Question regarding Beta cells, Insulin Resitence

Hi Folks,
So now I have some questions.

I was reading someplace (I've read so much on diabetes that I can no
longer keep track of my sources) taht 2 things happen with Diabetes.

1. Beta Cells which produce insulin deteriorate/weaken and we end up
with high BG.

2. bieng overweight we store too much fat and that makes us insuln
resistent such that the "insulin receptors" are not picking up the
insulin that we do have.

So my question is do we have to have both conditions?
Can type 2s have one without the other?


Does Metformin take care of problem 1 and Actos take cere of problem 2?

Does actos and/or Metformin cause further deterioration of the beta
cells over time because it is forcing the liver to produce more insulin
(making liver work overtime)?

Thanks,

Vic
PS I may not reply right away. working and going to school (ie LOTS of
homework) makes for very little free time)

Vic1375 <dontspamme@nospam.com> wrote:
> Hi Folks,
> So now I have some questions.

> I was reading someplace (I've read so much on diabetes that I can no
> longer keep track of my sources) taht 2 things happen with Diabetes.

> 1. Beta Cells which produce insulin deteriorate/weaken and we end up
> with high BG.

> 2. bieng overweight we store too much fat and that makes us insuln
> resistent such that the "insulin receptors" are not picking up the
> insulin that we do have.

> So my question is do we have to have both conditions?

The increasing weight and increasing insulin resistance which at first
simply means you have to produce more insulin than most to keep your
BGs normal is known as the metabolic syndrome. It only leads to T2
diabetes if your pancreas can't stand the strain of having to produce
such large amounts of insuln and starts collapsing.

> Can type 2s have one without the other?

It's very rare for a type 2 not to have developed by this route.

> Does Metformin take care of problem 1 and Actos take cere of problem 2?

Depends on how picky you are in defining "takes care".

> Does actos and/or Metformin cause further deterioration of the beta
> cells over time because it is forcing the liver to produce more insulin
> (making liver work overtime)?

(The beta cells are in the pancreas, not the liver.)

Stimulating the beta cells to produce more insulin is regarded by a
minority as increasing the strain which led to diabetes in the first
place and hastening their progressive death. That minority prefers
therapies which reduce the workload of the beta cells as much as
possible.

--
Chris Malcolm cam@infirmatics.ed.ac.uk DoD #205
IPAB, Informatics, JCMB, King's Buildings, Edinburgh, EH9 3JZ, UK
[http://www.dai.ed.ac.uk/homes/cam/]

Vic1375 wrote:
> Hi Folks,
> So now I have some questions.
>
> I was reading someplace (I've read so much on diabetes that I can no
> longer keep track of my sources) taht 2 things happen with Diabetes.
>
> 1. Beta Cells which produce insulin deteriorate/weaken and we end up
> with high BG.
>
> 2. bieng overweight we store too much fat and that makes us insuln
> resistent such that the "insulin receptors" are not picking up the
> insulin that we do have.
>
> So my question is do we have to have both conditions?
> Can type 2s have one without the other?
>
>
> Does Metformin take care of problem 1 and Actos take cere of problem 2?
>
> Does actos and/or Metformin cause further deterioration of the beta
> cells over time because it is forcing the liver to produce more insulin
> (making liver work overtime)?
>
> Thanks,
>
> Vic
> PS I may not reply right away. working and going to school (ie LOTS of
> homework) makes for very little free time)
>
>
>
Most T2's start off as insulin resistant, and may become insulin
deficient. Though it is possible to be insulin deficient and not
resistant as a T2 I think, but it's not a total insulin deficiency like
a T1, the body still makes some insulin, just not enough. Whether that
is merely an indication that one is heading towards T1, and not a true
T2 is probably up for debate in the medical community too. (i.e. LADA,
Type 1.5 etc.) Metformin works against resistance--doesn't cause more
insulin to be produced, but allows the body to use what is produced.
Forget what Actos does, but maybe it makes more insulin. I know the
sulfonylureas do. (glyburide etc.)

T1's Don't make any insulin at all (eventually, sometimes the autoimmune
process doesn't kill all the beta cells at once, so some insulin can be
made for a while, until all the beta cells (the cells in the pancreas
that make insulin) die). So, they Must inject insulin. It is also
possible to be a T1 and have some insulin resistance. Usually, this is
noticed when HUGE amounts of insulin must be injected to reach BG
control. Sometimes metformin will be added to the regimen at that point,
to combat the resistance, and then less insulin needs to be injected.

