Some new research: Evidently they have found that people who are lacking in the leptin receptors have more invasive disease. Leptin is a hormone that has to do with weight gain/loss. Unfortunately, there are no leptin supplements. Anything that advertises itself as leptin is not. If you look at the ingredients you will see they do not contain leptin. In any case, it's not clear that taking leptin or increasing it would help. I spoke with Dr. Galland about this. I sent him some research. He was interested. You may want to research leptin and Entamoeba histolytica to find the articles.
From what I have read, it seems to me that the parasites interfere with the leptin somehow.
Dr. William Petri
He is Chief of the Division of Infectious Diseases and International Health at University of Virginia, School of Medicine. In addition, he is President of the American Society of Tropical Medicine and Hygiene.
I believe that Dr. WA Petri, Jr. is also with the NIH in Maryland.
I wonder if enough of us contact Dr. Petri he can do more for us? Just a thought.
Do any of you ever research PubMed?
Gut Microbes. 2012 Jan 1;3(1). [Epub ahead of print]
Leptin signaling protects the gut from Entamoeba histolytica infection.
Vedantam G, Viswanathan VK.
& Microbiology; University of Arizona; Tucson, AZ USA.
The role of the adipose-derived hormone leptin, and leptin receptors, in signaling satiety to the central nervous system and regulating energy balance is well recognized. But leptin also acts on peripheral tissues such as skeletal muscles, adipose tissues, pancreas, liver, intestine and the immune system. The existence of different splice variants of leptin receptor and the numerous intracellular signaling pathways triggered by leptin make this a truly versatile system.
Two recent studies explore the link between malnutrition, leptin signaling and susceptibility to amebic infection.
These studies point to important and novel aspects of leptin signaling in maintaining gut homeostasis and warding off infections.
[PubMed - as supplied by publisher]
Infect Immun. 2012 Feb 13. [Epub ahead of print]
Leptin protects host cells from Entamoeba histolytica cytotoxicity by a STAT-3 dependent mechanism.
Marie CS, Verkerke HP, Paul SN, Mackey AJ, Petri WA Jr.
Drew University, Biology Department, Madison, New Jersey, United States of America.
The adipocytokine leptin links nutritional status to immune function.
Leptin signaling protects from amebiasis but the molecular mechanism is not understood.
We developed an in vitro model of ameba-host cell interaction to test the hypothesis that leptin prevents ameba induced apoptosis in host epithelial cells.
We demonstrated that activation of mammalian leptin signaling increased cellular resistance to amebic cytotoxicity, including caspase-3 activation.
Exogenous expression of the leptin receptor conferred resistance in susceptible cells and leptin stimulation enhanced protection. A series of leptin receptor signaling mutants showed that resistance to amebic cytotoxicity was dependent on activation of STAT3 but not SHP-2 or STAT5. A common polymorphism in the leptin receptor (Q223R) that increases susceptibility to amebiasis in humans and mice was found to increase susceptibility to amebic cytotoxicity in single cells. The Q223R polymorphism also decreased leptin-dependent STAT3 activation by 21% relative to the WT receptor (P-value = 0.035) consistent with a central role of STAT3 signaling in protection. A subset of genes uniquely regulated by STAT3 in response to leptin were identified. Most notable were TRIB1 and SOCS3, which have opposing roles in the regulation of apoptosis. Overall apoptotic genes were highly enriched in this gene set (P-value < 1E-05) supporting the hypothesis that leptin regulation of host apoptotic genes via STAT3 is responsible for protection. This is the first demonstration of a mammalian signaling pathway that restricts amebic pathogenesis, and represents an important advance in our mechanistic understanding of how leptin links nutrition and susceptibility to infection.
[PubMed - as supplied by publisher]