Another cure

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Another cure

Postby bromley » Fri Jan 13, 2006 3:33 am

If there is a God I would really like to come back as a mouse with EAE in my next life. When the mouse goes to the mouse neurologist the latter can say 'you've got EAE, but don't worry we got 300 cures available (unlike those poor humans with their MS)'. This times it's Italian researchers and something called Leptin. We'll outside my knowledge base, but I wonder if statins have any role in regulating Leptin?

Ian



Blockade of fat hormone helps halt and heal multiple sclerosis 13 January 2006
Italian researchers have found that blockade of the hormone leptin, which is primarily produced in fats cells, has beneficial effects on the induction and progression of experimental autoimmune encephalomyelitis (EAE) in mice – the animal model of human multiple sclerosis (MS). In their study appearing online on January 12 in advance of print publication in the February 2006 issue of the Journal of Clinical Investigation, Giuseppe Matarese and colleagues from Università di Napoli "Federico II" suggest that leptin neutralization may be a potential way to both prevent and treat MS.
MS is an inflammatory disease of the brain and spinal chord characterized by muscle weakness, numbness, and loss of coordination. These symptoms result in part from destruction of the nerve-insulating material myelin by activated T cells.

Leptin is known to play a critical role in the regulation of food intake, metabolism, and the immune response. Since it had been previously shown that leptin is expressed in active inflammatory lesions of the central nervous system during EAE and MS, Matarese and colleagues investigated the effects of leptin blockade on the induction and progression of EAE in mice. They found that leptin blockade by the use of either anti-leptin antibodies or a form of the leptin receptor unable to bind leptin, either before or after disease onset improved clinical symptoms of disease, slowed disease progression, reduced disease relapses, and reduced the number of antigen-specific T cells. The authors delved further to unravel the cellular signaling events underlying these beneficial effects. Taken together, the data provide a basis for the development and testing of novel strategies of leptin-based targeting for the potential treatment of MS.

TITLE: Leptin neutralization interferes with pathogenic T cell autoreactivity in autoimmune encephalomyelitis

AUTHOR CONTACT:
Giuseppe Matarese
Università di Napoli "Federico II", Napoli, Italy.
Phone: 39-081-7463311
Fax: 39-081-7463252
E-mail: gmatarese@napoli.com

Source: Journal of Clinical Investigation
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Postby Degerlache » Fri Jan 13, 2006 6:37 am

Although the study below was not done on mice, but on rats (are they already closer to humans?), the same question could be posed concerning pioglitazone. I believe pioglitazone is currently tested for MS. Pioglitazone might also have an impact on Leptin, if I understand the following correctly ?

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"Like pioglitazone, WY14643 lowered basal plasma levels of glucose, triglycerides (-16% vs. untreated), and leptin (-52%)"


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Postby Melody » Fri Jan 13, 2006 7:08 am

omega 3 fatty acids
What can high-omega-3 foods do for you?
Reduce inflammation throughout your body
Keep your blood from clotting excessively
Maintain the fluidity of your cell membranes
lower the amount of lipids (fats such as cholesterol and triglycerides) circulating in the bloodstream
decrease platelet aggregation, preventing excessive blood clotting
inhibit thickening of the arteries by decreasing endothelial cells' production of a platelet-derived growth factor (the lining of the arteries is composed of endothelial cells)
increase the activity of another chemical derived from endothelial cells (endothelium-derived nitric oxide), which causes arteries to relax and dilate
reduce the production of messenger chemicals called cytokines, which are involved in the inflammatory response associated with atherosclerosis
reduce the risk of becoming obese and improve the body's ability to respond to insulin by stimulating the secretion of LEPTIN, a hormone that helps regulate food intake, body weight and metabolism, and is expressed primarily by adipocytes (fat cells)

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Obesity

Vitamin D deficiency has been linked with obesity. (18, 19) Vitamin D has recently been shown to lower leptin secretion. (20) Leptin is a hormone produced by fat cells and is involved in weight regulation. It is thought that the hormone signals the brain when fat cells are "full," but exactly how the hormone controls weight is not entirely clear.

Additionally, obesity by itself probably further worsens vitamin D deficiency due to the decreased bioavailability of vitamin D(3) from skin and dietary sources, because of its being deposited in body fat. (36)
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John was diagnosed Jan 2005. On lipitor 20mg .On Copaxone since July 4,2005. Vitamin D3 2000iu-4000iu (depending on sunshine months)June 10 2005(RX::Dr. O'Connor) Omega 3 as well Turmeric since April 2005. Q10 60mg. 1500mg liquid Glucosamine Nov 2005.
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Postby Degerlache » Fri Jan 13, 2006 9:00 am

It is somehow contradictory, isn't it : Vit D lowers leptin secretion and omega 3 fatty acids stimulate leptin secretion, and both would be helpfull for MS ?

Hower, the impact of omega 3 acids on the brain may be different as suggested, in the way that there is a significant reduction of leptin concentration in the cerebrospinal fluid (according to the article below)


<shortened url>

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Postby dignan » Fri Jan 13, 2006 9:35 am

Be careful about this research, there has been contradictory information about the role of leptin.



Leptin and its soluble receptor in plasma of patients suffering from remitting-relapsing multiple sclerosis (MS) In vitro effects of leptin on type-1 and type-2 cytokine secretion by peripheral blood mononuclear cells, T-cells and monocytes of MS patients.

J Autoimmun. 2004 Sep;23(2):169-77.
Chatzantoni K, Papathanassopoulos P, Gourzoulidou E, Mouzaki A.
Experimental Hematology & Transfusion Medicine, Medical School & University Hospital, University of Patras, Patras, Greece.

