Dr. Mobeen presents the approach to managing a type II diabetic patient. Following classes of drugs are presented:

• Drugs that increase the levels of inuslin (insulin secretogogues).
  • Drugs that work on the beta cells.
  • Sulfonylureases.
    • Potassium channel blockade causing deploraization of a beta cell leading to the secretion of insulin.
  • Incretins.
    • GLP1
    • GIP
    • Exanatide
• Drugs that increase peripheral sensitivity to insulin.
  • Metformin
    • First line drug for managing type II diabetes mellitus.
    • Mechanism of action of metformin.
    • Actions of metformin on hepatocyte:
      • AMPK levels increased leading to the reduced cAMP levels. This reduces PKA levels. This leads to increased glycolysis and reduced gluconeogenesis.
      • FFA are reduced leading to increased insulin sensitivity.
      • Improves function of the insulin receptors.
      • Improves glucose transport inside the cell.
  • TZDs
    • Work on the lipid cells.
    • Open the genes in lipid and muscle cells leading to increased sensitivity to insulin.
    • LPL receptors are increased in density. Imprving triglyceride levels. Cholestrol levels are not improved.
    • Number of lipid cells increase. Lipogenesis increases. (Not a good effect. However, lipid storage will increase reducing glucose levels temporarily.)
• Drugs that increase ejection of the glucose from the gut. That is, reduce its absorption from the gut.
  • Alpha glucosidase enzyme's role.
  • Function of Acarbose.
  • Acarbose binding to alpha glucosidase. Preventing glucose polymer breakdown.
  • Diahrrhea, gas, discomfort, abdominal pain dur to increased glucose levels in the large intestine.
• Drugs that eject glucose in urine.
  • Sodium glucose co transporter type 2 (SGLT2) inhibitors.
  • Increased risk of UTIs especially in women.
  • Polyuria. Low blood volume leading to thirst and postural hypotension.
• Role of diet to reduce intake of glucose.
• Role of exercise to increase glucose uptake in the peripheral tissues.