RRzVRR wrote:
Jackie Patti wrote:
RRzVRR wrote:
Found this article very interesting... file it under "NO EASY
ANSWERS"

I was a bit disappointed there was nothing about amylin in there,
even though they discussed the company.

It's a fascianting hormone; I've posted some stuff on
alt.support.diabetes about it.

Looked around a little on amylin. Keeping glucagon under control
helps keep the bg lows from being too low and thereby keeping insulin
levels under control?

In both T1 and T2 diabetics, there's low serum amylin, which means
there's high postprandial glucagon. So postprandial, you have both the
bg rise from food and the bg rise from the liver production of glucose
happening simultaneously, a double wammy of elevating bg.

People who take the synthetic analog of amylin (Symlin) reduce their
insulin usage 25-50%. That's currently the only approved use of Symlin
- for T1s and insulin-using T2s who don't get good control with
insulins. I am plotting how to convince my doctor to write a script as
I don't have poor control, I'd just like to reduce insulin.

There's also some interesting animal studies - amylin reduces appetite
30% in rats - and it's a definite effect on the brain. They're doing
phase 2 clinical trials in non-diabetic humans now to use it as an
anti-obesity drug.

It does a lot of other things as well - slows gastric-emptying thus
slowing bg rise. I suspect we don't know the half of it yet; it's a
very interesting little molecule.


Even though the human body and can withstand a lot of extremes it
really thrives in homeostasis.

Hormones are fascinating to me; such tiny amounts of things that make
such a huge difference.

Heck, here's my most recent post from asd about this:

I have found another interesting piece in the puzzle with some
minimal look at the research in animals. T2s, while having low
levels of serum amylin, have fibers growing on the pancreas and
elsewhere that are made largely of amylin. The fibers are postulated
to be one of the causes of insulin resistance.

That kind of makes sense in a way. A T2 doesn't make less insulin
than a nondiabetic, but more. Since amylin is co-secreted with
insulin, you'd expect it to be high in T2s also. But it's low in the
blood, which sort of implies it's been taken out of the blood.

They originally called amylin "diabetes-associated peptide" because
they were finding it in these fibers that they postulate cause
insulin resistance.

There's also a big change with amylin not getting to the brain.
They've proven this in animals. If they give amylin to animals, they
eat a lot less - one study said up to 30%. If they destroy the bit
of the brain in rats that amylin works on, then amylin doesn't change
appetite anymore. So while everyone is talking about gastric
emptying, there's a huge effect of amylin on the brain directly.

This seems to imply T2s get fat because of the amylin being removed
from the blood before it gets to the brain. It might well be that
the amyloid fibers that form both cause insulin resistance and by
removing amylin from the blood, increase appetite.

The next interesting question is what causes the amylin to form these
fibers instead of staying in the blood...

There was a study of ethnic Japanese that showed that all T2s who
became so before the age of 50 had a genetic defect and made a
slightly different form of amylin.

It's very intriguing stuff - we might be on the verge of finding out
the root cause of T2.


--
http://www.ornery-geeks.org/consulting/