The role of dietary fatty acids in children's behaviour and learning

A growing awareness and understanding of the profiles of local children in County Durham, UK, experiencing learning and behavioural difficulties throughout the education system, has resulted in a number of school based nutritional intervention studies being undertaken. Evidence suggests that some children and young adults with developmental difficulties have a deficiency of particular omega 3 and omega 6 polyunsaturated fatty acids and supplementation with these nutrients can have an impact on their behaviour, concentration and performance on standardised assessments. The first randomised placebo controlled trial to be carried out on children in Durham with developmental coordination disorder has demonstrated significant effects of fatty acid supplementation on behaviour, reading and spelling performance. We are conducting further scientific studies within Durham and neighbouring Authorities in the North of England to be published at a future time. We have also carried out a number of open label treatment studies within schools to help us understand better the role that nutritional intervention can play across a broader range of age groups and abilities. The results suggest positive outcomes for a substantial proportion of children who are more able to engage with the educational opportunities presented to them. This is an important finding to be shared with educationalists, health professionals and importantly the parents.     

A changing role for dietary monounsaturated fatty acids

Evidence is accumulating that diets low in saturated fatty acids and high in monounsaturated fatty acids are effective in controlling blood lipid levels; a likely consequence could be a beneficial effect on the risk of coronary heart disease. Although as yet limited in number, studies have shown monounsaturated fatty acids to be the equivalent of polyunsaturated fatty acids or low-fat diets in lowering blood low-density-lipoprotein cholesterol. The monounsaturated acids apparently have the added advantage of not causing a decrease in high-density-lipoprotein cholesterol or an increase in blood triglycerides, which can be a consequence of other dietary modifications. In the past, olive oil was the only fat rich in monounsaturated acids that was generally available in the United States. Recently, canola oil, a fat also rich in monounsaturates, has appeared in retail food outlets. Other potential sources are high oleic sunflower and safflower oils. Because the culinary and organoleptic properties of the monounsaturated-rich oils can be identical to those of currently used oils, they should be readily accepted by the consumer. Whether the preferred healthful diet is one low in fat or one high in monoenes or polyenes, the primary dietary recommendation remains--decrease the intake of saturated fat and cholesterol.     

Protective effect of dietary n-3 polyunsaturated fatty acids on myocardial resistance to ischemia-reperfusion injury in rats

Dietary n-3 polyunsaturated fatty acids (PUFA) reduce coronary heart disease (CHD) complications, such as chronic arrhythmia and sudden cardiac death. Improved myocardial resistance to ischemia-reperfusion injury results in smaller myocardial infarction, which is a major factor in the occurrence of CHD complications. We hypothesized that a specific dietary fatty acid profile (low in saturated and n-6 PUFA but high in plant and marine n-3 PUFA) may improve myocardial resistance to ischemia-reperfusion injury and reduce infarct size. To test this assumption, we used a well-defined rat model of myocardial infarction. Based on our results, in comparison to a diet that is high in either saturated or n-6 PUFA but poor in plant and marine n-3 PUFA, a diet that is low in saturated fats and n-6 PUFA but rich in plant and marine n-3 PUFA results in smaller myocardial infarct size (P < .01). The effects of the 3 diets were also examined by analyzing the fatty acid composition of plasma, erythrocyte cell membranes, and the phospholipids of myocardial mitochondria. The results show a great accumulation of n-3 PUFA and a parallel decrease in arachidonic acid, the main n-6 PUFA, in plasma, cell membranes, and cardiac mitochondria (P < .0001). We conclude that improved myocardial resistance to ischemia-reperfusion may be one of the critical factors explaining the protective effects of dietary n-3 PUFA against CHD complications in humans. In addition to increasing n-3 PUFA intake, an optimal dietary pattern aimed at reducing cardiovascular mortality should include a reduction of the intake of both saturated and n-6 PUFA.     

