FERRET-SEARCH Archives

Searchable FML archives

FERRET-SEARCH@LISTSERV.FERRETMAILINGLIST.ORG

Options: Use Forum View

Use Monospaced Font
Show Text Part by Default
Show All Mail Headers

Message: [<< First] [< Prev] [Next >] [Last >>]
Topic: [<< First] [< Prev] [Next >] [Last >>]
Author: [<< First] [< Prev] [Next >] [Last >>]

Print Reply
Subject:
From:
Sukie Crandall <[log in to unmask]>
Date:
Sun, 19 Sep 2010 15:43:56 -0400
Content-Type:
text/plain
Parts/Attachments:
text/plain (158 lines)
Hopefully, my brain is not too frazzled by a ragweed allergy related
sinus head I've had all day.

Why might this have implications? Partly because with domestic ferrets,
domestic cats, and domestic dogs we are talking about animals who were
recently nocturnal (with mostly crepuscular peak activity -- meaning
dawn and dusk -- and burrow darkness otherwise for polecats) which
people have been shifting to being largely diurnal, so the question
arises of how much effect that has on their liver and pancreatic
functions, and measuring this protein and comparing it to that of wild
polecats or zoo polecats kept in natural lighting and other living
conditions might be useful. More why?: Partly because we already know
that light exposure reduces melatonin production. (The blue wavelength
range is the worst, while the second worst is the green wavelength
range -- used in many equipment lights and night lights. The least
disruptive is amber colored lighting (yellowy-orange) so prefer any
type of light that looks amber at dusk and afterward for ferrets, and
if you can ***safely*** cover or block the blue or green then do so.)
Now, too little melatonin production increases luteinizing hormone
production. Increased luteinizing hormone production is the trigger
for adrenal tumors. OPPS!

Individuals with their biological clocks off resulting in too much
light exposure for their species are going to produce too little
melatonin. (Aging also reduces the amount of melatonin that a body
can naturally make.)

http://www.eurekalert.org/pub_releases/2010-09/uoc--bdb091710.php
Press Release on cryptochrome in part (to fit in the FML size limit):
> University of California -- San Diego
> ...
>Biologists have found that a key protein that regulates the biological
>clocks of mammals also regulates glucose production in the liver

...
>Their discovery, detailed in this week's advanced online publication
>of the journal Nature Medicine, provides an entirely new biochemical
>approach
...
>This reciprocal relationship between circadian rhythm and the
>maintenance of a constant supply of glucose in the body had been
>known for some time. But what we found that's so significant is
>that a particular biological clock protein, cryptochrome, is actually
>regulating how the hormone that regulates glucose production in the
>liver works in a very specific way."
>
>"We used to think that our metabolism was regulated primarily by
>hormones that are released from the pancreas during fasting or
>feeding. This work shows that the biological clock determines how well
>these hormones work to regulate metabolism," says Marc Montminy, a
>professor in the Clayton Foundation Laboratories for Peptide Biology
>at the Salk Institute for Biological Studies....
>
>Cryptochrome was first discovered by scientists as a key protein
>regulating the biological clocks of plants. It was later found to
have >the same function in fruit flies and mammals. But its role in
>regulating glucose production in the liver came as a complete surprise
>to the UCSD and Salk team, which included scientists from the Genomics
>Institute of the Novartis Research Foundation in San Diego, the
>University of Memphis and the Chinese Academy of Sciences in Shanghai.
>
>...What we showed was that cryptochrome has a role outside the nucleus
>as well."
>
>That additional function of cryptochrome in mammalian cells, the
>scientists discovered, is to regulate a process known as
>"gluconeogenesis," in which our bodies supply a constant stream of
>glucose to keep our brain and the rest of our organs and cells
>functioning. When we're awake and eating, sufficient glucose is
>supplied to our bloodstream. But when we're asleep or fasting, glucose
>needs to be synthesized from the glycogen stored in our liver to keep
>our glucose levels up.
>
>"That is how our energy metabolism evolved to function in concert with
>our diurnal activity, or in the case of the mice, their nocturnal
>activity," said Kay. "This molecular mechanism involving cryptochrome
>presumably evolved to coordinate our energy metabolism with our daily
>activity and feeding levels.
  ...
>Zhang and his UCSD colleagues conducted a series of experiments that
>found that the production of the next step after cyclic AMP, a protein
>called Creb, ebbed and flowed rhythmically in the livers of mice. That
>led the scientists to their initial discovery that cryptochrome was
>regulating the production of Creb in the liver.
>
>In their studies with fasting and insulin-resistant mice at the Salk
>Institute, the scientists found that cryptochrome was regulating how
>the hormone glucagon, which controls gluconeogenesis, works in a very
>specific way. By controlling the production of cyclic AMP, crytochrome
>regulates the activity of Creb in the liver. In this way, the
>production of glucose in the liver is tied through our daily eating,
>sleeping and fasting activities through the biological clock.
>
>The scientists say their discovery may open up a whole new area of
>research into how cryptochrome may be regulating other cell functions
>outside the nucleus.
>
>"There's a wide role that the biological clock may be playing in
>influencing other hormones, not just glucagon, that are important
>for metabolism...

This appears to be a different but related very recent study on
cryptochrome:
http://www.biomedcentral.com/content/pdf/1471-2199-11-69.pdf
That is not the final pdf version, but rather a provisional one because
it is a brand new publication so it might disappear or disappear on and
off depending on how they assign URLs.

Abstract:
http://www.ncbi.nlm.nih.gov/pubmed/20840750

A bit more:
http://www.biomedcentral.com/1471-2199/11/69

Oh, and there is currently quite a bit of work in multiple species
that ties eating a lot (the food type did not matter) to increased LH
production, while LH production goes down if the food amount returns
to a better level for the species. See PubMed or for summaries:
http://ferrethealth.org/archive/FHL12184 and
http://ferrethealth.org/archive/FHL12185

(There is some recent preliminary human food work that indicates that
due to being processed, some types of processed foods are digested more
efficiently so it might be easier to become over-weight or to over-eat
with some types of processed food, indicating the extra physical
activity becomes even more important (says she who is currently slowed
down from thyroid problems). This should not be a complete surprise; it
is already very ( very, very, very, very , very) well documented that
even just cooking can "pre-digest" foods which is why cooked foods
break down more efficiently in the body, and that is so for both animal
origin foods and plant foods.)

This recent work also has possible implications for both pancreatic and
adrenal health of ferrets:

http://www.cell.com/cell-metabolism/abstract/S1550-4131%2810%2900270-6

<http://www.sciencenews.org/view/generic/id/63109/title/Study_clarifies_obesity-infertility_link>

Notice that the pituitary does not become insulin-resistant. That has
cascading implications for the mechanisms involved in a whole range
of endocrinological health problems, since it tosses out a number of
earlier hypotheses in any species for which that is the case and
creates a need for new hypotheses on why some observations happen.

>A new study in mice shows that the pituitary gland, which helps
>regulate the release of fertility-associated hormones, remains
>sensitive to insulin. But in obese mice, insulin's constant signaling
>to release the fertility hormones leads to an overabundance of those
>hormones

LH is among the hormones increased in the mice (but LH production in
such a situation has to be compared across species). Again, LH is the
trigger for adrenal growths in ferrets.

[Posted in FML 6826]


ATOM RSS1 RSS2