I have a question about Diabetes M., type II. I recently got q. about it on Kaplan that thoroughly confused me.
If a pt is newly diagnosed as a type II diabetic, what will be the activity of his pyruvate dehydrogenase (PDH)?
According to Kaplan it will be high, since the pt is gonna have hyperinsulinemia, and thus his liver will prefer gylcolysis over gluconeogenesis.
But why is this? I thought the whole "point" of type II DM is that there is insulin resistance, so that yes, there will be hyperinsulinemia, but the organs will not react to it.
Before you answer, read this:
I tried to look this up and the best explanation I got was that the insulin resistance is differential between extrahepatic sites (muscle, adipose), and liver. So, early in diabetes, only the extrahep. sites are resistant, and one gets postprandial hyperglycemia. However, the liver still reacts to insulin, so in fasting states you are "ok," and glycolysis occurs. It is only in advanced insulin resistance that the hepatocytes fail to recognise insulin, and are constitutively gluconeogenetic...hence you get a fasting hyperglycemia.
IS THIS TRUE? I am concerned, since I (think I) never learned this at school, despite me having x leactures on DM in almost every organ system class. I am also a little upset, since I feel that 99% of all resources and classes discuss "how diabetes is so, so, so important" and "how every doctor should know everything about it" and then almost no book offers a resonable explanation of the metabolic processes and just spits out the annoying cliche of "insulin resistance of unknown mechanism" I had to spend app. 1 hr of my valuable boards time looking up the info above in REVIEW ARTICLES...not text books...what the heck. (or is this something American kids learn in elementary schools and I just look stupid asking it? I was born in Europe...)
If a pt is newly diagnosed as a type II diabetic, what will be the activity of his pyruvate dehydrogenase (PDH)?
According to Kaplan it will be high, since the pt is gonna have hyperinsulinemia, and thus his liver will prefer gylcolysis over gluconeogenesis.
But why is this? I thought the whole "point" of type II DM is that there is insulin resistance, so that yes, there will be hyperinsulinemia, but the organs will not react to it.
Before you answer, read this:
I tried to look this up and the best explanation I got was that the insulin resistance is differential between extrahepatic sites (muscle, adipose), and liver. So, early in diabetes, only the extrahep. sites are resistant, and one gets postprandial hyperglycemia. However, the liver still reacts to insulin, so in fasting states you are "ok," and glycolysis occurs. It is only in advanced insulin resistance that the hepatocytes fail to recognise insulin, and are constitutively gluconeogenetic...hence you get a fasting hyperglycemia.
IS THIS TRUE? I am concerned, since I (think I) never learned this at school, despite me having x leactures on DM in almost every organ system class. I am also a little upset, since I feel that 99% of all resources and classes discuss "how diabetes is so, so, so important" and "how every doctor should know everything about it" and then almost no book offers a resonable explanation of the metabolic processes and just spits out the annoying cliche of "insulin resistance of unknown mechanism" I had to spend app. 1 hr of my valuable boards time looking up the info above in REVIEW ARTICLES...not text books...what the heck. (or is this something American kids learn in elementary schools and I just look stupid asking it? I was born in Europe...)