脂肪酸对糖尿病模型大鼠血磷脂脂肪谱的影响

目的　观察富含n - 6和n - 3多不饱和脂肪酸 (PUFA)饲料对自发性 2型糖尿病模型OtsukaLong -E vansTokushimaFatty(OLETF)大鼠糖代谢及血清磷脂 (S -PL)中脂肪酸 (FA)组成的影响。 方法　将 2 0只 14周龄雄性OLETF大鼠随机分为 2组。两组大鼠饲料总能量相同 ,其中饱和脂肪酸 (SFA)、单不饱和脂肪酸 (MUFA)和PU FA的百分含量亦相同 ,但分别富含n - 6PUFA〔4 1 6mol/ (10 0mol·脂肪 )〕和n - 3PUFA〔2 0 4mol/ (10 0mol·脂肪 )〕 ,饮食干预 10周。第 2 4周时实施口服糖耐量试验 (OGTT)、胰岛素水平测定和S -PL中FA组成测定。结果　干预期间 ,两组大鼠总进食量及体重增长无显著性差异 ;干预后OGTT及胰岛素水平测定表明 ,n - 3组相对于n - 6组具有较好的胰岛素敏感性。n - 3组大鼠S -PL中 18∶1(n - 9)、MUFA总量、18∶2 (n - 6 )、各n - 3系PUPA百分含量较n- 6组高 ,n - 6PUFA总量、2 0∶4 (n - 6 )百分含量较低。结论　n - 3PUFA的摄入相对于n - 6PUFA对OLETF大鼠的糖代谢有益 ,OLETF大鼠S -PL的FA组成受到饲料中FA的影响 ,但并不是其直接反应。     

Hepatic fatty acids and acyl desaturases in rats: effects of dietary carbohydrate and essential fatty acids

For a 9-week period, six groups of weanling male rats were fed either a fat-free diet or a diet containing 10% hydrogenated coconut oil (HCO) or 10% safflower oil (SAF), respectively. Each of these diets contained either glucose or sucrose as the only carbohydrate. In the fat-free diets, the carbohydrate level was 67.3% and in the fat-supplemented diets 44.8%. Including HCO in the fat-free diet did not significantly alter hepatic 5-, 6-, and 9-desaturase activity, whereas addition of SAF significantly depressed all these activities. As compared to glucose, sucrose induced higher 9-desaturase activity in the rats on the fat-free diets. Adding HCO or SAF to the diet, simultaneously with lowering the carbohydrate level, diminished the stimulatory effect of dietary sucrose versus glucose on 9-desaturase activity. Levels of 20:4n6 and 20:3n9 in the fatty acid profiles of the liver microsomes were not influenced by dietary carbohydrate source, neither were the activities of the 5- and 6-desaturases, providing indirect evidence that dietary sucrose, as compared to glucose, did not differently affect biosynthesis of 20:4n6 and 20:3n9.     

The health effects of dietary unsaturated fatty acids

• 2.1 The chemistry of fatty acids
• 2.2 Digestion, absorption and metabolism
• 2.3 Functions of unsaturated fatty acids

3 Unsaturated fatty acids in the UK diet

• 3.1 Sources of fat in the diet
• 3.2 Dietary recommendations for fat
• 3.3 Intakes of unsaturated fatty acids
• 3.4 Major contributors to unsaturated fatty acid intake
• 3.5 Trends in intake

4 Unsaturated fatty acids in health and disease

• 4.1 Unsaturated fatty acids and cardiovascular disease
• 4.2 Unsaturated fatty acids and diabetes
• 4.3 Unsaturated fatty acids and cancer
• 4.4 Unsaturated fatty acids and inflammatory conditions
• 4.5 Unsaturated fatty acids in fetal and infant development
• 4.6 Unsaturated fatty acids and cognitive function and behaviour
• 4.7 Emerging aspects of unsaturated fatty acids and health

5 Unsaturated fatty acids and public health

• 5.1 Labelling of unsaturated fatty acids
• 5.2 Are current UK recommendations adequate?
• 5.3 Opportunities to increase intake of long chain n‐3 PUFAs
• 5.4 Implications of optimising intakes of unsaturated fatty acids

