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Diet, Fatty acids, and regulation of genes important for heart disease.

Conjugated linoleic acid inhibits proliferation and modulates protein kinase C isoforms in human prostate cancer cells.

Conjugated linoleic acid supplementation, insulin sensitivity, and lipoprotein metabolism in patients with type 2 diabetes mellitus.

The effect of conjugated linoleic acid on calcium absorption and bone metabolism and composition in adult ovariectomised rats.

Conjugated linoleic acid prevents the development of essential hypertension in spontaneously hypertensive rats.

Activation of PPAR gamma and delta by conjugated linoleic acid mediates protection from experimental inflammatory bowel disease.

Safety profile of conjugated linoleic acid in a 12-month trial in obese humans.





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Title: Conjugated linoleic acid inhibits proliferation and modulates protein kinase C isoforms in human prostate cancer cells.

Author(s): Song HJ, Sneddon AA, Barker PA, Bestwick C, Choe SN, McClinton S, Grant I, Rotondo D, Heys SD, Wahle KW.

Source: Nutr Cancer. 2004;49(1):100-8.

Content: The Rowett Research Institute, Bucksburn, Aberdeen, Scotland, UK.

Prostate cancer is the second most common cancer in men. The disease etiology is poorly understood, but diet and lifestyle are contributory factors. Conjugated linoleic acids (CLAs), naturally occurring fatty acids in ruminant food products, have antitumor properties in animal models of cancer and antiproliferative effects on cancer cells in vitro.

The cellular mechanisms by which CLAs elicit these effects are unclear, particularly for prostate cancer cells. We have previously identified protein kinase C (PKC) isoforms, alpha, delta, iota, mu, and zeta in LNCaP prostate cancer cells.

The objective of this study was to determine the effects of CLAs (individual cis-9, trans-11 and trans-10, cis-12 isoforms and a 50:50 mixture) on PKC isoform abundance in LNCaP cells. Confluent cells were treated with 6, 25, and 50 microM CLA for 0.5, 6, and 24 h. Cytosol and membrane protein fractions were assayed for PKC isoforms (mainly alpha and delta but also iota, mu, and zeta) by Western blot analysis using specific antibodies.

CLAs clearly modulated the abundance of these PKC isoforms, both positively and negatively, depending on the isoform, concentration of CLAs, and period of treatment. Increased PKC-delta and decreased PKC-iota membrane abundance was consistent with CLAs eliciting increased apoptosis and, in part, with their antitumor effects.



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Many studies reported herein have been performed on laboratory animals and not on humans. While some results of animal trials are later found to be similar in human trials, we have no way of knowing whether or not this will be the case.

This information is not presented as medical advice and no conclusions regarding the effectiveness or lack of such should be drawn from this information.

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