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16 Cards in this Set

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Insulin Synthesis?
in beta cell. First, Proinsulin made and packaged in golgi into granules. Proteolytic cleavage in granules result in formation of insulin and C peptide. The Insulin portion has disulfide bonds in them.

Stored in granules with C peptide with Zn, usually in hexamers.
Glc and Insulin Release?
Glc metabolism result in increased ATP >> inhibition of K ch >> beta cell depolarization >> Increase in Ca influx and insulin release
Glc vs AA effects on insulin?
Glc releases insulin and inhibits glucagon.

AA, however, release both insulin and glucagon.
Insulin action on glc uptake?
everywhere, it's enhanced except in CNS, PNS, blood vessels, renal medullary cells and hepatocytes
Classifications of Insulin preps?
either fast, intermediate, and long lasting. They differ by whethere there's a peak, time for onset etc.
Insulin glargine
ultralong acting, does not produce peak, so give constant concentration throughout the day.
Protamine zinc insulin
reacting insulin with Zn and basic protein, protamine. The complex causes insulin to be released slowly, hence making it LONG LASTING.
Insulin Lispro
absorbed more rapidly than regular insulin following injection, and can be injected just prior to eating, rather than 30 minutes prior to eating.
Strategies in Type II
first use metformin. Once metformin (inhibits gluconeogenisis) isn't sufficient, add oral hypoglycemic such as glyburide (K efflux inhibitor in beta cells).
Sulfonylureas
Mech: binds K ch and inhibit K efflux, causing depolarization, Ca++ entry and insulin release (similar to insulin which instead causes ATP increase that then inhibits K channel).

ex: tolbutamide (first gen), glyburide and glipizide (2nd gen.)
rapaglinide
oral hypoglycemic, same mech of action as sulfonylureas (K ch inhibition).
Metformin
Mech; inhibit gluconeogenis, reducing BOTH fasting and postprandial hyperglycemia.

NEVER causes hypoglycemia.

may cause LACTIC ACIDOSIS!.
acarbose [think: a:absence of carbose: carbohydrates]
Mech: works in gut by inhibiting breakdown of sucrose to glc (through inhibtion of alpha-glucosidase enzyme).
Pioglitazone and rosiglitazone
Mech: increase synth and translocation of glc transporters in tissue, and by decreasing gluconeogensis.

They decrease insulin resistance via activation of PPARgmamma
Sitagliptin phosphate
GLP-1 (endogenous) stim insulin rlease and inhibits glucagon release.

this drug inhibits the enzye DPP-4 which breaksdown GLP-1, so results in elevation of GLP-1, more insulin release and less glucagon release.
What drug to use to prevent nephrotoxicity in diabetics chronically?
Captopril, an ACE-i