Leptin and leptin receptor polymorphisms are associated with increased risk and ...

[RhondaH]

poor prognosis of breast cancer.

I can't help but wonder that with the growing obesity epidemic that we will see a growth in HER2 cancers Low Fat doesn't help...BAH, I think we ALL are in agreement that it is the TYPE of fat AND how much.

Rhonda

http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Citation


http://www.ncbi.nlm.nih.gov/entrez/q...list_uids=2064

Leptin definition:

http://www.vivo.colostate.edu/hbooks...ht/leptin.html

I in my very very amateur way become more and more convinced that the intitiating factor is the omega three six balance and excess omega six intake.

Excess omega six historically is a problem the body has never had to deal with, and so why should it have a mechanism to do so.


Very interesting links, with lots of sub links.


Thanks for posting this, I am the middle of book crunching on the subject.

RB

One of the threads in your attachment.

Leptin increasing the oncogenic potential of erbB2 (HER 2).

From what I read high leptin levels are found in those with high body fat content.

Is it acting in concert or independently of oestrogen?

Interesting.

RB

http://www.ncbi.nlm.nih.gov/entrez/q...=pubmed_docsum

1: FEBS Lett. 2004 May 7;565(1-3):139-42. Related Articles, Links
Click here to read
Transactivation of erbB2 by short and long isoforms of leptin receptors.

Eisenberg A, Biener E, Charlier M, Krishnan RV, Djiane J, Herman B, Gertler A.


http://www.ncbi.nlm.nih.gov/entrez/q...=pubmed_docsum

Faculty of Agricultural, Food and Environmental Quality Sciences, The Hebrew University of Jerusalem, P.O. Box 12, Rehovot 76100, Israel.

We generated kinase-positive and kinase-negative erbB2 tagged with YFP and the long form of leptin receptor (LEPRb) tagged with CFP. Both were as active as their untagged analogs. Both short and long isoforms of leptin receptor phosphorylated and thereby activated erbB2 upon leptin binding and enhanced MAPK activity. Our results unveil a novel route by which leptin may provoke erbB2's phosphorylation and thus enhance its oncogenic potential independently of HER family ligands or its overexpression. Using FRET technology in living cells, we found no evidence of complex formation between erbB2 and prolactin or leptin receptors, indicating that the transactivation occurs through an indirect interaction.

PMID: 15135067 [PubMed - indexed for MEDLINE]

[Gina]

I have been fascinated with this Leptin BC connection for sometime. Just wondering, have you see all the data on how infection with H. pylori causes the leptin in the local cells surrounding the primary point of infection to over-express??? Most of these studies relate to h. pylori infection of the gastric mucosa, but the same cascade happens in intracellular h. pylori disease of the epithelial cells, regardless of their location. Eradication of the organism leads to downgrading of the excess leptin. Also, as you know, there is an inverse relationship between ghrelin and leptin. Ghrelin can be increased by fasting and sometimes leptin can be decreased by using insulin..fyi.

Also, RB, is there any way to e-mail you directly? I have some important questions about the omega-3's that I would like to run by you. My e-mail is Gpopp@Comcast.net.

Thanks for your VERY informative posts...,
Gina

Another thought provoking leptin link - and re previous suggestions read on this site HER is linked to reproductive functions.

Thanks for the posts above Rhondah.

RB


http://www.ncbi.nlm.nih.gov/entrez/q...=pubmed_docsum

1: Endocrinology. 2005 Aug;146(8):3334-42. Epub 2005 May 19. Related Articles, Links
Click here to read
Leptin and adiponectin stimulate the release of proinflammatory cytokines and prostaglandins from human placenta and maternal adipose tissue via nuclear factor-kappaB, peroxisomal proliferator-activated receptor-gamma and extracellularly regulated kinase 1/2.

Lappas M, Permezel M, Rice GE.

Department of Obstetrics and Gynaecology, University of Melbourne and Mercy Perinatal Research Centre, Mercy Hospital for Women, East Melbourne, Victoria, Australia. mlappas@unimelb.edu.au

Beyond their effects on central metabolic functions, leptin, resistin, and adiponectin have profound effects on a number of other physiologic processes, including immune function and inflammation. Although leptin, resistin, and adiponectin are produced in human placenta and adipose tissue, their immunoregulatory actions in these tissues are not known. Therefore, the aim of this study was to determine the effect of leptin, resistin, and adiponectin on the release of proinflammatory mediators in human placenta and sc adipose tissue. Samples were obtained from normal pregnancies at the time of cesarean section. Tissue explants (n = 5) were incubated in the absence (basal control) or presence of a leptin (1, 10, and 100 ng/ml), resistin (1, 10, and 100 ng/ml), and adiponectin (0.1 and 0.5 microg/ml). After 6 h incubation, the medium was collected, and the release of IL-1beta, IL-6, TNFalpha, prostaglandin (PG)F2alpha and PGE2 was quantified by ELISA. There was no effect of resistin on proinflammatory cytokine or prostaglandin release; however, leptin at 100 ng/ml and adiponectin at 0.1 and/or 0.5 microg/ml significantly increased the release of IL-1beta, IL-6, TNFalpha, and PGE2 from human placenta and adipose tissue. Although both leptin and adiponectin significantly increased PGF2alpha release from human placenta, there was no effect of these hormones on PGF2alpha release from adipose tissue. Furthermore, this leptin- and adiponectin-induced proinflammatory response could be abrogated by treatment with the antiinflammatory ERK1/2 MAPK inhibitor U0126, the peroxisomal proliferator-activated receptor-gamma ligand troglitazone, and the nuclear factor-kappaB inhibitor BAY 11-7082. Collectively, these data indicate that leptin and adiponectin activate proinflammatory cytokine release and phospholipid metabolism in human placenta and adipose tissue, and antiinflammatory agents can abrogate leptin- and adiponectin-induced inflammation.

PMID: 15905315 [PubMed - indexed for MEDLINE]