Hyperglycemia Question..

Not 100% sure, but try checking the insulin use of people with high blood sugar. I'm imagining a diabetic with high blood sugar mis / over dosing on insulin or not following insulin with an appropriate meal, resulting in hypoglycemia.

its all in the insulin. the body uses and stores glucose passively (without insulin) and actively (with the help of insulin). passively is a lot slower and can't handle rapid changes in glucose levels, while insulin is like a gatekeeper unlocking the storage chambers or releasing supplies rapidly when needed. insulin facilitates most the entry of glucose into fat and muscle cells for storage. so if you're a type one diabetic (the kind with lower levels of insulin) then you can have way to much glucose in the system (because it isn't being utilized) after consuming a meal. but the other extreme can happen as well where since you don't have the capacity to store glucose very well - so you end up peeing/excreting all the extra glucose that was meant for storage (for times when you're not eating) and end up with low blood sugar. this is coupled with the passive utilization of glucose that was already stored.

type II diabetes' pathology has to do with cells resistance to insulin - so you can figure out how it causes high blood sugar (and consequently low blood sugar) as well.

ah ok. so to be diagnosed (or assessed) with with high blood sugar you need to have high blood sugar (hyperglycemia).

so to have hyperglycemia it means you have high blood sugar and thats it.

there are many causes of hyperglycemia, a common one being diabetes.

being diabetic doesn't mean you're are exclusively hyperglycemic (or hypoglycemic), the disease can cause both states. its defined broadly on how you deal with glucose storage and insulin production/resistance.

I am not grasphing how you wrote that last sentence but here is some more info:

As stated above, Insulin stores the sugar. Type I Diabetics completely lack Insulin production and therefore have unregulated Glucagon response. Glucagon leads to conversion of stored sugars, fats, protein to glucose. The normal kidney reabsorbs 100% of glucose. However, type I's have an overload of glucose to kidney, and the overloaded kidney cannot reclaim the sugar and it is lost via urination.

Without the use of insulin: Type I's will continue to convert body stores to energy. Eventually, there will be a mass production of Ketones (from fat breakdown), severe volume depletion, and coma.

A normal person who misses a meal, their blood sugar will continue to be maintained by the release of glucagon and some other factors. But you have to factor in the use of Insulin with the diabetic patient, did they take their insulin? Do they use to much insulin, causing hypoglyemia? A diabetic patient who takes too much insulin, will cause irreversible brain damage because the brain relies on glucose and the excessive insulin causes storage of glucose.

Reread your texts, doc.

As to the OP: people with hyperglycemia tend to pretty much always have hyperglycemia. Insulin-dependent diabetics can take too much insulin and become hypoglycemic, but generally hyperglycemics will always have high blood sugar.

type II can get bad enough where an insulin resistance (the pathology in type II) where patients eventually require insulin in addition to the prescriptions to decrease blood sugar levels.


lol... thanks i actually did break out my old text books (sorry i'm a dumb cutter).

i was trying to explain the glucose transporters (GLUT 1-4) and how insulin is involved and kinda had to work myself back and around diabetes.

so insulin dependent diabetes do have hyperglycemia and can't utilize the glucose (glucose starvation in the face of its abundance).

They may feel symptoms, but that doesn't mean they really are hypoglycemic. A lot of those symptons are shared between hyperglycemia and hypoglycemia.

Some pre-diabetics (and I guess diabetics too) may oversecrete insulin since their endocrine system is so messed up. Also, what Lawrence said about glucose utilization.

The answer to the original question is reactive hypoglycemia. It happens sometimes with borderline diabetics, but more commonly with Type 1 diabetics via a different mechanism.

In a Type 2, which is what was asked about, it tends to be cause by a change in insulin resistance. When you eat the body releases insulin to soak up the glucose, and then releases glucagon which makes the liver release stored glucose to soak up any left over insulin. If that isn't done the remaining insulin will take needed glucose out of the bloodstream and you get hypoglycemia.

So what you see is an initial upward spike as the blood glucose levels go high which down-regulates the glucagon response, there is going to be a lot of insulin so not much clean up work, followed by a downward spike as the insulin finding less resistance than it expected strips more glucose out of the blood than needed. The glucagon response is now overwhelmed, it wasn't expecting all that insulin, and the glucose levels crash low. The body notices this and dumps epinephrine (the fall back because glucagon failed) which in turn causes the liver to dump stored glucose and restore the glucose levels in the blood. This leaves you with the side effects of epinephrine which are rather unpleasant.

There is a similar effect where going low results in a rebound high (Somogyi phenomenon) but I think that is limited to Type 1. There, more than you ever wanted to know on the topic - I am not a doctor but as a Type 1 diabetic this is my life (literally).

My understanding (correct me if I'm wrong) is that insulin triggers the storage of glucose in cells, while glucagon triggers the release (from cells and liver).

yup you're right. glucagon triggers glucose release. glucagon is mostly used in fasting states (where the body needs a non dietary source of glucose). i tried to oversimplify how insulin and sugar work in relation to specific hyperglycemic states. i was just trying to explain a negative feedback loop where in states of high blood glucose (high blood sugar) normally insulin would be released so that it would be taken into cells for storage. high blood sugar would also trigger a decrease in glucagon production (so that less glucose would be released from cells). so in cases on insulin dependent diabetes? not only do you have a problem with glucose storage, but because of the lack of insulin, the resultant states of hyperglycemia can actually result in a decrease of glucagon compounding effects . high blood sugar +lack of glucose uptake storage (lack of insulin) +lack of utilization release of glucose from cells when it might be actually needed (glucagon production inhibition). the results of which can be disastrous.

I am not so sure what condition we are talking about here. It sounds like you are talking about diabetic ketoacidosis (DKA). As you say there is a down-regulation of the glucagon response in the presence of hyperglycemia (the body doesn't want to worsen the situation by putting out more insulin). As the insulin level is low and the body cannot get glucose from the blood so it starts burning fat instead (an involuntary Atkins diet). This produces ketones that in the absence of insulin turn the blood acidic with potentially fatal results (2% of people die even with hospital intervention).

The problem happens when there are repeated hypoglycemic attacks close together that deplete the liver's glucose stores to the point where it can no longer dump glucose to save you in an attack.

Managing Type 1 diabetes is a juggling act and you become quite familiar with your local ER.