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PDA 1 Diabetes Drugs

Diabetes Drug Mechanisms

QuestionAnswer
intermediate/long-acting basal insulin
rapid and short-acting bolus insulin
replace proline at B28 with aspartic acid residue insulin aspart (bolus)
proline at B28 and lysine at B29 are reversed insulin lispro (bolus)
protamine-insulin (bolus) complex; disassociates after cleavage making it intermediate acting netral protamine hagedorn (NPH) (basal)
add fatty acid moiety to LysB29; increases self-aggregation and reversible albumin binding insulin detemir (basal)
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)
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
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
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
increases activity of AMPK - mech unknown (not direct activation) metformin (an AMPK agonist)
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)
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
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
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
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
small AA peptide with sequence similar to that of amylin pramlintide
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
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
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
Created by: astephens5