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L Deloyers Laboratory of Experimental Surgery
Avenue J Wybran 40
Université Libre de Bruxelles
1070 Brussels
Belgium
E-mail: nutrisub{at}ulb.ac.be
Dear Sir:
The comments of Oda concerning our article on the role of n–3 polyunsaturated fatty acids (PUFAs) in the metabolic syndrome (1) are well understood. Oda speculates that the beneficial effects of n–3 fatty acids in the metabolic syndrome would result (at least in part) from an inhibition of the peripheral endocannabinoid system, with long-lasting effects on body weight regulation. Indeed, some arachidonoyl derivatives may act as agonists of cannabinoid receptor 1 (CB 1). Changes in n–3 PUFA intakes markedly affect arachidonic acid (20:4n–6) concentrations in different tissues and may alter the activation of the CB 1 system. For instance, the data provided in Table 1 indicate that the relative concentration of C20:4n-6 is significantly increased in the brain, liver, soleus muscle, heart muscle and heart endothelium of second generation n–3-depleted rats, as recently studied in our laboratory. In addition, n–3 and n–6 PUFAs may exert opposing effects on the endocannabinoid system, but this remains to be determined.
View this table:
TABLE 1. Fatty acid pattern in tissue phospholipids of n–3 fatty acid–depleted and control female rats1
Likewise, beneficial effects of n–3 PUFAs on obesity-related metabolic risk factors may result from changes in tissue concentration of specific very long-chain monounsaturated fatty acids, such as 24:1n-9 (nervonic acid). As a matter of fact, we recently observed a decrease in the relative content of C22:1n-9 (the immediate precursor of C24:1n-9) in phospholipids of the brain, soleus muscle, and endocardium (but not liver and cardiomyocytes) of the same second generation n–3-depleted rats, when compared with measurements obtained in control rats of same sex (female) and age (Table 1).
ACKNOWLEDGMENTS
None of the authors had a conflict of interest.
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