Polyunsaturated Fatty Acid Deficient Diet Research Articles

Maternal n-3 polyunsaturated fatty acids restructure gut microbiota of offspring mice and decrease their susceptibility to mammary gland cancer.

Our previous studies have revealed that a maternal diet rich in n-3 polyunsaturated fatty acids (PUFAs) is associated with decreased mammary cancer risk in offspring. However, the underlying mechanism remains unclear. The present study aimed to investigate the possible mechanism by which maternal n-3 PUFAs decrease the mammary cancer risk of offspring in terms of gut microbiota. C57BL/6 pregnant mice were fed a control standard chow (CON), fish oil supplemented diet (n-3 Sup-FO), flaxseed oil supplemented diet (n-3 Sup-FSO) or n-3 PUFA deficient diet (n-3 Def) (n = 10) throughout gestation and lactation. After weaning, all offspring were fed a AIN-93G diet. The tumor incidence and volume were significantly increased in n-3 Def offspring compared with the other groups. Maternal n-3 PUFA supplementation resulted in a significantly increased α-diversity of the gut microbiota in n-3 Sup-FO and n-3 Sup-FSO offspring compared with that in n-3 Def offspring. The relative abundances of Akkermansia, Lactobacillus and Mucispirillum observed in adult offspring of both the n-3 Sup-FO and n-3 Sup-FSO groups were higher than those observed in the control group, whereas the maternal n-3 Def diet was associated with decreased abundances of Lactobacillus, Bifidobacterium and Barnesiella in 7-week-old offspring. The levels of the pro-inflammatory factors IL-1β, IL-6 and TNF-α were significantly lower in n-3 PUFA supplemented offspring than in n-3 Def offspring. In addition, the abundance of Mucispirillum was positively associated with the concentration of the anti-inflammatory factor IL-10, whereas the abundances of Bifidobacterium and Akkermansia were negatively associated with IL-1β and IL-6, respectively. Based on the bacterial composition of the gut microbiota, metabolites were predicted and the results showed that arachidonic acid metabolism and the MAPK signaling pathways were more enriched, while the butyric acid metabolic pathway was less enriched in offspring of the n-3 Def group than in those of the other three groups. Our findings suggest that decreased pro-inflammatory factors and changed gut microbiota are associated with the protective effects of maternal n-3 PUFAs against offspring's mammary tumorigenesis.

Depressive-like phenotype evoked by lifelong nutritional omega-3 deficiency in female rats: Crosstalk among kynurenine, Toll-like receptors and amyloid beta oligomers

Depression is one of the most common psychiatric diseases and the prevalence of depressive symptoms in women is almost twice compared to men, although the reasons of this gender difference are not fully understood yet. Recently, soluble amyloid beta (Aβ)1-42 peptide has been receiving great importance in the development of depression, also considering that depression is highly comorbid with Alzheimer’s disease and other neurodegenerative illnesses. The central role played by Aβ in the development of depressive-like symptoms in rodents has been evidenced in environmental rodent model of depression. Indeed, we have previously found that lifelong exposure to n-3 polyunsaturated fatty acids (PUFA) deficient diet in female rats at 8 weeks of life leads to depressive like- symptoms and higher susceptibility to stress associated with increased Aβ levels. In order to understand if such effects were maintained over time, rats were exposed to the same diet regimen until 6 or 21 weeks of life. We found that both timepoints of exposure to n-3 PUFA deficient diet lead to depressive-like phenotype. Furthermore, a significant alteration in brain neurochemistry was retrieved. In particular, in hippocampal area a significant reduction in serotonin (5-HT) and noradrenaline (NA) content was evidenced. Considering the prominent role of NA in counterbalancing neuroinflammatory state, we quantified in the same brain area kynurenine levels, a metabolite of tryptophan implicated in inflammatory state and brought to the fore for its implication in depression. Interestingly, kynurenine levels were significantly increased in hippocampus (HIPP) of female rats exposed to such diet. In addition, lifelong deficiency in n-3 PUFA dietary intake led to systemic increase of corticosterone, hence hypothalamic pituitary adrenal (HPA) axis hyperactivation, and higher proinflammatory cytokine production. Increased production of kynurenine, along with HPA axis hyperactivation, have been associated with immune system modulation, particularly through Toll-like receptor type 2 (TLR2) and Toll-like receptor type 4 (TLR4) involvement. In addition, it has been shown that soluble forms of Aβ1-42 can induced depressive like-phenotype in consequence to a crosstalk between TLR4 and 5-HTergic system. Thus, considering that in this model we have previously reported increased plasma Aβ1-42 level, we quantified TRL2 and 4 expression in HIPP of treated rats. We found that chronic exposure to a diet characterized by very low n-3 PUFA content led to higher expression of TLR2 and TLR4 in HIPP of female treated rats, indicating an activation of the immune system and was accompanied by increased expression of oligomeric Aβ.Taken together, our data indicate that the pro-depressive effects induced by a diet poor in n-3 PUFA can be attributable to a shift of hippocampal tryptophan metabolism toward inflammatory metabolite ultimately corresponding to altered immune response and increased Aβ oligomerization.