6 Conclusions

Acknowledgements

References

Appendix 1

Summary Fat provides energy; indeed it is the most energy dense of all the macronutrients, with 1 g providing 37 kJ (9 kcal). However, the constituent parts of fat, fatty acids, are required by the body for many other functions than simply as an energy source, and there is an increasing awareness of the potential health benefits of specific types of fatty acids. Fatty acids are long hydrocarbon chains, with a methyl group at one end (the omega or n‐end) and an acid group at the other. Unsaturated fatty acids are hydrocarbon chains containing at least one carbon–carbon double bond; monounsaturated fatty acids contain one double bond, and polyunsaturated fatty acids (PUFAs) contain many double bonds. The position of the double bond relative to the omega end determines whether a PUFA is an n‐3 (omega 3) or an n‐6 (omega 6) fatty acid. Most fatty acids can be synthesised in the body, but humans lack the enzymes required to produce two fatty acids. These are called the essential fatty acids and must be acquired from the diet. In humans, the essential fatty acids are the n‐3 PUFA α‐linolenic acid and the n‐6 PUFA linoleic acid. Although humans can elongate dietary α‐linolenic acid to the long chain n‐3 PUFAs eicosapentaenoic acid and docosahexaenoic acid, the rate of synthesis may not be sufficient to meet requirements, and it is, therefore, recommended that good sources of these fatty acids, namely, oil‐rich fish, are also included in the diet. Fat is found in most food groups, and foods containing fat generally provide a range of different fatty acids, both saturated and unsaturated. In the UK, the major dietary sources of unsaturated fatty acids include meat & meat products, cereals & cereal products and potatoes & savoury snacks; primarily as a result of the vegetable oil used in processing. Recommended intakes of both total fat and the different types of fatty acids have been set for the UK population, and it is possible to monitor fat intake from the data collected in nationwide dietary surveys. As a population, we are not currently meeting these recommendations, so there is still scope for dietary change. In Western diets, n‐6 fatty acids are the predominant PUFAs, and this is in line with current dietary advice to consume a minimum of 1% energy as n‐6 PUFAs and 0.2% energy as n‐3 PUFAs. The balance of n‐3 and n‐6 PUFAs in Western diets has changed substantially over the last 100 years or so, and as the two families of PUFAs share a common metabolic pathway, concerns have been raised that this might be detrimental to health; what is becoming increasingly clear is that both n‐3 and n‐6 PUFAs have independent health effects in the body, and as intakes of the n‐6 PUFAs are within the guidelines for a healthy diet, concerns about the n‐6 to n‐3 ratio are driven by low intakes of n‐3 rather than high intakes of n‐6. Currently in adults n‐6 PUFAs contribute to 5.3% energy. Detecting associations between components of the diet and risk of various diseases is notoriously complex and in many cases, the evidence is still accumulating. Cardiovascular disease, characterised by hardening and narrowing of blood vessels and/or the development of blood clots, is one of the leading causes of mortality and morbidity worldwide. The type and total amount of dietary fat has a clear part to play in affecting an individual’s disease risk, yet the precise mechanisms by which unsaturated fatty acids reduce cardiovascular disease risk are still unclear. A number of mechanisms whereby dietary fatty acids could influence the progression of cardiovascular disease and its risk factors have been identified. These include effects on blood lipid concentrations, blood pressure, inflammatory response, arrhythmia and endothelial function, along with many other effects, both known and as yet undefined. A well‐established risk factor for cardiovascular disease is an elevated plasma low density lipoprotein (LDL) cholesterol concentration. Replacing saturated fatty acids with either monounsaturated fatty acids or n‐6 PUFAs reduces LDL (the ‘bad’) cholesterol, and so reduces the risk of developing the disease. Unsaturated fatty acids, such as linoleic acid or monounsaturated fatty acids, also slightly raise high density lipoprotein (HDL) (the ‘good’) cholesterol, which assists in the removal of triacylglycerols from the bloodstream. Interest in the health effects of the long chain n‐3 PUFAs found in fish oils is also increasing. There is strong