From:
Sukie Crandall
Date: 2006-03-22 18:44:51 UTC
Subject: [ferrethealth] another benefit of melatonin for ferrets with adrenal disease and more
To: FHL <ferrethealth@smartgroups.com>
FHL members who have read up on melatonin will recall that when too
much light exposure happens the the body creates very little
melatonin. This in turn (well known fast) causes the release of more
Luteinizing Hormone (LH) which is one of at least two things (another
being neutering) which do so. As you will note in a study mentioned
today in a different post, increased LH levels are increasingly
linked to the development of adrenal tumors, as per multiple studies
which are progressively filling in the few blanks remaining.
Decreased melatonin production also causes an increase in the
production of Follicle Stimulating Hormone (FSH) which has been
linked to bone loss, and is postulated to possibly be at least part
of ***why bone mass is lost in conjunction with adrenal disease in
ferrets*** so very often.
This study, though not on ferrets, points out yet another benefit of
giving melatonin to adrenal ferrets who are at risk of losing bone mass:
> J Clin Neurosci. 2006 Mar 17; [Epub ahead of print]
>
> The effect of exogenous melatonin administration on trabecular
> width, ligament thickness and TGF-beta(1) expression in degenerated
> intervertebral disk tissue in the rat.
>
> Turgut M, Oktem G, Uslu S, Yurtseven ME, Aktug H, Uysal A.
>
> Department of Neurosurgery, Adnan Menderes University School of
> Medicine, Aydin, Turkey.
>
> Intervertebral disk (IVD) degeneration, a complex pathological
> condition of varying origins, causes low back pain. Degenerative
> changes in IVD tissue affect the adjacent vertebral structure,
> resulting in a decreased vertebral trabecular width. It has been
> suggested that transforming growth factor-beta 1 (TGF-beta(1)) may
> have a role in the repair of connective tissue, as it occurs in the
> IVD degeneration process. In this study, we investigated the
> effects of exogenous melatonin (MEL) administration on vertebral
> trabecular width, ligament thickness and TGF-beta(1) expression in
> degenerated IVD tissue. Fifteen adult male Swiss Albino rats were
> divided randomly into three groups; nonoperated control, operated
> degeneration, and MEL treatment groups. In the operated
> degeneration and MEL treatment groups, cuts were made parallel to
> the end plates in the posterior annulus fibrosus at the fifth and
> tenth vertebral segments of the tail to induce IVD degeneration. In
> each group, TGF-beta(1) immunoreactivity and morphometry of
> vertebral trabecular width and anterior and posterior ligament
> thickness were evaluated. Histologically, disorganisation and
> irregularity of collagen fibres was seen in the degenerated
> (operated) IVD. Increased TGF-beta(1) expression in multinuclear
> chondrocytes was also observed as was decreased vertebral
> trabecular width. Importantly, the reduction of trabecular width
> observed in the operated degenerated group was reversed after MEL
> administration (p<0.0001). Similarly, TGF-beta(1) expression in
> multinuclear chondrocytes was dramatically increased after
> exogenous MEL application. Thus, there was a regression in
> histopathological changes after MEL treatment, with disk
> appearances similar to those of the control group. Based on our
> findings, we suggest that MEL activates the recovery process in the
> degenerated IVD tissue, possibly by stimulating TGF-beta(1)
> activity. This is the first report investigating the involvement of
> the pineal hormone MEL in the repair of rat IVD.
>
-- Sukie (not a vet)
Ferret Health List co-moderator
http://www.smartgroups.com/groups/ferrethealth
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