Maternal n-3 PUFAs deficiency during pregnancy inhibits neural progenitor cell proliferation in fetal rat cerebral cortex

The aim of this study was to evaluate the in vivo impacts of maternal n-3 polyunsaturated fatty acids (PUFAs) deficiency during pregnancy on the proliferation of neural progenitor cells (NPCs) in the developing cerebral cortex of fetal rats. Our results showed that about 5 weeks of maternal dietary n-3 PUFAs deprivation resulted in a substantial n-3 PUFA deficiency in fetal rat cerebral cortex. Importantly, by two survival schemes and two quantitative methods, we found that maternal intake of n-3 PUFAs deficient diet during the gestation significantly inhibited the proliferation of NPCs in fetal rat cerebral cortex. Moreover, the decreased cortical NPCs proliferation induced by nutritional n-3 PUFAs restriction did not originate from the increased NPCs apoptosis. Finally, our observations indicated that the down-regulation of cyclin E protein might be involved in the inhibitory effects of maternal n-3 PUFAs deficient diet on the proliferation of cortical NPCs. These findings highlight the importance of maternal intake of appropriate n-3 PUFAs and deepen our understanding of the exact effects of n-3 PUFAs on mammalian brain development.

Dietary Omega-3 Polyunsaturated Fatty Acid Deprivation Does Not Alter Seizure Thresholds but May Prevent the Anti-seizure Effects of Injected Docosahexaenoic Acid in Rats.

Background: Brain concentrations of omega-3 docosahexaenoic acid (DHA, 22:6n-3) have been reported to positively correlate with seizure thresholds in rodent seizure models. It is not known whether brain DHA depletion, achieved by chronic dietary omega-3 polyunsaturated fatty acid (PUFA) deficiency, lowers seizure thresholds in rats.Objective: The present study tested the hypothesis that lowering brain DHA concentration with chronic dietary n-3 PUFA deprivation in rats will reduce seizure thresholds, and that compared to injected oleic acid (OA), injected DHA will raise seizure thresholds in rats maintained on n-3 PUFA adequate and deficient diets.Methods: Rats (60 days old) were surgically implanted with electrodes in the amygdala, and subsequently randomized to the AIN-93G diet containing adequate levels of n-3 PUFA derived from soybean oil or an n-3 PUFA-deficient diet derived from coconut and safflower oil. The rats were maintained on the diets for 37 weeks. Afterdischarge seizure thresholds (ADTs) were measured every 4–6 weeks by electrically stimulating the amygdala. Between weeks 35 and 37, ADTs were assessed within 1 h of subcutaneous OA or DHA injection (600 mg/kg). Seizure thresholds were also measured in a parallel group of non-implanted rats subjected to the maximal pentylenetetrazol (PTZ, 110 mg/kg) seizure test. PUFA composition was measured in the pyriform-amygdala complex of another group of non-implanted rats sacrificed at 16 and 32 weeks.Results: Dietary n-3 PUFA deprivation did not significantly alter amygdaloid seizure thresholds or latency to PTZ-induced seizures. Acute injection of OA did not alter amygdaloid ADTs of rats on the n-3 PUFA adequate or deficient diets, whereas acute injection of DHA significantly increased amygdaloid ADTs in rats on the n-3 PUFA adequate control diet as compared to rats on the n-3 PUFA deficient diet (P < 0.05). Pyriform-amygdala DHA percent composition did not significantly differ between the groups, while n-6 docosapentaenoic acid, a marker of n-3 PUFA deficiency, was significantly increased by 2.9-fold at 32 weeks.Conclusion: Chronic dietary n-3 PUFA deficiency does not alter seizure thresholds in rats, but may prevent the anti-seizure effects of DHA.

