Understanding DM II, please help!

[amyhart34]

I understand the difference between type I and type II; however, what I don't understand is if insulin resitance is not the insulin not responding properly, it is the cells not responding properly to insulin, then how does administering more insulin help??? I get that if the body isn't producing insulin, such as in type I, giving insulin would work. But if the problem is with the cells and their receptors (type II), I can't wrap my brain around why giving more insulin is the answer!

Thanks!

2nd semester overwhelmed student

[BostonFNP, APRN]

You can think of it in basic terms:

1.) Insulin resistance means that more insulin is require to produce the same physiologic effect in the body.

2.) Initially the body is able to compensate by producing more insulin. During this period we can use oral antidiabetic agents to help preserve this state an maintain glycemic control.

3.) Resistance progresses and the body is unable to produce sufficient amount of insulin to maintain homeostasis/euglycemia. In order to help maintain euglycemia, we give exogenous insulin.

[eva123]

Also, you have to think about the mechanism of action. Oral antidiabetics can work like insulin or produce more insulin, so when they do not work or when there is a medical emergency (hospitalization usually results in a patient needing insulin instead of just oral agents) insulin is given.

[hodgieRN]

I see what you are saying. Don't think of insulin as merely a messenger to the pancreas. It acts directly on a cellular level within the body. If insulin was only a hormone that simply triggered a receptor, then it would only be as useful as the receptors itself, but this is not the case. Insulin has it own action and it's own effect on the body. The pancreas just secretes it. And, there are many factors that affect secretion. Once the insulin is released, then it goes to work on the body. That's why giving someone insulin works. It's not acting on the pancreas, it's acting on it's own within the body. You are basically cutting out the middle man.

Insulin itself acts as a metabolic process. It promotes energy conservation, cell growth, and cell division. (Bodybuilders who take steroids often take insulin. Not for the glucose control, but for muscle growth and cellular energy. It actually has anabolic effects, meaning it helps build). It stimulates glucose uptake via cellular transport, it promotes synthesis of organic molecules by converting glucose in glycogen and amino acids into proteins (see why bodybuilders take it). Without insulin, glycogen breaks down into glucose and proteins break down in amino acids. That's one of the reasons obese pts need more and more insulin. More is required to keep up with metabolic demand and all the different processes required to keep functioning.

Insulin can also help drive electrolytes into the cell. If someone gets IV insulin, potassium will shift from outside the cell into the cell.

And, obviously, it help lower glucose levels by blah, blah, blah.

All this happens despite the pancreas. Insulin is it's own beast.

When you have insulin resistance, the body is not reacting (on a metabolic level) as it did before. As Boston FNP, more is required to cause the same physiologic response. Insulin acts independently on liver cells, muscle cells, fat cells, etc. If you have resistance, that means insulin is not working as well in the liver cells, muscle cells, and fatty cells, regardless of the pancreas (so to speak). So, you have to up the dosage.

[classicdame, MSN, EdD]

if the cells absorb about 60% (hypotehtical number) of insulin that is circulating, then it makes sense to circulate more. 60% of 100 is 60 units. 60% of 200 is 120 units.