Volume 12, Number 1, Janvier-Février 2005
|Page(s)||32 - 36|
|Published online||15 January 2005|
Les CLA peuvent-ils prévenir l’athérogenèse ?
UMR Inserm 476/Inra 1260, Faculté de Médecine La Timone, 27, Boulevard Jean Moulin, 13360
2 LEN, bâtiment 447, Université Paris-Sud, 91405 Orsay
3 Inserm U465, Centre biomédical des Cordeliers, 15, rue de l’Ecole de Médecine, 75270 Paris Cedex 06
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.
Key words: atherosclerosis / CLA / inflammationlipoproteins
© John Libbey Eurotext 2005
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