Treatment of Type 2 Diabetes: Oral Agents Flashcards Preview

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Flashcards in Treatment of Type 2 Diabetes: Oral Agents Deck (19)
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Organ systems targeted by glucose-lowering therapies + role in regulating glucose homeostasis

  • Pancreas
    • Secretes insulin and glucagon
  • Liver
    • Major player in gluconeogenesis, glycogen synthesis, etc
  • Muscle
    • Stores glycogen, undergoes glycogenolysis, takes up glucose when insulin is high
  • Adipose tissue
    • Takes up glucose when insulin is high
  • GI
    • Secretes incretin enhancers which assist insulin-mediated reduction of glucose levels


Main classes of non-insulin medications

  • Sulfonylureas
    • ex. glipizide, glyburide
  • Biguanide
    • ex. Metformin
  • Thiazolidinediones
    • ex. Pioglitazone, rosiglitazone
  • Incretin enhancers (GIP, GLP, DDP)
  • GLP-1 Agonists
    • ex. exenatide, liraglutide
  • DPP4 inhibitors
    • ex. sitagliptin
  • Amylin analogue
    • ex. pramlintide


Sulfonylureas: examples

ex. glipizide, glyburide


Sulfonylureas: MOA

  • MOA: Increase endogenous insulin secretion by closing ATP sensitive K+ channels → depolarization → Voltage gated Ca2+ channels → exocytosis of insulin
  • SOA: Pancreas


Biguanide: examples, MOA

  • ex. Metformin
  • MOA: Acts at the liver to potentiate suppressive effects of insulin on hepatic glucose production
  • SOA: Liver


Thiazolidinediones: examples

ex. Pioglitazone, rosiglitazone



Thiazolidinediones: MOA

  • Insulin sensitizing → activates PPAR ɣ receptor ==> increases insulin action ==> transcription of genes involved in adipocyte differentiation, glucose & lipid metabolism amongst other.
  • SOA:
    • Mainly skeletal muscle & adipose tissue
    • (liver - decreases gluconeogensis)


Incretin enhancers (GIP,GLP, DDP): MOA

  • MOA: Incretins contribute to the control of postprandial glycemia by ↑ insulin
  • SOA:
    • GI
    • pancreas


GLP-1 Agonists: exmaples

ex. exenatide, liraglutide


GLP-1 Agonists: MOA

  • MOA: GLP-1 amplifies glucose stimulated insulin secretion, inhibits glucagon secretion, slows gastric emptying, and increases satiety in the CNS
  • SOA: 
    • GI
    • pancreas


DPP4 inhibitors: examples



DPP4 inhibitors: MOA

  • MOA:  DPP4 inhibition prevents GLP-1 degradation ==> Enhance pancreatic insulin secretion and suppress glucagon, no effect on appetite or gastric emptying
  • SOA:
    • GI
    • pancreas


Amylin analogue: examples



Amylin analogue: MOA

  • MOA: Amylin is a peptide co-secreted with insulin, and inhibits gastric emptying and glucagon secretion acutely, leading to reduced food intake and weight loss
  • SOA:
    • GI
    • pancreas


Blood glucose and HbA1c goals for adults w/DM

  • Hemoglobin A1c (HbA1c or A1c)
    • < 7% (general), 6% (individual)*
    • without significant hypoglycemia
  • Fasting glucose
    • 70-130 mg/dL
  • 2 hour postprandial glucose
    • < 180 mg/dL


Routine monitoring for adults with diabetes

  • home blood glucose monitoring
    • check fingerstick blood glucoses at least twice per day at specific timepoints:
    • fasting, before lunch, before dinner, and at bedtime
  • record: glucose results, insulin admin, diet, physical activity


Characteristics of incretin enhancers

  • Incretin enhancers are GI mediated molecules that assist insulin-mediated glucose reduction post-prandium
  • serum insulin levels increase significantly more upon oral dosage of glucose vs. IV due to incretin enhancers
  • main incretin enhancers: GLP-1 & GIP
    • GLP-1 = glucagon-like peptide-1
    • GIP = glucose-dependent insulinotropic polypeptide


GLP-1 and T2D

Type 2 diabetics have normal or elevated levels of GLP-1 but are resistant to its insulin stimulatory actions


Fxn of DPP-4 (dipeptidyl peptidase-IV)

an enzyme that rapidly inactivates (within minutes) GLP-1 & GIP