Search

For several decades, studies have reported that n-3 polyunsaturated fatty acids (PUFAs) play a beneficial role in cardiovascular, immune, cognitive, visual, mental and metabolic health. The mammalian intestine is colonized by microbiota, including bacteria, archaea, viruses, protozoans, and fungi. The composition of the gut microbiota is influenced by long-term dietary habits, disease-associated dysbiosis, and the use of antibiotics. Accumulating evidence suggests a relationship between n-3 PUFAs and the gut microbiota. N-3 PUFAs can alter the diversity and abundance of the gut microbiome, and gut microbiota can also affect the metabolism and absorption of n-3 PUFAs. Changes in the populations of certain gut microbiota can lead to negative effects on inflammation, obesity, and metabolic diseases. An imbalanced consumption of n-3/n-6 PUFAs may lead to gut microbial dysbiosis, in particular, a significant increase in the ratio of Firmicutes to Bacteroidetes, which eventually results in being overweight and obesity. N-3 PUFA deficiency disrupts the microbiota community in metabolic disorders. In addition, accumulating evidence indicates that the interplay between n-3 PUFAs, gut microbiota, and immune reactions helps to maintain the integrity of the intestinal wall and interacts with host immune cells. Supplementation with n-3 PUFAs may be an effective therapeutic measure to restore gut microbiota homeostasis and correct metabolic disturbances associated with modern chronic diseases. In particular, marine extracts from seaweed contain a considerable dry weight of lipids, including n-3 PUFAs such as eicosapentaenoic acid (EPA, C20: 5) and docosahexaenoic acid (DHA, C22: 6). This review describes how gut microbiota function in intestinal health, how n-3 PUFAs interact with the gut microbiota, and the potential of n-3 PUFAs to influence the gut-brain axis, acting through gut microbiota composition., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Background: Although it is believed that fish omega-3 fatty acids may decrease breast cancer risk, epidemiological evidence has been inconclusive. This study examined the association between fish and fish omega-3 fatty acids intake with the risk of breast cancer in a case-control study of Korean women., Methods: We recruited 358 incident breast cancer patients and 360 controls with no history of malignant neoplasm from the National Cancer Center Hospital between July 2007 and April 2008. The study participants were given a 103-item food intake frequency questionnaire to determine their dietary consumption of fish (fatty and lean fish) and omega-3 fatty acids derived from fish (eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA))., Results: Using a multivariate logistic regression model, high intake of fatty fish was associated with a reduced risk for breast cancer in both pre- and postmenopausal women (OR [95% CI] for highest vs. lowest intake quartiles, p for trend: 0.19 [0.08 to 0.45], p < 0.001 for premenopausal women, 0.27 [0.11 to 0.66], p = 0.005 for postmenopausal women). Similarly, reductions in breast cancer risk were observed among postmenopausal subjects who consumed more than 0.101 g of EPA (OR [95% CI]: 0.38 [0.15 to 0.96]) and 0.213 g of DHA (OR [95% CI]: 0.32 [0.13 to 0.82]) from fish per day compared to the reference group who consumed less than 0.014 g of EPA and 0.037 g of DHA per day. Among premenopausal women, there was a significant reduction in breast cancer risk for the highest intake quartiles of omega-3 fatty acids (ORs [95% CI]: 0.46 [0.22 to 0.96]), compared to the reference group who consumed the lowest quartile of intake., Conclusion: These results suggest that high consumption of fatty fish is associated with a reduced risk for breast cancer, and that the intake of omega-3 fatty acids from fish is inversely associated with postmenopausal breast cancer risk.

Docosahexaenoate is usually considered to be the principal endpoint of alpha-linolenate metabolism in mammals. Nevertheless, several studies over the past 30 y have shown that more carbon from alpha-linolenate is recycled into newly synthesized lipids than is used to make docosahexaenoate. Our objective in this study was to assess carbon recycling from alpha-linolenate in suckling rats made deficient in n-3 polyunsaturated fatty acids (PUFA). Female Long-Evans rats were given a diet deficient in n-3 PUFA at weaning and then bred 8 wk later. Pups from the second generation were nursed by their respective dams and gavaged with 1 mg [U-13C]-alpha-linolenate at 10 d old. Brain and liver were obtained 24 h later, and the fatty acid profiles and 13C enrichment analyzed. Docosahexaenoate was markedly depleted in brain (-82%) and liver (-97%) of the n-3 PUFA-deficient rats. In the controls, 13C enrichment in products of carbon recycling (cholesterol and fatty acids other than n-3 PUFA) exceeded that in docosahexaenoate by 2.4-fold (liver) and 7.5-fold (brain). n-3 PUFA deficiency reduced the ratio of 13C enrichment in products of carbon recycling compared with 13C incorporated into docosahexaenoate by 63% in the brain but not in the liver. Despite severe n-3 PUFA deficiency, carbon recycling still consumed 50% more 13C from alpha-linolenate than went into docosahexaenoate in the liver and 2.8-fold more in the brain. We conclude that carbon recycling is an integral part of neonatal metabolism of alpha-linolenate and is not simply an overflow pathway arising from excess availability of preformed docosahexaenoate.

