Diabetes Drug Mechanisms
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| intermediate/long-acting | basal insulin
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| rapid and short-acting | bolus insulin
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| replace proline at B28 with aspartic acid residue | insulin aspart
(bolus)
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| proline at B28 and lysine at B29 are reversed | insulin lispro
(bolus)
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| protamine-insulin (bolus) complex; disassociates after cleavage making it intermediate acting | netral protamine hagedorn (NPH)
(basal)
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| add fatty acid moiety to LysB29; increases self-aggregation and reversible albumin binding | insulin detemir
(basal)
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| two arginine residues added to C terminus of B chain + asparagine at A21 is replaced with glycine - exists as a hexamer in solution at pH 4, dissociates at pH 7 (provides prolonged predictable absorption fro SC injection) PEAKLESS ABSORPTION | glargine
(basal insulin)
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| imitates increase of ATP - inhibits K efflux channel: (increase of intracellular ATP results in inhibition of K+ efflux protein channel; results in depolarization & activation of the Ca channel, which results in exocytosis of insulin granules into blood) | sulfonylureas
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| imitates increase of ATP - inhibits K efflux channel: (increase of intracellular ATP results in inhibition of K+ efflux protein channel; results in depolarization & activation of the Ca channel, which results in exocytosis of insulin granules into blood) | K+ channel modulators
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| mimic the insulin pathway! (AMPK is naturally activated when cellular ATP stores are reduced - AMPK phosphorylates AS160 in a manner similar to Akt/PKB (a part of the insulin receptor pathway!)) | AMPK agonists
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| increases activity of AMPK - mech unknown (not direct activation) | metformin
(an AMPK agonist)
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| substrate for PPAR gamma (which is a group of nuclear receptors responsible for the regulation of genes involved in glucose and lipid metabolism) --> when these drugs bind to PPAR g, results in activation of AMPK | thiazolidinediones
(PPAR gamma agonists)
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| binds to GLP-1 receptors in the pancreas and hypothalamus resulting in: 1) stimulation of insulin secretion 2) inhibition of glucagon release 3) delay of stomach emptying - reduces food intake b/c you think you're full | GLP-1 receptor agonists
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| inhibits DPP-4 so that GLP-1 (normal substrate for it) does not bind --> increases GLP-1 conc causing: 1) stimulation of insulin secretion 2) inhibition of glucagon release 3) delay of stomach emptying - reduces food intake b/c you think you're full | DPP-4 inhibitors
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| work in brush border of small intestine! these drugs stop a-glucosidase from breaking down starches, dextrin, and disaccharides into sugars that can be absorbed: 1) slow absorption of carbs from GI tract 2) increase release of GLP-1 | alpha-glucosidase inhibitors
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| mimic actions of amylin! (amylin is a 37 AA peptide produced by the B cells of the pancreas) actions: 1) reduced glucagon release 2) delayed gastric emptying 3) satiety (hunger satisfaction) --> plasma glucose levels reduced | amylin receptor agonists
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| small AA peptide with sequence similar to that of amylin | pramlintide
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| lower plasma glucose - mech unknown but could be: 1) good at binding fat, bile acid, and glucose in plasma OR 2) act as a nuclear receptor signaling molecule | bile acid binding resins
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| released by the pancreas naturally in response to low blood sugar - bind with Gs-protein coupled receptor (results in synthesis of cAMP) stimulates production of glucose by: 1) gluconeogenesis 2) glycogen breakdown | glucagon
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| interacts with the K+ channel on the pancreatic B cells results: 1) prevents closing of channel 2) prolongs open time of channel --> prevents release of insulin | diazoxide
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Created by:
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