Diabetes

Genetic, Autoimmune destruction of pancreatic beta cells that produce insulin

Genetic, Metabolic abnormalities, environmental factors

childhood or early childhood before puberty

any age, usually after age 35

insulin, +/- thiazolidine dione

• 1. oral hypoglycemic agents
• 2.Antihyperglycemic agents

sulfonylurea, meglitinide, Incretin Analogues, DPP-IV inhibitors

metformin, thiazolidinediones, alpha glucosidase inhibitors

Carbohydrate metabolism, lipid metabolism, protein metabolism

hypoglycemia, visual disturbances, peripheral edema, local or systemic allergic reactions

Promote insulin release by binding to and inhibiting K+ conductance by Kir6.2

hypoglycemia, gastrointestinal disterbances, hematological disturbances, ethanol intolerance, Contraindicated in patients with hepatic renal insufficiency

Inhibit K+ conductance by Kir 6.2 ----> result in membrane depolarization and insulin release

• Increase glucose uptake results in closure of the Kir6.2
• (mostly used as adjunct therapy)
• SC injection

Decreases the inactivation of endogenous incretin hormones ----> Results in a glucose - dependent increase of insulin release and decrease in glucagon levels (used in adjunct therapy)

• Mostly oral administration
• Highly protein bound

Lower elevated levels of blood glucose with relatively little potential to produce hypoglycemia. They do not promote insulin release

Biguanides, Thiazolidinedione, alpha-Glucosidase inhibitor, Modified amyline peptide

• decreases the hepatic glucose output
• Inhibits absorption of glucose from the gut
• Increases glucose uptake by muscle and fat cells
• Its mechanism of action appear to involve activation of cAMP dependent protein kinase
• Activation of this kinase in skeletal muscle and adipocytes leads to increase glucose transport by promoting translocation of GLUT4 to the cell surface

Lactic acidosis and gastrointestinal problems

increases insulin sensitivity by binding ligand activated transcription factor PPAR - y which then activates PPAR - y and increases the expression of mRNAs encoding enzymes and proteins required for optimal insulin sensitivity

weight gain, edema, possible hepatic toxicity, cardiovascular side effects

Inhibit alpha - glucosidases, enzymes in the GI tract involved in degradation of complex carbohydrates which stall the rise in blood glucose concentrations after a meal (does not enter the blood stream)

• abdominal pain
• diarrhea
• flatulence

• acts like insulin to inhibit glucagon secretion
• It also delays gastric emptying
• It also has appetite suppressive properties
• SC administration

• Mostly oral
• TZD are highly protein bound

inhibits sodium glucose cotransporter 2 and block resorption of glucose in the kidney, leading to an increase in urinary glucose excretion and lowering of both plasma glucose levels and body weight