Hi awthrawthr ,
uhhhh ... the inactivation of the beta cells is not the first event.
They became inactive because they were destroyed by suvailing T-cells see
what I read in the original article explained above.....

hth a little bit
Gys

[Default] On 17 Dec 2006 05:09:17 -0800, awthrawthr@yahoo.com Giggled
into the madness of usenet:

eating hot peppers in raw or pill form does not do this.  lying about
curing type 1 and 2 will only get you kill filed by some and mocked by
the rest.

now go back to scamming at your health scam store little clerk.

<snipped some speculative theory>

Hi Jeff,
why do you think that the difference between the gangglia and the body is
important ?

My impression is that their main hypothesis is that TRPV1+  is the cause of
the problem and they show an immuun fluorescence picture of pancreas
preparations which is positive (green) for TRPV1 in the controls that were
not treated with capsaicin.They also show a western blot of TRPV1 (protein )
of spinal cord extracts which is positive for the control.So which part of
the neuron is secreting a peptide because of activation by TRPV1 does not
seem very important to me.

If I look up TRPV1 with "TRPV1 AND sapiens" in Gene at the NCBI :

Summary Capsaicin, the main pungent ingredient in hot chili peppers, elicits
a sensation of burning pain by selectively activating sensory neurons that
convey information about noxious stimuli to the central nervous system. The
protein encoded by this gene is a receptor for capsaicin and is a
non-selective cation channel that is structurally related to members of the
TRP family of ion channels. This receptor is also activated by increases in
temperature in the noxious range, suggesting that it functions as a
transducer of painful thermal stimuli in vivo. Four transcript variants
encoding the same protein, but with different 5' UTR sequence, have been
described for this gene.

For me , T2 1000 mg Metformin/day ,100 mg Tramadol /day ,300 mg Lyrica / day
, diet and exercise with lots of neuropatic pain this literature is
encouraging :

1) TRPV1 antagonists, including TRPV1 siRNAs, have potential in the
treatment of both, neuropathic and visceral pain . 2) PAR2 activates
PKCepsilon and PKA in sensory neurons, and thereby sensitizes TRPV1 to cause
thermal hyperalgesia 3)Opioid receptor agonist morphine acts via inhibition
of adenylate cyclase to inhibit protein kinase A-potentiated TRPV1 responses
4)Review notes that high expression of TRPV1 has been detected in
inflammatory diseases of the colon and ileum, whereas neuropeptides released
upon sensory nerve stimulation triggered by TRPV1 activation may play a role
in intestinal motility disorders.5)VR1 is widely distributed in the skin,
suggesting a major role for this receptor, e.g. in nociception and
neurogenic inflammation

My 2 cents
Gys

[Default] On Thu, 21 Dec 2006 09:10:17 -0700, desert dweller
<private@privateemail.org> Giggled into the madness of usenet:

and from that article the store clerk I was referring to claims that
eating peppers will do the same.

"The capsaicin was not directly injected into the pancreas. It was
inject s.c. (subcutaneously). It affected pain fibers all over the body.
Which is one reason why it is not a good way to prevent diabetes."

I read the full article, it was injected into the pancreous.