supportive, but not yet conclusive, evidence that these fatty acids protect against fatal heart disease. On the basis of this conclusion, in 2004 the Scientific Advisory Committee on Nutrition advised the UK government to adopt the population‐wide dietary recommendation to eat at least two portions of fish per week, of which one should be oil‐rich, equivalent to 0.45 g of the long chain n‐3 PUFAs per day. In recent years, the potential health benefits of α‐linolenic acid has attracted attention, and evidence is mounting on the role that this n‐3 fatty acid may play in preventing the progression of cardiovascular disease, although it is currently unclear what, if any, association exists. Brain cells are especially rich in certain long chain PUFAs. This has led to the suggestion that dietary status of these long chain fatty acids might influence cognitive function and behaviour. Research in this field is still in its early stages, but there is a small amount of evidence to suggest improvements in cognitive function following fatty acid supplementation. In contrast, it is well established that pregnant women must have an adequate supply of the long chain n‐3 PUFAs before and throughout pregnancy and lactation to support normal growth, neurological development and cognitive function of the baby. As n‐6 PUFAs are more abundant in the diet, achieving an adequate intake is less problematic. However, this is not the case for the n‐3 PUFAs; increasing fish consumption beyond two servings of oil‐rich fish per week or relying on fish oil supplementation is not appropriate during pregnancy due to the potential problems associated with heavy metal contamination of fish, or the high vitamin A level in some fish oil supplements. Unsaturated fatty acids have also been associated with a number of other diseases and although the evidence is by no means conclusive, it is an area that is attracting a huge amount of interest. Dietary fat affects a number of different metabolic pathways, including those involved with glycaemic control, so the types and amounts of dietary fat may have a role to play in the management of type 2 diabetes. Unsaturated fatty acids may also be associated with a reduced risk of developing certain cancers, including cancers of the colon, breast and prostate, although currently the level of evidence is not deemed sufficient by authoritative bodies, such as the World Cancer Research Fund, World Health Organization and the Department of Health, to make any specific dietary recommendations. There are a number of inflammatory conditions, such as asthma, Crohn’s disease and arthritis, which could potentially be alleviated by dietary modification. The fatty acid composition of cell membranes can be altered by consumption of both n‐3 and n‐6 PUFAs, and this can result in reduced inflammatory activity. However, whether this effect brings about a significant reduction in clinical symptoms is still unclear. It is also important to note that there are concerns that the beneficial effects on certain disease outcomes are only observed with very high intakes of unsaturated fatty acids, which could realistically only be achievable by supplementation. Few nutritionists would be comfortable recommending supplement use as the only alternative to fish, as this can be expensive and goes against the idea that all the nutrients that our bodies require can be obtained from the food that we eat if the right choices are made. Unsaturated fatty acids are now a nutritional hot topic, and their presence in foods has attracted both public and industrial interest. There is currently no specific legislation to control the use of health claims relating to the fatty acid content of foods. However, a European Union (EU) Directive is expected imminently which will formally set down the criteria that a product will have to meet in order to make any nutrition or health claim. With regards to the current recommendations, those for the UK are in line with those around the world. However, as a population, we need to increase our consumption of long chain n‐3 PUFAs and decrease intake of saturated fatty acids. To facilitate this, food technologists are looking at ways in which the fatty acid profile of a food can be modified in order to bring dietary improvements without requiring a major change in dietary habits. However, public health messages surrounding the optimum intakes of fatty acids must be clear and consistent to ensure that a favourable change in the fatty acid profile of the UK diet occurs.     

