It's like "water resistant" and "water repellant."  If a coat is "water
resistant" it'll keep you dry in a mist or a light shower, but if a
thunderstorm comes through, you're drenched.  If that coat is "water
repellant," however, you'll stay dry even in the thunderstorm.  (Well,
OK, your feet will still get wet, but you get the point.)

Insulin resistance is not insulin repellence.  If you've got *enough*
insulin, you can overcome it, which is why people with "pre-diabetes"
show as making massive amounts of insulin.  The problem in T2 is that
eventually we lose the ability to make enough insulin to overcome it.  
Then we can either lower the insulin resistance or get some more insulin
from outside.  

Priscilla, simplifying madly

Lynn...

In the case of IR, it's not that someone with IR is not using the
insulin... it's that they're not using it efficiantly.

For many years before dx, most people with IR are pumping out vast
amounts of insulin and their bodies need vast amounts just to stay
"normal"... and they do stay normal for a time.

In time even the vast amounts their bodies make can't keep up with their
inefficiant cells.  So injecting more does help... they just need more
and more to stay normal.

Now... while it does keep their glucose in range, there can be problems
with having too much circulating insulin in a body... so it's a trade off.

Jennifer

Basically, it is a case of "if you throw enough mud at the wall, SOME of it
is going to stick"

While the body doesn't use the insulin properly, there is still some
succeeding in opening those locks in the cells to get the glucose in there.
The more keys (insulin) there are, the more chance of having some fit into
the locks (opening the cell walls).

Kelly
T2 10 years, yada yada

Lynn wrote in message ...

Insulin Resistance means you need more insulin than a non-insulin resistant
person would need to accomplish some insulin dependent task.    You can
overpower that Insulin Resistance by adding more insulin to the blood.
Millions and millions of non-diabetics with high Insulin Resistance do it
every hour of every day by just manufacturing more insulin than non-Insulin
Resistant people do.

However,  diabetics have problems making enough insulin to overpower their
Insulin Resistance.   That's why they're diabetic.    If they wish to
approximate the insulin present in non-diabetic,  high insulin resistant
people,  they must inject the extra insulin into their bodies.

A better approach is to reduce their needs by eating low carb,  and to
reduce their insulin resistance by one of several lifestyle changes and/or
anti-Insulin resistance drugs.

As a G.D.,  you are facing one,  two or all of three problems:

   1.   Pregnant women need more insulin than not-pregnant women,  at least
twice as much by the 3rd trimester.

   2.  Since you are G.D.,  you probably have Type 2 diabetes genes and
their effect is the death of quite a few beta cells in past years.   Thus,
your ability to manufacture insulin has declined and you can't meet the
higher insulin needs of pregnancy.

   3.  You may or may not have elevated Insulin Resistance.    If you do,
many docs won't counter it with anti-Insulin Resistance drugs during
pregnancy.

The standard techniques for reducing Insulin Resistance are:

     1.  Lose fat lb
     2.  Exercise vigorously every day
     3.  Take anti-Insulin Resistance meds

Pregnant women have difficulties with these techniques.     Not impossible
difficulties but difficulties nevertheless.    (Many docs are offering
metformin to G.D. ladies)

High blood sugars lead to problems during pregnancy,  among them,  premature
birth and miscarriage.     Insulin injections are the 800-lb gorilla of
blood sugar control.    If you as a pregnant lady can't control your blood
sugar via  a low carb diet ,  fat loss,  vigorous daily exercise and
metformin anti-insulin resistance med,  then insulin injections are your
only remaining option.

I have never seen a reference which claimed insulin injections raised
Insulin Resistance.   It was always the other way around.  But that doesn't
really matter.   you must gain control over your blood sugars right now and
insulin injection is the most powerful tool available.

Remember:   normal human insulin needs double by the end of the pregnancy;
you've got to come up with that insulin somehow.

Bizarre humor:    One of my friends had two G.D. pregnancies.    During the
first one,  she had her husband bring shortbread cookies and sugared soda
pop (her absolute favorite snack,  forbidden during her pregnancy)  to the
delivery room.     She gobbled the cookies and drank the pop in the delivery
room during one of the waiting periods after delivery**.   When she
measured** her blood sugar,  it was rock steady normal.     An hour earlier
and that same snack would have sent her sky-high.

(**We both worked in Research.    Perhaps we Researchers are bizarre,  not
the humor)

Regards
 Old Al

the injected insulin does not increase insulin resistance.  But it
does over come, or maybe overwhelm is a better word, the insulin
resistance.  And the injected insulin is NOT exactly like your body's
natural insulin.  You are actually less resistant to the injected
brands.  The added benefit is that you will not be forcing your body
to produce so much extra of it's own insulin.  Meaning your natural
production will be slowed to a more normal rate, actually giving your
pancreas a rest.  Less stress on the endocrine system and the rest of
the body.

But do not forget that the IR "will" still be there.  The reason you
cannot or should not attempt to treat the IR with oral meds while
pregnant is the very real health risks to the fetus that the oral meds
pose.

In the context of IR the body is still using insulin, it just takes a
whole lot of it to get the job done and the amount produced isn't enough.

Adding more will bring down blood sugars.

In the context of GD your need for insulin is much more than the insulin
your body produces whether because of IR or marginal insulin production
before pregnancy.  Whatever the reason, the body needs more insulin and
adding it will help.

For example. Looking at basal insulin alone taken to control fasting
blood sugar.  A person who is not insulin resistant might take anywhere
from 3-15 units a day.  An insulin resistant type 2 might take anywhere
from 30-120 units a day to get the same effect. (These are doses real
people have reported to me.)

So the IR person will need a lot more, but it will achieve the same effect.

It's not clear to me that hyperinsulemia by itself increases insulin
resistance.  But in combination with high bg, it does:

Sustained Exposure of L6 Myotubes to High Glucose and Insulin
Decreases Insulin-Stimulated GLUT4 Translocation but Upregulates GLUT4
Activity

http://diabetes.diabetesjournals.org/cgi/content/full/51/7/2090

Hyperglycemia and hyperinsulinemia are cardinal features of acquired
insulin resistance. In adipose cell cultures, high glucose and insulin
cause insulin resistance of glucose uptake, but because of altered
GLUT4 expression and contribution of GLUT1 to glucose uptake, the
basis of insulin resistance could not be ascertained. Here we show
that GLUT4 determines glucose uptake in L6 myotubes stably
overexpressing myc-tagged GLUT4. Preincubation for 24 h with high
glucose and insulin (high Glc/Ins) reduced insulin-stimulated GLUT4
translocation by 50%, without affecting GLUT4 expression. Insulin
receptor and insulin receptor substrate-1 tyrosine phosphorylation,
phosphatidylinositol 3-kinase activation, and Akt phosphorylation also
diminished, as did insulin-mediated glucose uptake. However, basal
glucose uptake rose by 40% without any gain in surface GLUT4. High
Glc/Ins elevated basal p38 mitogen-activated protein kinase (MAPK)
phosphorylation and activity, and a short inhibition of p38 MAPK with
SB202190 corrected the rise in basal glucose uptake, suggesting that
p38 MAPK activity contributes to this rise. We propose that in a
cellular model of skeletal muscle, chronic exposure to high Glc/Ins
reduced the acute, insulin-elicited GLUT4 translocation. In addition,
basal state GLUT4 activity was augmented to partially compensate for
the translocation defect, resulting in a more robust glucose uptake
than what would be predicted from the amount of cell surface GLUT4
alone.

DRT