Treating Diabetes Flashcards
What is neurogenic diabetes insipidus?
A vasopressin deficiency
What is nephrogenic diabetes insipidus?
A resistance to vasopressin
What is type I diabetes mellitus?
No insulin produced due to lack of beta cells
What is type II diabetes mellitus?
A resistance to insulin
Describe the function of vasopressin
Increases water permeability in the collecting duct so more water is reabsorbed into the blood from the kidneys
How can vasopressin deficiency be treated?
Oral, intranasal or subcutaneous desmopressin which mimics the function of vasopressin over a longer half life
Describe the function of insulin
Increases glucose uptake, glycolysis and glycogenesis
What is the mechanism for insulin induced glucose uptake?
Insulin binds to tyrosine kinases on the cell surface which causes translocation of glucose transporters from intracellular vesicles to the cell surface to allow glucose transport into the cell
Describe rapid vs long-lasting insulin treatment
Rapid treatment - mimics insulin release after a meal, usually administered in solution
Long-lasting treatment - mimics basal insulin release, administered in complexes with zinc
How has lispro been modified to alter it’s half-life?
The formation of hexamers and dimers is inhibited which decreases the half life
How has glargine been modified to alter it’s half-life?
It is insoluble at physiological pH
Why can’t type II diabetes mellitus be treated with insulin?
The disease causes resistance to insulin and so the insulin is already present in the body and adding more will have little to no effect
How can type II diabetes mellitus be treated?
Oral metformin - reduces gluconeogenesis, increases GLUT-4 translocation to increase glucose uptake
Outline the mechanisms behind insulin release
High levels of blood glucose and ATP closes the ATP dependent potassium ion channels in the beta cells which depolarises the membrane. This opens the voltage gated calcium ion channels which trigger the exocytosis of insulin
What causes glucose intolerance?
Defects in metabolism prevent sufficient ATP to close potassium ion channels