The role of dietary polyunsaturated fatty acids and prostaglandins in reducing blood pressure and improving thrombogenic indices

Evidence linking dietary fats to blood pressure and thrombogenic indices is reviewed. Results of dietary studies performed at Beltsville, Maryland, have demonstrated that under controlled dietary conditions, i.e., when total fat intake is maintained at 25% fat calories with a P/S ratio of 1, at either a fixed or free-choice salt intake and where the body weight is maintained relatively constant, blood pressure can be lowered and platelet aggregation indices can be improved in men and women in the 40–60 age group. Results of a pilot epidemiologic study of farmers aged 40–45 in Finland and Italy generally confirm the experimental nutrition studies reported above. A possible explanation of these results based on the conversion of linoleic acid to prostaglandins as well as the physiological actions of prostaglandins is discussed.     

Effects of dietary fatty acids and exercise on body-weight regulation and metabolism in rats

OBJECTIVE: To assess the interaction of high-fat diets (HF) made with different dietary fatty acids and exercise on body-weight regulation, adiposity, and metabolism. RESEARCH METHODS AND PROCEDURES: Male Wistar rats born to dams fed HF diets (40% w/w) made with either fish oil (FO), soybean oil (SO), or palm oil (PO) were fed diets similar to their dams and divided randomly into exercise (EX, swimming) or sedentary control (SD) groups when they were 9 weeks old. EX lasted for 6 weeks. Twenty-four hours after the last EX bout, fasted rats were killed by decapitation. Chemical analyses and body composition analysis were conducted. RESULTS: The results demonstrated that different fatty acids had different effects on body weight, composition, and metabolism. SO-fed rats gained the most weight and fat. EX reduced body weight of FO- and PO-fed rats, but SO-fed rats were still heavier and fatter than other rats. Data from SO- and PO-fed rats suggested that they are insulin resistant and that EX normalized this abnormality. Of the three HF diets used, FO produced the least adverse effects compared with PO and SO. DISCUSSION: Not only the quantity of dietary fat, but also the type of fat used, will produce different effects on body weight and metabolism. EX ameliorates the suggested insulin resistance induced in rats fed either highly saturated or n-6 polyunsaturated fatty acids. Long-chain n-3 polyunsaturated fatty acids, as found in fish oil, are more beneficial than n-6 polyunsaturated fatty acids when fed in high amounts to rats.     

Effect of dietary fat on the utilization of fatty acids by myocardial tissue in the rat

Weanling rats were fed high fat diets containing 40% of energy as fat for 23 d. Diets were formulated to contain equivalent content of essential nutrients per calorie for the nonfat components. Four oil mixtures provided high dietary levels of either oleic, linoleic, linolenic or erucic acid. Effect of dietary fatty acid composition on the fatty acid composition of phosphatidylcholine, phosphatidylethanolamine and cardiolipin isolated from cardiac mitochondria was examined in conjunction with the effect of diet on the oxidative activity of cardiac mitochondria. Dietary treatments that reduced the content of C16:0 in the sn-1 and sn-2 positions of phosphatidylcholine were associated with increased content of C20:1 and C22:1 fatty acids into the sn-2 position and resulted in decreased oxidative activity of cardiac mitochondria utilizing palmitylcarnitine as a substrate for oxidation. Diets high in linoleic acid did not increase membrane phospholipid content of omega 3 fatty acids, but resulted in decreased level of C20:4 omega 6. In a subsequent perfusion experiment, hearts were removed from animals fed either high erucic or high linoleic acid diets and were perfused to examine rates of fatty acid oxidation and simultaneous synthesis of high energy phosphate compounds in cardiac muscle. Diet did not affect the levels of creatine phosphate or adenine nucleotides present in the tissue on a per-gram-wet-weight basis, but production of 14CO2 from beta-oxidation of palmitic acid was lower for animals fed the high erucic acid diet than for those fed the high linoleic acid diet. Since this diet did not alter oxidation of palmitylcarnitine in vitro and as beta-oxidation of lauric acid was not decreased in the perfused heart, we conclude that mitochondrial oxidation of fatty acid was not altered by diet and that low rates observed for palmitate oxidation are attributable to reduced palmitylcarnitine synthesis.     

The confusion about dietary fatty acids recommendations for CHD prevention

A recent meta-analysis of prospective cohort studies has not found an association between dietary saturated fat intake and CHD incidence. This funnelled the discussion about the importance of the recommendation to lower the intake of saturated fat for the prevention of CHD. At the same time a document of the European Food Safety Authority has suggested that specific quantitative recommendations are not needed for individual fatty acids but that more general statements can suffice. In this review, we discuss methodological aspects of the absence of association between SFA intake and CHD incidence in prospective cohort studies. We also summarise the results of the controlled dietary experiments on blood lipids and on CHD incidence in which saturated fat was replaced by either cis-unsaturated fat or carbohydrates. Finally, we propose a nutritionally adequate diet with an optimal fatty acid composition for the prevention of CHD in the context of dietary patterns. Such diets are characterised by a low intake of saturated fat, and as low as possible intake of trans-fat and fulfil the requirements for the intake of n-6 and n-3 fatty acids. No recommendation is needed for the intake of cis-MUFA.     