Mitochondrial and Oxidative Stress Aspects in Hippocampus of Rats Submitted to Dietary n-3 Polyunsaturated Fatty Acid Deficiency After Exposure to Early Stress.

Chronic dietary long-chain polyunsaturated fatty acids (PUFAs) deficiency may lead to changes in cortex and hippocampus neuronal membrane phospholipids, and may be linked to impaired central nervous system function. Particularly docosahexaenoic acid deficiency appears to be involved in neuropsychiatric disorders. On the other hand, adverse events early in life may also profoundly affect brain development, leading to long-lasting effects on neurophysiology, neurobiology and behavior. This research assessed if neonatal stress and a dietary n-3 PUFAs deficiency could interact to produce hippocampal alterations related to mitochondrial functions in adult rats. There were no effects of diet, neonatal intervention or interactions on superoxide dismutase or catalase enzymatic activities, mitochondrial membrane potential and respiratory chain complexes. Rats fed n-3 PUFAs deficient diet displayed higher levels of glutathione peroxidase and catalase activity, higher free radicals production and higher thiol content compared to rats fed n-3 PUFAs adequate diet. There were interactions among diets and neonatal stress, since glutathione peroxidase, free radicals production and thiol content were increased in groups that were subjected to neonatal interventions fed n-3 PUFAs deficient diet. Additionally, reduced mitochondrial potential was observed in handled animals. Total thiol revealed a neonatal stress effect, since animals subjected to neonatal interventions displayed lower thiol content. In conclusion, we observed that a chronic treatment with deficient n-3 PUFAs diet, from the puberty period on, increased free radicals production and imbalanced antioxidant enzymes activities, and these increases were higher in animals subjected to neonatal interventions.

Nutritional n-3 PUFAs deficiency during perinatal periods alters brain innate immune system and neuronal plasticity-associated genes.

Low dietary intake of the n-3 polyunsaturated fatty acids (PUFAs) is a causative factor of neurodevelopmental disorders. However the mechanisms linking n-3 PUFAs low dietary intake and neurodevelopmental disorders are poorly understood. Microglia, known mainly for their immune function in the injured or infected brain, have recently been demonstrated to play a pivotal role in regulating maturation of neuronal circuits during normal brain development. Disruption of this role during the perinatal period therefore could significantly contribute to psychopathologies with a neurodevelopmental neurodevelopmental component. N-3 PUFAs, essential lipids and key structural components of neuronal membrane phospholipids, are highly incorporated in cell membranes during the gestation and lactation phase. We previously showed that in a context of perinatal n-3 PUFAs deficiency, accretion of these latter is decreased and this is correlated to an alteration of endotoxin-induced inflammatory response. We thus postulated that dietary n-3 PUFAs imbalance alters the activity of microglia in the developing brain, leading to abnormal formation of neuronal networks. We first confirmed that mice fed with a n-3 PUFAs deficient diet displayed decreased n-3 PUFAs levels in the brain at post-natal days (PND)0 and PND21. We then demonstrated that n-3 PUFAs deficiency altered microglia phenotype and motility in the post-natal developing brain. This was paralleled by an increase in pro-inflammatory cytokines expression at PND21 and to modification of neuronal plasticity-related genes expression. Overall, our findings show for the first time that a dietary n-3 PUFAs deficiency from the first day of gestation leads to the development of a pro-inflammatory condition in the central nervous system that may contribute to neurodevelopmental alterations.

