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From:
Sukie Crandall <[log in to unmask]>
Date:
Sun, 4 Feb 2007 13:33:56 -0500
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With insulinoma seizures occur from sugar (energy) starvation in the
brain. These will be of interest as related to insulin and the brain
to illustrate general functions since in some posts there seems to be
confusion about what occurs when glucose levels get too low for the
brain:

http://www.boston.com/news/globe/health_science/articles/2006/01/30/insulin_in_the_brain/

http://diabetes.diabetesjournals.org/cgi/content/full/51/12/3384

http://www.medicalnewstoday.com/medicalnews.php?newsid=41017

http://www.eurekalert.org/pub_releases/2005-03/l-rdl030205.php

http://www.eurekalert.org/pub_releases/2006-03/l-rii031606.php

http://scienceweek.com/2005/sw050520-5.htm

Recently, I carried info here from a mouse study done among researchers
in U. Calgary, Toronto Children's Hospital, and a research facility in
Maine (Jackson?) on how damage to a specific type of sensory neuron
appears to be able to be a trigger for Type 1 Diabetes, and may be for
other glucose management problems. Work has begun on Type 2 Diabetes,
too. (Intriguingly, damaged nerves can become either hyporesponsive or
hyperresponsive -- sometimes even neighboring nerves, as people here
with neuropathy of several types can attest. I've had both in different
ways and different areas in my widely separated years of both bouts of
severe sensory neural disease and some left over problems in both
directions even after my body healed.)

For whatever reasons Steve and I have had low levels of insulinoma
among our ferrets over the space of 26 years. We feed kibble on demand
mostly, give no starch treats (though a few steal some), provide a lot
of exercise, and provide a lot of darkness available at any time. The
body produces its own melatonin in darkness -- and we are talking
darkness rather than dimness. New studies are indicating previously
unknown functions for melatonin in pancreatic actions. In fact, it
plays a part in two actions that oppose each other so some vets argue
that melatonin might be good for some ferrets with insulinoma while
others argue that it might be bad for some ferrets with insulinoma. The
second is under study. That is all largely hypothetical now, though,
and telling which may be helped from which may be harmed, or even if
either occurs in significant numbers is truly iffy for now.

Our own levels of insulinoma have been low enough that we have to
combine them with the cases here of other pancreatic neoplasias such as
lymphoma and carcinoma to get up barely 20% over ferrets' lifespans.

I can tell you this: back in the early days of our having ferrets, back
when it was all kibble and when there were almost no fancy ferrets the
rates of both insulinoma and adrenal disease were lower -- way lower --
among the ferrets of the people we knew.

Rumor has it that a preliminary announcement from the ferret genetics
study at U.C. Davis did find at least one form of genetic variant which
creates endocrinological tumor vulnerabilities.

BTW, for a very interesting, and very accessible lecture on genetics
which gets into the interplay of physical stresses and malignancy
formation there one for non-biologists here by Arnold Levine:

http://online.kitp.ucsb.edu/online/bblunch/

It is technical and up to date BUT it is NOT given for biologists let
alone geneticists, but instead for physicists, so non-biologists should
have no trouble with it. (BTW, the caloric restriction longevity effect
is also seen with core cooling which itself is a result of caloric
restriction so more is going on than oxidation reduction with caloric
restriction (and interestingly in the sole study I know of that broke
down the type of caloric source the flat worms studied had longer
lives with higher carbohydrate proportions but not with higher protein
proportions so there are obviously a number of surprises to understand
better in that area of study.))

I suspect that as happened with adrenal disease where multiple factors
(being neutered and exposed to too much light, for example) wound up
working together to produce the trigger of LH over- production (and the
associated FSH over-production may also play a role beyond reducing
bone density) -- the rate of which can be increased by genetic
vulnerability -- that insulinoma in ferrets may be triggered by an
interplay of several factors which result in one or two triggering
alterations and that genetic vulnerability plays a factor. Anyone who
recalls how rare both adrenal disease and insulinoma used to be in U.S.
ferrets a quarter century ago can not help but think about what things
have changed and which have not changed. Those who weren't around then
(most people here) would be startled by a short ride back in time to
when those were so rare.

It would be good if even a foundation study on rates of insulinoma in
general existed. Meanwhile, we all look at what studies exist, try to
not accidently build upon our own biases ourselves by avoiding the
studies and experiences that oppose our own preferred hypotheses nor by
refusing to strongly challenge our own concepts, recognize how mixed
the picture still is and how much really rigorous study is needed, and
just make our own choices and respect differing choices others have
made. There is so much more to learn.

Sukie (not a vet)
Current FHL address:
http://groups.yahoo.com/group/ferrethealth
People can join there or can send a blank mail to the automated
joining address:
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and then follow the directions.
(The second is recommended for those having problems with Yahoogroups
web settings, and afterward send a blank mail from your subscribed
address to
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to get the digest instead of individual mails. )
Recommended ferret health links:
http://pets.groups.yahoo.com/group/ferrethealth/
http://ferrethealth.org/archive/
http://www.afip.org/ferrets/index.html
http://www.miamiferret.org/fhc/
http://www.ferretcongress.org/
http://www.trifl.org/index.shtml

[Posted in FML 5509]


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