Docosahexaenoic acid (DHA) is a major structural component of the nervous system, and depletion may lead to losses in neural function. Our objective was to demonstrate a deficit in spatial task performance in rats with low brain DHA due to a low n-3 fatty acid intake using a first-generational artificial rearing technique. Newborn rat pups were separated on d 2 and assigned to two artificial rearing groups or a dam-reared control group. Pups were hand fed artificial milk via custom-designed nursing bottles containing either 0.02% (n-3 Def) or 3.1% (n-3 Adq) of total fatty acids as LNA. At d 21, rats were weaned to either n-3 Def or n-3 Adq pelleted diets and several behavioral tasks were evaluated at 9 wk of age. Brain DHA was lower (58% and 61%, p < 0.001) in n-3 Def in comparison to n-3 Adq and dam-reared rats, respectively. At adulthood, the n-3 fatty acid-deficient rats had a significantly greater moving time than the dam-reared group (p < 0.05), but there were no differences among the three groups in the elevated plus maze test. The n-3 fatty acid deficient rats exhibited a longer escape latency (p < 0.05) and poorer memory retention in the Morris water maze compared with n-3 fatty acid adequate and dam-reared rats. We concluded that artificial rearing can be used to produce n-3 fatty acid deficiency in the first generation. This deficiency was associated with significantly reduced spatial learning. Adequate brain DHA levels are required for optimal spatial learning.

The fatty acid (FA) docosahexaenoic acid (DHA, 22: 6n-3) is highly enriched in membrane phospholipids of the central nervous system and retina. Loss of DHA because of n-3 FA deficiency leads to suboptimal function in learning, memory, olfactory-based discrimination, spatial learning, and visual acuity. G protein-coupled receptor (GPCR) signal transduction is a common signaling motif in these neuronal pathways. Here we investigated the effect of n-3 FA deficiency on GPCR signaling in retinal rod outer segment (ROS) membranes isolated from rats raised on n-3-adequate or -deficient diets. ROS membranes of second generation n-3 FA-deficient rats had approximately 80% less DHA than n-3-adequate rats. DHA was replaced by docosapentaenoic acid (22:5n-6), an n-6 FA. This replacement correlated with desensitization of visual signaling in n-3 FA-deficient ROS, as evidenced by reduced rhodopsin activation, rhodopsin-transducin (G(t)) coupling, cGMP phosphodiesterase activity, and slower formation of metarhodopsin II (MII) and the MII-G(t) complex relative to n-3 FA-adequate ROS. ROS membranes from n-3 FA-deficient rats exhibited a higher degree of phospholipid acyl chain order relative to n-3 FA-adequate rats. These findings reported here provide an explanation for the reduced amplitude and delayed response of the electroretinogram a-wave observed in n-3 FA deficiency in rodents and nonhuman primates. Because members of the GPCR family are widespread in signaling pathways in the nervous system, the effect of reduced GPCR signaling due to the loss of membrane DHA may serve as an explanation for the suboptimal neural signaling observed in n-3 FA deficiency.

Background/aims: We investigated the dose-response effect of egg-phosphatidylcholine (PC) on the maze-learning ability and brain fatty acid composition in aged mice., Method: Male Crj:CD-1 mice aged 18 months were fed the following diets for 4 months: (i) 5 g palm oil/100 g diet (n-3-deficient control group); (ii) 1 g egg-PC/100 g diet plus 4 g palm oil/100 g diet (egg-PC 1% group); (iii) 2.5 g egg-PC/100 g diet plus 2.5 g palm oil/100 g diet (egg-PC 2.5% group), and (iv) 5 g egg-PC/100 g diet (egg-PC 5% group). Maze-learning ability was assessed 3 months after the start of the experiment. All animals were maintained on the n-3 fatty acid-deficient diets to examine the direct effect of egg-PC on maze behavior. The time required to reach the maze exit and the number of times that a mouse strayed into blind alleys in the maze were measured in 3 trials every 4 days., Results: Our results showed that the 2.5 and 5% egg-PC groups needed less (p < 0.05) time to find the exit and strayed into blind alleys fewer times (p < 0.05) than the control group. In order to determine the relationship between maze-behavior and brain docosahexaenoic acid (DHA) and arachidonic acid (AA) levels in aged mice fed various doses of egg-PC, the plasma and brain fatty acid composition was examined. Dose-response increases in the percentage of DHA were found in plasma lipids. However, based on our data on the brain fatty acid composition of mice fed various doses of egg-PC, no significant differences in the percentages of DHA and AA among the dietary groups were observed., Conclusion: These results suggest that the intake of egg-PC improves maze-learning ability in aged mice fed n-3 fatty acid-deficient diets but it does not influence the percentage of brain DHA and AA., (Copyright 2002 S. Karger AG, Basel)