition of these enzyme systems reduces the
    • rate of digestion of complex carbohydrates. Less glucose is absorbed because the carbohydrates are not broken down into glucose molecules.
  9. DPP-IV hæmmere: sitagliptin
    • Sitagliptin works to competitively inhibit the enzyme dipeptidyl peptidase 4 (DPP-4). This enzyme breaks down the incretins GLP-1 and GIP, gastrointestinal hormones released in response to a meal.[14]
    • By preventing GLP-1 and GIP inactivation, they are able to increase the
    • secretion of insulin and suppress the release of glucagon by the alpha
    • cells of the pancreas. This drives blood glucose levels towards normal.
    • As the blood glucose level approaches normal, the amounts of insulin
    • released and glucagon suppressed diminishes, thus tending to prevent an
    • "overshoot" and subsequent low blood sugar (hypoglycemia) which is seen
    • with some other oral hypoglycemic agents.
  10. GLP1 analoger: exenatid
    • Exenatide augments pancreas response
    • (i.e. increases insulin secretion) in response to eating meals; the result is the release of a higher, more appropriate amount of insulin
    • that helps lower the rise in blood sugar from eating. Once blood sugar levels decrease closer to normal values, the pancreas response to
    • produce insulin is reduced; other drugs (like injectable insulin) are effective at lowering blood sugar, but can "overshoot" their target and cause blood sugar to become too low, resulting in the dangerous condition of hypoglycemia.Exenatide also suppresses pancreatic release of glucagon in response to eating, which helps stop the liver from overproducing sugar when it is unneeded, which prevents hyperglycemia (high blood sugar levels).Exenatide helps slow down gastric emptying and thus decreases the rate at which meal-derived glucose appears in the bloodstream.
  11. GLP1 analoger: Liraglutide
    It reduces meal-related hyperglycemia (for 12 hours after administration) by increasing insulin secretion, delaying gastric emptying, and suppressing prandial glucagon secretion.
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Farma tema C virkning