Differential oxidation of individual dietary fatty acids in humans

BACKGROUND: Dietary fatty acids that are more prone to oxidation than to storage may be less likely to lead to obesity. OBJECTIVE: The aim of this study was to determine the effect of chain length, degree of unsaturation, and stereoisomeric effects of unsaturation on the oxidation of individual fatty acids in normal-weight men. DESIGN: Fatty acid oxidation was examined in men consuming a weight-maintenance diet containing 40% of energy as fat. After consuming the diet for 1 wk, subjects were fed fatty acids labeled with (13)C in the methyl or carboxyl position (10 mg/kg body wt). The fatty acids fed in random order were laurate, palmitate, stearate, oleate, elaidate (the trans isomer of oleate), linoleate, and linolenate blended in a hot liquid meal. Breath samples were collected for the next 9 h and the oxidation of each fatty acid was assessed by examining liberated (13)CO(2) in breath. RESULTS: Cumulative oxidation over the 9-h test ranged from a high of 41% of the dose for laurate to a low of 13% of the dose for stearate. Of the 18-carbon fatty acids, linolenate was the most highly oxidized and linoleate appeared to be somewhat conserved. (13)C recovery in breath from the methyl-labeled fatty acids was approximately 30% less than that from the carboxyl-labeled fatty acids. CONCLUSIONS: In summary, lauric acid is highly oxidized, whereas the polyunsaturated and monounsaturated fatty acids are fairly well oxidized. Oxidation of the long-chain, saturated fatty acids decreases with increasing carbon number.     

The effects of dietary n-3 polyunsaturated fatty acids on neutrophils

The studies of dietary fish oil supplementation in healthy volunteers demonstrate a significant increase in neutrophil EPA content, a concomitant reduction in neutrophil AA content, and suppression of neutrophil LTB4 synthesis by supplementation with dietary fish oil containing approximately 3-4 g EPA daily for a minimum of 4 weeks. Suppression of neutrophil chemotactic responsiveness to LTB4 and FMLP was observed after dietary n-3 PUFA supplementation at these levels. Dietary EPA is more active than DHA in eliciting these effects in human neutrophils. Dietary n-3 PUFA supplementation inhibits neutrophil chemotaxis to these ligands through the inhibition of the signal transduction pathway between the receptor and phospholipase C, as demonstrated by the inhibition of chemotaxin-stimulated IP3 formation, in the absence of an effect on the number or affinity of the respective chemotaxin receptors. In patients with RA, dietary supplementation with n-3 PUFA resulted in decreased AA content of cellular lipids, with an augmented EPA content and decreased LTB4 generation by neutrophils. Dietary supplementation with n-3 PUFA also resulted in augmentation of depressed neutrophil chemotaxis to LTB4 and FMLP. Preliminary findings suggest that the decreased responsiveness to chemotaxins of neutrophils from RA patients is due to down-regulation of chemotaxin receptor number, resulting in decreased signaling via chemotaxin receptors. Dietary fish oil PUFA partially reversed the down-regulation of the chemotaxin receptor of neutrophils of RA patients, but had a lesser effect on chemotaxin receptor signaling and function, probably due to a post-receptor inhibition induced by fish oil PUFA, as was previously observed in healthy controls. Several small clinical trials have each suggested that dietary supplementation with n-3 PUFA resulted in modest improvements in disease activity. Meta-analysis of these studies confirms statistically significant improvements in tender joint count and morning stiffness after 3 months of dietary fish oil supplementation in patients with RA. Dietary supplementation with gamma-linolenic acid-rich oils also inhibits neutrophil LTB4 formation, has other anti-inflammatory and immunosuppressive effects, and shows promise of therapeutic efficacy in RA.     