Leptin is synthesized by adipocytes to regulate appetite. Leptin has also been implicated in the pathogenesis of multiple sclerosis (MS) leading to speculation about a beneficial effect of fasting to autoimmune patients. We measured plasma leptin and its soluble receptor (OB-Rs) in 52 MS patients and 50 controls. We also cultured MS and control peripheral blood mononuclear cells (PBMC), T-cells and monocytes +/- recombinant leptin (rleptin), to assess leptin's direct effect on pro- and anti-inflammatory cytokine secretion. We found similar leptin and OB-Rs plasma levels between patients and controls. Untreated patients in the acute phase or in remission, or patients treated with methylprednisolone, had lower leptin levels than patients in the acute phase or in remission receiving IFN-beta. OB-Rs levels were low in patients refractory to IFN-beta but higher in patients receiving methylprednisolone or patients in remission receiving IFN-beta. PBMC from untreated patients in the acute phase, secreted spontaneously IFN-gamma, TNF-alpha and IL-10. IFN-gamma was contributed by T-cells, TNF-alpha and IL-10 primarily by monocytes and to a lesser extent by T-cells.

The overall effect of rleptin on PBMC was a net increase in IL-10 production and a net reduction in IFN-gamma production. These results do not warrant a beneficial effect of fasting to MS patients.

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Postby Melody » Fri Jan 13, 2006 10:15 am

Does anyone here understand what exactly they mean? Do they mean that if you eat less you still have leptin it just isn't released and if you over eat the leptin gets released? Or do they mean that you only produce excessive leptin if you overeat and produce next to none if you eat smaller quantities? John is not liking this one he thinks I take to much control now over his food let alone his intake. :lol:
John was diagnosed Jan 2005. On lipitor 20mg .On Copaxone since July 4,2005. Vitamin D3 2000iu-4000iu (depending on sunshine months)June 10 2005(RX::Dr. O'Connor) Omega 3 as well Turmeric since April 2005. Q10 60mg. 1500mg liquid Glucosamine Nov 2005.
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Postby Brownsfan » Fri Jan 13, 2006 10:43 am

Could this be construed as supportive of the Swank protocol? I'm no scientist, but it seems to be widely accepted that "bad fats" increase inflammation in the blood, whereas "good fats" decrease this inflammation. If MS is indeed an inflammatory disorder, then this seems like common sense that reducing sat fats and replacing with omega 3's and 6's would resuld in decreased inflammation and therefore fewer MS attacks. Dr. Swank's long-term study, albeit not scientific by today's standards, was still pretty convincing in my mind. Of course my neuros insist that fats play no part in MS onset or progression.
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Postby dignan » Tue Jan 17, 2006 11:44 am

Leptin, Leptin everywhere. Here's another study about leptin and depression. It's becoming clear that the role of leptin is far from clear.



Leptin fights depression: Fat-hormone study highlights role in mood.

January 17, 2006 - Nature - The appetite-control hormone leptin staves off symptoms of stress in rats, and might lead to new ways to fight human depression, say researchers in the United States.

Leptin is famed for controlling our weight and appetite. But the hormone, which is released by fat cells and gives the brain a reading of our fat stores, is also thought to act in brain areas involved in emotion.

To explore this link, Xin-Yun Lu and her colleagues at the University of Texas Health Science Center in San Antonio stressed rats by, for example, separating them from other animals. The rats' leptin levels plunged at the same time that they showed behavioural changes such as losing interest in a sugary drink, the kind of apathy that is often associated with human depression.

The team found that injections of leptin into otherwise healthy animals were as good as at least one known treatment in a test widely used to screen for new antidepressants. In this test, the researchers showed that leptin could help the animals to evade depression-induced behaviour when forced to swim.

The results, which the team report in the Proceedings of the National Academy of Sciences1, are sure to trigger interest in those working on alternative therapies for depression. Many patients do not respond to existing treatments and doctors are keen to find more.

But they caution that much more work is needed before leptin becomes a candidate treatment for the blues. Because the hormone also exerts effects on appetite, reproduction and the immune system, medical researchers would probably need to find molecules that can specifically mimic leptin's anti-depressant effects on the brain without causing unwanted side effects.

It also isn't clear how well leptin's effect in animals is mirrored in people. The findings do fit with a few small studies suggesting that leptin levels are altered in people with depression. "It's very, very interesting," says Giovanni Cizza, who studies hormones and depression at the National Institute for Diabetes and Digestive and Kidney Disease in Bethesda, Maryland. But, he adds, "Depression is a very human phenomenon, so I take it with a grain of salt."

Leptin shot to fame in the mid 1990s when scientists discovered that a strain of immensely fat mice that eat voraciously lack a working copy of the gene. They found that leptin injections could help the mice to shed weight, raising the prospect that the hormone might be a miraculous fat fighter for the obese.

That hope was dealt a blow when leptin failed to fight flab for most people in clinical trials. Since then, scientists have realized that obese people often have high levels of leptin and seem to have become resistant to its effects. And now they know that the hormone has a host of other roles in the body too.

The new study raises questions about the link between appetite and mood. Many depressed patients lose weight and their interest in eating; a minority start to eat more. Experts say that low levels of leptin could conceivably fuel both depression and changes in appetite.

Lu and other researchers acknowledge that many factors, including the availability of tempting food and associations between eating and comfort, influence what and how much we consume. "It's affected by many, many things," says Cizza. "But leptin is a big player."

http://www.nature.com/news/2006/060116/ ... 116-3.html
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