These researchers seem to think there is a link between elevated leptin
levels and autoimmune disease which .. theoretically .. can be targeted
..

<<snip>>
modulating leptin concentration through dietary approaches, and/or the
administration of drugs that interfere with the bodys own production of
leptin, may have potential utility in the treatment of MS and other
autoimmune diseases.
<<snip>>

<<snip>>
excess iron elevated plasma leptin level
<<snip>>

Leptin regulates the immune response to friend and foe

The hormone leptin, primarily produced in fat cells, helps regulate
food intake, metabolism and reproduction. It has also been shown to
promote and sustain the body's immune response by binding to T
lymphocytes - the frontline cells that protect against infection. The
disease experimental autoimmune encephalomyelitis (EAE) in mice is
currently used by researchers as a model of human multiple sclerosis
(MS). Italian researchers now reports that just prior to developing the
clinical symptoms of EAE, mice experience a significant burst of leptin
which correlates with a reduction in food intake and weight loss.
Furthermore, subjecting mice to acute starvation, which prevents the
production of leptin, was found to delay the onset and reduce the
severity of disease.

Leptin regulates the immune response to friend and foe

The hormone leptin, primarily produced in fat cells, helps regulate
food intake, metabolism and reproduction. It has also been shown to
promote and sustain the bodys immune response by binding to T
lymphocytes - the frontline cells that protect against infection.

The disease experimental autoimmune encephalomyelitis (EAE) in mice is
currently used by researchers as a model of human multiple sclerosis
(MS). The disease is characterized by the production of autoreactive T
lymphocytes that turn against the body and attack cells within the
brain and spinal cord, first inducing weight loss and ultimately
resulting in paralysis.

In the January 15 issue of the Journal of Clinical Investigation,
Giuseppe Matarese and colleagues at IEOS-CNR at Università di Napoli
"Federico II", Napoli, Italy report that just prior to developing the
clinical symptoms of EAE, mice experience a significant burst of leptin
which correlates with a reduction in food intake and weight loss.
Furthermore, subjecting mice to acute starvation, which prevents the
production of leptin, was found to delay the onset and reduce the
severity of disease. In addition, leptin secretion from T lymphocytes
was found to further contribute to overall leptin production during
EAE.

"Once again we witness the remarkable choreography of molecules related
to body weight and energy metabolism and the parallel roles of these
same molecules in the finely tuned immune response" stated Dr. Lawrence
Steinman and colleagues at Stanford University, California in their
accompanying commentary. They go on to say that "these results imply
that in autoimmunity, stress may be beneficial, and that short-term
starvation may help reverse disease". Stress is detrimental and eating
is recommended when fighting bacterial infections, however it appears
that in the case of autoimmunity, the opposite holds true - stress and
fasting is helpful.

These results suggest that leptin actively contributes to the
pathogenesis of EAE, influencing both its onset and clinical severity.
Interestingly, leptin is produced at much higher levels in females than
males, which may account for the higher susceptibility of females to
autoimmune diseases, a fact that has long puzzled scientists. The
authors suggest that modulating leptin concentration through dietary
approaches, and/or the administration of drugs that interfere with the
bodys own production of leptin, may have potential utility in the
treatment of MS and other autoimmune diseases.

###
CONTACT:
Giuseppe Matarese
Gruppo di ImmunoEndocrinologia
Instituto di Endocrinologia e Oncologia Sperimentale
Consiglio Nazionale delle Richerche (IEOS-CNR) and Cattedra di
Immunologia
Dipartmento di Biologia e Patologia Cellulare e Molecolare
Università di Napoli "Federico II", via S. Pansini 5 - 80131
Napoli
ITALY
Phone: +39-081-7463311
Fax: +39-081-7463252
E-mail: gmatarese@napoli.com

Eur J Med Chem. 2005 Sep 8; [Epub ahead of print] Related Articles,
Links

Novel synthesized aminosteroidal heterocycles intervention for
inhibiting iron-induced oxidative stress.

Elmegeed GA, Ahmed HH, Hussein JS.

Hormones Department, National Research Center, Dokki, Giza, Egypt.

The objective of this study was to elucidate the potential role of
novel synthesized aminosteroidal heterocyclic compounds 2, 5, 9b and
10c against iron-induced oxidative stress with particular insight on
erythrocyte ghosts in male rats. Chronic iron supplementation (3000 mg
kg(-1) diet) for 6 weeks significantly increased plasma iron and
ferritin levels. It also produced significant increase in plasma
TNF-alpha and NO levels. Lipid metabolism was also affected by excess
iron, so that plasma and erythrocyte membrane total cholesterol,
triglycerides, phospholipids and total lipid levels were significantly
elevated. In consequence, a significant increase in plasma leptin level
was detected. Iron overload clearly induces oxidative stress as
indicated by the significant increase in both plasma and erythrocyte
membrane lipid peroxidation levels. Noteworthy, excess iron not only
decreased the mean value of erythrocyte membrane protein but also
caused marked alterations in the membrane protein fractions with
concomitant inhibition in erythrocyte membrane ATPases activity. On the
other hand, treatment with the aminosteriodal heterocyclic compounds
especially compounds 5, 2, and 10c in an oral dose of 5 mg kg(-1) B.W.
per day could ameliorate almost all of the changes in plasma and
erythrocyte ghosts components induced by iron overload. The efficacious
role of these novel synthesized aminosteriods in preventing
iron-induced oxidative stress may be mediated through their iron
chelating properties, anti-lipid peroxidation activities and membrane
stabilizing actions. The encouraging results obtained in the present
study lend credence to substantial investigation to assess the use of
these compounds as a potent line of therapy to retard the pathogenesis
of iron overload diseases.

PMID: 16154236 [PubMed - as supplied by publisher]

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