饮食n-3脂肪酸对小鼠脑脂类中多不饱和脂肪酸构成的影响

【目的】观察饮食鱼油n-3多不饱和脂肪酸(n-3 PUFAs)对脑内不同脂类中PUFAs构成的影响。【方法】使用C57BL/6J雌性小鼠,在胎儿期和幼年期分别给予不同种类高脂饲料(18%脂肪,供能比为36%)喂养-高脂豆油饲料、高脂鱼油饲料和高脂豆油:鱼油(5∶1)混合饲料,以正常饲料(6%脂肪来自豆油,供能比为12%)为对照,时间为4个月。采用薄层层析分离脑组织中各主要脂类成份,然后采用甲酯化-气相色谱分析对各脂类成份中的脂肪酸进行测定。【结果】鱼油饲料喂养改变了小鼠脑内主要脂类中PUFAs的构成。在磷脂中,虽然5种PUFAs在各饲料组之间差异均无显著性(P>0.05),但二十二碳六烯酸(DHA)/花生四烯酸(AA)(1.94±0.41)以及n-3/n-6 PUFAs比值(2.31±0.75)在鱼油组较其它三组显著升高(P<0.05);在甘油一和二酯中,与豆油组相比,鱼油组和豆油:鱼油混合组LA含量(0.31±0.09%,0.65±0.58%)降低,而鱼油组DHA/AA(2.60±1.66)以及n-3/n-6 PUFAs比值(2.31±0.75)升高(P<0.05);在甘油三酯中,与豆油组相比,鱼油组和豆油:鱼油混合组AA含量(1.62±0.53%,1.12±0.36%)和EPA含量(0.98±0.58%,1.34±0.31%)显著降低,而DHA/AA比值(1.14±0.21,1.46±0.58)升高(P<0.05),但DHA含量在三组之间无差异(P>0.05);在游离脂肪酸中,5种PUFAs在各饲料组之间无差异(P>0.05)。【结论】饮食鱼油n-3 PUFAs摄入增多虽然不影响脑内DHA的聚积,但改变了DHA/AA以及n-3/n-6PUFAs的比值。甘油酯类可能是脑摄取、聚积DHA的主要直接来源之一。     

膳食脂肪酸与燃煤型氟中毒的相关性研究

目的 探讨脂肪酸摄入与燃煤型氟中毒之间的关系。方法 随机整群抽取毕节市织金县燃煤型氟中毒病区居住年限超过10年且年龄为18～75岁的居民1 101名进行横断面调查,采用logistic回归分析脂肪酸及分类摄入量与燃煤型氟中毒之间的关系。结果 多因素分析得出总脂肪酸摄入与燃煤型氟中毒呈负相关（回归系数为-6.408）;将氟中毒分为氟骨症和氟斑牙进行分层分析,与总脂肪酸摄入量最低四分位比较,在氟骨症中第二到第四分位的OR值分别0.53,0.51和0.43,95%置信区间分别为（0.35,0.81）,（0.35 ,0.78）和（0.27,0.66）;在氟斑牙中第二到第四分位的OR值分别0.74,0.60和0.37,95%置信区间分别为（0.47,1.16）,（0.38,0.95）和（0.24,0.58）;脂肪酸亚类中,多不饱和脂肪酸最具有意义。结论 膳食脂肪酸可能对燃煤型氟中毒具有保护作用。     

(N-3) long-chain polyunsaturated fatty acids prolong survival following myocardial infarction in rats

Many clinical studies report that (n-3) PUFAs decrease the incidence of sudden death in patients with coronary artery disease after myocardial infarction (MI). However, the mechanisms for the beneficial effects of (n-3) PUFAs are unknown. The objectives of the present study were to confirm the findings from clinical trials using an animal model of MI in which dietary intake could be closely controlled and to utilize the model to investigate molecular mechanisms for the beneficial effects of (n-3) PUFAs. Male rats were subjected to coronary ligation to induce MI and were randomly assigned to diets high in (n-6) (58% of lipid) or (n-3) (28% of lipid) PUFAs for 6 mo. A diet high in (n-3) PUFAs was associated with an improvement in 6-mo survival (89.2% vs. 64.9%, P = 0.013) compared with rats consuming a diet high in (n-6) PUFAs (n = 37/group). In a separate study (n = 5 rats/diet group), the (n-3) PUFA diet decreased the (n-6):(n-3) PUFA ratio in plasma (0.6 +/- 0.1 vs. 7.9 +/- 1.8, P < 0.05) and cardiac tissue (0.9 +/- 0.1 vs. 11.8 +/- 1.6, P < 0.05) of rats fed for 4 wk. The increased survival in the (n-3) diet group was associated with decreased cardiac activities of protein kinase A and calcium calmodulin-dependent kinase II by 33-38% (P < 0.05) and a 28% decrease (P < 0.05) in phosphorylation (activation) of the ryanodine receptor calcium release channel. Based upon our results, we speculate that decreased activities of protein kinases induced by diets high in (n-3) PUFAs are associated with a decrease in sudden death after MI in rats.