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In the present study, macular pigment density was associated not only with plasma lutein and zeaxanthin but also with omega-3 long-chain PUFAs, particularly with EPA and DPA. Further studies will be needed to confirm these findings and to identify the underlying mechanisms.

Epidemiologic studies suggest that intake of high energy from fat, inducing overweight, increases the risk of cancer development and promotes colon carcinogenesis. It is therefore important to understand which parameters are affected early on by a high-fat diet in order to devise and improve protective nutritional strategies. We investigated the effect of high energy/fat intake on colon mucosa of male Wistar rats induced by a single 1,2-dimethylhydrazine (DMH) injection. Aberrant crypt foci (ACF) were numbered and modifications in cyclooxygenase-2 (COX-2) and b-catenin levels assessed. Peroxisome proliferator-and retinoic acid-activated receptors (PPAR and RAR, RXR) are key transcription factors regulating gene expression in response to nutrient-activated signals. A short-term study was designed to evaluate whether alterations in mRNA expression of nuclear receptors can be detected at the beginning of the weight gain phase induced by an appetizing hyperlipidic diet (HLD). HLD consumption induced early downregulation of PPARc (-33.1%) and RARb (-53.1%) mRNA expression concomitant with an increase in levels of COX-2 (145.5%) and b-catenin (184.56%) and in the number of ACF (191.56 6 88.60 vs. 21.14 6 11.64, p < 0.05). These findings suggest that HLD increases ACF occurrence, possibly through alterations in the mRNA expression profile of nuclear receptors. Moreover, the use HLD rich in retinyl esters or supplemented with all-trans retinoic acid led to a reduction in the number of ACF. Vitamin A also prevented HLD-induced alterations and the increase in levels of COX-2 and b-catenin. The present observations show a protective role for vitamin A against disturbances associated with HLD exposure in induced colon carcinogenesis. ' 2005 Wiley-Liss, Inc.Key words: colon carcinogenesis; nuclear receptor; high energy/fat intake; vitamin A The incidence of obesity and colon cancer is increasing in all industrialized countries. Colon carcinogenesis is a multifactorial disease, and diet is strongly involved in its etiology. A prospective cohort study has reported that increased body weight was associated with increased death rates form cancer.1 Thus, the high prevalence of obesity, explained by a lifestyle characterized by high energy/fat intake, led to increased risk of colon cancer development. These conclusions are reinforced by data suggesting that the number of preneoplastic colonic lesions 2-4 induced by a high-fat diet is reduced by restriction of energy intake 5 or by fiber-and vitamin-rich diets. 6,7 These data illustrate the potential of nutritional methods for reducing the deleterious consequences of high fat/energy intake on the risk of colon cancer.It is likely that diet affects cancer occurrence at the level of the cell signaling pathways rather than at the level of mutations. Nuclear receptors have a central role in the regulation of gene expression in response to diet. Thus, growing evidence points to the involvement of nuclear receptors in colon tumorigenesis. Indeed, they function as ligand-activated transcr...

( P < 0.0001), alcohol intake ( P = 0.0006), and female gender ( P = 0.02), and decreased with intensive consumption of n-6 oils ( P = 0.02). The positive association between fi sh consumption and plasma DHA was highly signifi cant whatever the APOE genotype ( P < 0.0001) but stronger in APOE4 noncarriers than in carriers ( P = 0.06 for interaction). Plasma DHA increased signifi cantly with age ( P = 0.009) in APOE4 noncarriers only. These fi ndings suggest that dietary habits, gender, and APOE4 genotype should be considered when designing interventions to increase n-3 PUFA blood levels in older people. -Samieri, C., S. Lorrain, B. Buaud, C. Vaysse, C. Berr, E. Peuchant, S. C. Cunnane, and P. Barberger-Gateau. Relationship between diet and plasma long-chain n-3 PUFAs in older people: impact of apolipoprotein E genotype. Long-chain n-3 PUFAs [eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)] could potentially exert a protective effect against brain aging due principally to their vascular, anti-infl ammatory, and neuroprotective properties ( 1 ). Accordingly, several epidemiological studies have observed an inverse association between habitual consumption of long-chain n-3 PUFAs or fi sh, their main dietary source, and risk of cognitive decline or dementia ( 1 ). However, this protective association may be limited to Abbreviations: 3C, Three-City; AD, Alzheimer's disease; ALA, ␣ -linolenic acid; APOE4 , 4 allele of the APOE gene; DHA, docosahexaenoic acid; EPA, eicosapentaenoic acid; FFQ, food frequency questionnaire; HR, hazard ratio; RCT, randomized controlled trial.

Such disequilibrium in PUFA dietary intakes in favor of n-6 PUFA could have adverse impact on cell membrane incorporation of long-chain n-3 PUFA and deleterious impacts on the health of children and adolescents. Promoting the consumption of both vegetable oils and margarines rich in ALA, and oily fish rich in long-chain n-3 PUFA might improve such PUFA disequilibrium.