QUESTIONS

1. Insulin comes from the beta cells.  What comes from the alpha cells?  How about the delta cells?
    
2. What is "Gut Glucagon?"
    
3. What is somatostatin's effect on glucagon? on insulin?
    
4. Glipizide is in what class of drug & how does it work?
    
5. We all know Eddie Feldman, Rick Nelson, Rhett Nichols, and even Duncan Ferguson :)  Who on Earth are Banting & Best?
    
6. What does NPH stand for?
    
7. Soon we will probably all be using Humulin.  How do K9 & Feline insulins differ from human insulin?
   
8. What effect do insulin antibodies have on our patients?
    
9. What is "glucose toxicity?"
    
10. How does Diabetes mellitus lead to cataracts in the dog?
    
    
    
    
     

ANSWERS

1. The beta cells produce glucagon & the delta cells produce somatostatin.
   
   
   
   
    
2. There are duodenal cells - sometimes called "GI alpha cells" - which appear to make glucagon.  This is  "gut glucagon."
   
   
   
   
    
3. Somatostatin inhibits both insulin & glucagon.  (Recall that somatostatin lately has been found effective in treating insulinoma cases.)
   
   
   
   
    
4. Glipizide is a sulfonylurea.  It stimulates pancreatic beta cells to secrete insulin.  It also reduces gluconeogenesis in the liver and seems to have a potentiating effect on insulin in the periphery.
   
   
   
   
    
5. Banting & Best discovered insulin.  Insulin was used in dogs before in was used in humans.  (Insulin was an absolute miracle in treating diabetes mellitus as you might guess - this was in the 1920's)
   
   
   
   
    
6. NPH stands for Neutral Protamine Hagedorn.  Hagedorn was apparently the guy who invented NPH insulin.
   
   
   
   
    
7. Human & K9 insulin differ in only one spot
   Human & feline insulin differ in 4 spots
   
   Beef & K9 insulin differ in 3 sites
   Beef & Feline insulin differ in 1  site
   
   Pork & K9 insulin are identical
   Pork & feline insulin are very different
   
   
   
   
    
8. It takes 70-80% antibody binding to create insulin resistence.  When you have only 10-15% binding, the insulin simply lasts longer, peak concentration is prolonged & absorption is slowed.  These may be desirable depending on how you want to change things for a particular patient.
   
   
   
   
    
9. "Glucose toxicity" refers to the effects of chronic hyperglycemia.  Chronic hyperglycemia causes reduced insulin receptors, reduced glucose transport & physically damages the beta cells.   :(
   
   
   
   
    
10. In hyperglycemia there is an increase in fructose & sortbitols, levels of which increase in the canine lens.  These sugars soak up water which makes the lens fibers swell. Voila, a cataract!