someone brought up a conversation in our study group last night. we couldn't think of the "why", but it's probably right in front of our eyes-- but we were too exhausted to know it!
in dka, we all know that lipolysis is happening and that the free fatty acids are converted into ketone body in the liver because of the lack of insulin.
in hhns, the basic defect is the lack of effective insulin and the extracellular fluid is sucking the water out of the intracellular fluid.
ok, now the question is "why". why doesn't the person with hhns (say a type 2 diabetic that is insulin dependent) go into ketoacidosis and turn fat into ketone bodies?
any help would be very much appreciated.
Mar 1, '07
There is a great deal of debate about that. One of the leading hypotheses is that ketogenesis is held off because the pancreas can still secrete some insulin. (You need a lot less insulin for lipogenesis and inhibition of lipolysis than you would for glucose uptake.)
It is also thought that the hyperosmolar, dehydrated state in HHNK can inhibit release of fatty acids from adipose tissue.