Emily

"Vic1375" <dontspamme@nospam.com> wrote in message
news:et2mj4$3ge$1@new7.xnet.com...
> Hi Folks,
> So now I have some questions.
>
> I was reading someplace (I've read so much on diabetes that I can no
> longer keep track of my sources) taht 2 things happen with Diabetes.
>
> 1. Beta Cells which produce insulin deteriorate/weaken and we end up with
> high BG.
>
> 2. bieng overweight we store too much fat and that makes us insuln
> resistent such that the "insulin receptors" are not picking up the insulin
> that we do have.
>


This prompts me to ask a related question that's been bothering me.

If one is insulin resistant, but still producing enough insulin to keep
glucose levels out of the diabetic range, are the higher than normal insulin
levels themselves damaging in any way?

Google hasn't helped much in finding an answer.

Peter

Vic1375 <dontspamme@nospam.com> wrote:
: Hi Folks,

: So my question is do we have to have both conditions?
: Can type 2s have one without the other?
I believe that some can. Jenny has somthing like tht.

: Does Metformin take care of problem 1 and Actos take cere of problem 2?

As far as my understanding is cncerned, tht seems to be the way II see it.
Metformin surpressd the liver's production of glycogen so the beta cells
don't have to produce insulin to deal with it and Actos works to counter
the IR factor , largely related to belly fat.


: Does actos and/or
Metformin cause further deterioration of the beta
: cells over time because it is forcing the liver to produce more insulin
: (making liver work overtime)?

The liver does not produce insulin, the Beta cellsin the pancreas do that.
The liver stores sugar in the form of glycogon9sp?) and the Metformin
keeps it from realeasing the sugary stuff inot the blood stream. If it
were released, the beta cells would have to produce more insulin to deal
with it.

Wendy

In article <EefJh.134193$HO5.53819@fe1.news.blueyonder.co.uk> ,
"Peter" <peternorthlondon0001@lycos.co.uk> wrote:

> "Vic1375" <dontspamme@nospam.com> wrote in message
> news:et2mj4$3ge$1@new7.xnet.com...
> > Hi Folks,
> > So now I have some questions.
> >
> > I was reading someplace (I've read so much on diabetes that I can no
> > longer keep track of my sources) taht 2 things happen with Diabetes.
> >
> > 1. Beta Cells which produce insulin deteriorate/weaken and we end up with
> > high BG.
> >
> > 2. bieng overweight we store too much fat and that makes us insuln
> > resistent such that the "insulin receptors" are not picking up the insulin
> > that we do have.

You picked up #2 in mid-cycle. It's the insulin resistance that starts
the cycle of added fat --> insulin resistance --> high levels of
endogenous insulin --> added fat --> insulin resistance.... etc.

It's only when your #1 shows up that the diagnosis of type 2 diabetes
comes into play. Without #1 you're just insulin resistant and fat.
Once the stress on your beta cells burns enough of them out so you can't
produce sufficient insulin, then your BG starts going up into DM
territory. And phase 1 insulin (the stuff that waits around in case you
eat something) is liable to be first to go, which means that
post-prandial spikes will likely be the first sign of the DM arriving.
The malfunctioning of the "off switch" on the phase 2 insulin (that
which is pumped out in response to BG increase) will show up as reactive
hypoglycemia. Once phase 2 dies out as well, you've got to start
injecting insulin.

> This prompts me to ask a related question that's been bothering me.
>
> If one is insulin resistant, but still producing enough insulin to keep
> glucose levels out of the diabetic range, are the higher than normal insulin
> levels themselves damaging in any way?

Yup. They're packing on the poundage thus worsening the insulin
resistence, plus hyperinsulinemia can be damaging to various organ
systems, including cardiac.

I'm hoping Susan will post some references. I think she's got a few (or
more).

Priscilla

x-no-archive: yes

Priscilla H. Ballou wrote:

> Yup. They're packing on the poundage thus worsening the insulin
> resistence, plus hyperinsulinemia can be damaging to various organ
> systems, including cardiac.
>
> I'm hoping Susan will post some references. I think she's got a few (or
> more).
>

High insulin levels are associated with high incidence of cancers,
especially of the colon, prostate, breast and ovaries.

High insulin levels also promote inflammatory conditions in the body,
hence the high levels of inflammatory cytokines found where insulin is
high. One mechanism for this is the suppression of adrenal function by
insulin.

For cancer references, just do a Medline search using the term
hyperinsulinemia AND (name of cancer).

There are also quite a few references for insulin reduces CBG and SHBG
(cortisol binding protein and sex hormone binding globulin, the proteins
that carry these hormones to target cells so they can exert their action).

I'm too busy trying to assemble a decades long coherent medical history
for my trip to an out of town endocrinology researcher to dig these up now.

Susan