Les CLA peuvent-ils prévenir l’athérogenèse ?

Autor: Martin Jean-Charles, Amsler Ghislaine, Valeille Karine, Férézou Jacqueline, Parquet Michel, Gripois Daniel, Quignard-Boulangé Annie
Jazyk: English<br />French
Rok vydání: 2005
Předmět:
Zdroj: Oléagineux, Corps gras, Lipides, Vol 12, Iss 1, Pp 32-36 (2005)
Druh dokumentu: article
ISSN: 1258-8210
1950-697X
DOI: 10.1051/ocl.2005.0032
Popis: The anti-atherogenic properties of CLA are now illustrated in many animal studies (Rabbit, Mice and Hamster) or cell culture experiments. These properties can be observed while using either the CLA isomeric mixture (cis9,trans11- and trans10,cis12-, 50 :50) or selected CLA isomers (cis9,trans11- or trans10,cis12-). Especially, these fatty acids consistently attenuate the outcome of primary vascular lesions (fatty streaks), or can even induce a regression of pre-established lesions. There is, paradoxically, no clear relationship between this beneficial effect and an improvement of the lipid status in blood (triglycerides, total cholesterol, LDL-cholesterol, HDL-cholesterol) usually considered as a hallmark in the etiology of atherosclerosis. On the other hand, recent data obtained both in vitro and in vivo indicate that part of the beneficial effects of CLA occurs through the modulation of vascular inflammatory and oxidant stress factors (cytokines and cyclooxygenase), as well as from the expression of adhesion molecules (VCAM, ICAM) in the aorta. This regulation involves the interaction of CLA with transcription factors such as PPARs, LXR and NF-kB targeting the gene expression dowstream. In human, clinical trials are no more conclusive than the animal experiments with regards to the contribution of CLA to modulate the lipid status in blood. Nevertheless, some data highlight the pro-atherogenic role of CLA and especially of the trans10,cis12-isomer, as demonstrated by the increase in the various markers of oxidative stress (isoprostanes) and inflammatory status (C-reactive protein). In conclusion, whereas there is compelling evidence that feeding mixed or pure isomers of CLA attenuates atherosclerosis initiation and progression in several experimental models, human studies are less convincing. Nevertheless, clinical trials addressing sufficient risk factors and risk markers together are still lacking to draw a definitive conclusion and to set up obvious recommandations. The use of the sole blood lipids do not seem to be appropriate for such an evaluation.
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