Re: Al's Post Regarding Weight Gain And Breast Cancer

[Lani]

THIS ANGIOTENSIN II inhibitor also has an effect on PPAR--comments?:

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Telmisartan Curbs Weight Gain in Rats


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By David Douglas

NEW YORK (Reuters Health) May 23 - The angiotensin II receptor blocker telmisartan increases caloric expenditure and protects against weight gain in rats fed a high-fat, high-carbohydrate diet, researchers report in the May issue of Hypertension.

"Our findings," senior investigator Dr. Theodore W. Kurtz told Reuters Health, "are consistent with the results of a preliminary clinical study from Japan in which telmisartan also reduced visceral fat accumulation and improved glucose tolerance in patients with the metabolic syndrome."

"This raises the possibility," he added, "that some antihypertensive drugs may be useful not only for treating high blood pressure, but also for treating the metabolic disturbances that often go hand in hand with hypertension."

Specifically, Dr. Kurtz of the University of California, San Francisco and colleagues found that rats given telmisartan, but not those fed valsartan, which lacks the peroxisome proliferator-activated receptor gamma partial agonist activity of telmisartan, had lower absolute food intake.

Telmisartan also increased expression of genes known to play important roles in mitochondrial energy metabolism, as well as reducing the accumulation of visceral fat and decreasing adipocyte accumulation to a much greater extent than valsartan.

Dr. Arya M. Sharma, author of an accompanying editorial, told Reuters Health that the work "clearly opens a new perspective on the metabolic effects of telmisartan in humans."

Dr. Sharma of McMaster University, East Hamilton, Ontario went on to observe that "the potential role of this compound in weight maintenance or even the prevention of weight regain may deserve further evaluation."

Hypertension 2006;47:1003-1009.

[R.B.]

PPARs are intimately linked into the body's metabolism systems.

Fats are PPAR activators.

PPAR gamma is linked to fat storage.

PPAR alpah to fat burning.

Fat intake - the omega three six balance may through its realtionship with PPARs. leptin, insulin etc play a large part in obesity.

Omega six seems to have to have more to do with storage.

Omega three more to do with burning off.

There is some cross over.

RB

[R.B.]

More info

RB


http://www.medpagetoday.com/Hematolo...Cancer/tb/3386

ABSTRACT

Review
ATLANTA, May 23 — A purported link between breast cancer risk and lifetime weight gain holds true for every type, stage, and grade of estrogen receptor-positive tumor, according to American Cancer Society researchers.

"Despite the growing body of literature examining the increased risk of breast cancer from obesity and weight gain, the relation between body weight and the histopathologic characteristics of breast carcinomas has received less attention," reported Heather Spencer Feigelson, Ph.D., M.P.H., and colleagues in the July 1 issue of Cancer.

The study drew on data from more than 44,000 post-menopausal women not taking hormone therapy who participated in the ACS Cancer Prevention Study II Nutrition Cohort, established in 1992. Of these, the study focused on 1,200 women with incident invasive breast cancers.

Compared with women who gained only 20 pounds or less after the age of 18, those who gained 60 or more pounds had elevated risk of:

* Ductal carcinoma (odds ratio=1.89; 95% confidence interval=1.53 to 2.34)
* Lobular carcinoma (OR=1.54; 95% CI=1.01 to 2.33)
* Regional or distant metastases (OR=3.15; 95% CI=2.21 to 4.48)
* Higher grade tumors. The association was strongest with Grade 3 tumors (OR=2.84; 95% CI=1.99 to 4.06).

The study found no significant link between weight gain and estrogen- or progesterone-negative tumors, the investigators said.

[R.B.]

Heres another trial. There are a number on NCBI. I just looked it up.

Please note the last scentence. Is this a PPAR alpha activator as well.


RB



1: Rev Med Liege. 2005 Feb;60(2):89-95. Related Articles, Links

[PPAR-gamma receptors, new therapeutic target in metabolic and cardiovascular diseases]

[Article in French]

Scheen AJ, Paquot N.

Universite de Liege.

PPARs ("Peroxisome Proliferator-Activated Receptors") belong to a superfamily of nuclear receptors with several isoforms, among which PPAR-alpha mainly located in the liver and PPAR-gamma mainly located in the adipose tissue. These receptors are considered as major pharmacological targets since the discovery of their activation by specific agonists, which lead to various favourable metabolic effects. Improvement of lipid profile by fibrates is explained by the activation of liver PPAR-alpha receptors. However, PPAR-gamma receptors have focused most fundamental and clinical research in recent years after the demonstration of their activation by thiazolidinediones (pioglitazone, rosiglitazone), a new class of antidiabetic agents. Beyond their effects on insulin sensitivity, glitazones exert pleiotropic effects that may result in cardiovascular protection in high risk patients. It has been recently demonstrated that certain angiotensin AT1 receptor blockers (sartans) can also exert a partial agonist activity on PPAR-gamma. Among the molecules of this class, telmisartan appears to exert this effect at the lower concentrations. Thus, PPAR-y, as common pharmacological target, may, at least partially, explain some of the effects observed with both thiazolidinediones and inhibitors of the renin-angiotensin system, in particular the improvement in insulin sensitivity (in particular via an increase in adiponectin levels), the protection against type 2 diabetes, the reduction in arterial blood pressure and the prevention of cardiovascular complications. There is currently a major interest from the pharmaceutical industry in the development of new molecules able to activate both PPAR-alpha and PPAR-gamma.

Publication Types:

* Review


PMID: 15819371 [PubMed - indexed for MEDLINE]

[AlaskaAngel]

Why is it taking so long to realize that we need to think of and treat the body as an integrated system? How many of us had the chance at diagnosis to have an endocrinologist's influence in plans for our treatment? When will there be an endocrinologist sitting on each tumor board?

AlaskaAngel