Dietary n-3 polyunsaturated fatty acid deprivation together with early maternal separation increases anxiety and vulnerability to stress in adult rats

Low concentrations of n-3 polyunsaturated fatty acid (PUFA) and chronic stress are implicated in susceptibility to mood disorders. We have investigated the combined effects of chronic n-3 PUFA dietary deficiency and early maternal separation (MS) stress on the reactivity to stressful situations of rats as adults. Pups fed a control or an n-3 PUFA deficient diet were daily separated for two weeks before weaning They were all tested at 3 month-old to determine their anxiety, and their ability to learn two aversive tasks differing in the control they could exert on the situation: auditory fear conditioning and brightness avoidance discrimination. Neither the n-3 PUFA-deficient diet nor MS alone significantly affected behavior. But n-3 PUFA-deficient rats that had been separated were more anxious and fearful in inescapable situations, while their ability to cope with an aversive avoidance task remained unaffected. These results support the notion that PUFA-unbalanced diet, together with stress, may be a determinant risk factor in emotional disorders.

Dietary n-6 PUFA deprivation downregulates arachidonate but upregulates docosahexaenoate metabolizing enzymes in rat brain

BackgroundDietary n-3 polyunsaturated fatty acid (PUFA) deprivation increases expression of arachidonic acid (AA 20:4n-6)-selective cytosolic phospholipase A2 (cPLA2) IVA and cyclooxygenase (COX)-2 in rat brain, while decreasing expression of docosahexaenoic acid (DHA 22:6n-3)-selective calcium-independent iPLA2 VIA. Assuming that these enzyme changes represent brain homeostatic responses to deprivation, we hypothesized that dietary n-6 PUFA deprivation would produce changes in the opposite directions. MethodsBrain expression of PUFA-metabolizing enzymes and their transcription factors was quantified in male rats fed an n-6 PUFA adequate or deficient diet for 15weeks post-weaning. ResultsThe deficient compared with adequate diet increased brain mRNA, protein and activity of iPLA2 VIA and 15-lipoxygenase (LOX), but decreased cPLA2 IVA and COX-2 expression. The brain protein level of the iPLA2 transcription factor SREBP-1 was elevated, while protein levels were decreased for AP-2α and NF-κB p65, cPLA2 and COX-2 transcription factors, respectively. ConclusionsWith dietary n-6 PUFA deprivation, rat brain PUFA metabolizing enzymes and some of their transcription factors change in a way that would homeostatically dampen reductions in brain n-6 PUFA concentrations and metabolism, while n-3 PUFA metabolizing enzyme expression is increased. The changes correspond to reported in vitro enzyme selectivities for AA compared with DHA.

Sodium appetite in adult rats following ω-3 polyunsaturated fatty acid deficiency in early development

We examined the effect of ω-3 polyunsaturated fatty acid (PUFA) deficiency during development on sodium appetite. Being raised on an ω-3 PUFA deficient diet increased the intake of 0.5 M NaCl following furosemide-induced sodium depletion by 40%. This occurred regardless of the diet they were maintained on later in life, and the increased consumption persisted for 3 days. In a second study, animals were administered furosemide and low-dose captopril. Sodium consumption of deficient raised animals was again higher than that of the control raised. Fos immunoreactivity in brain areas associated with sodium appetite and excretion were not influenced by diet. Our findings indicate that inadequate dietary ω-3 PUFA during development results in an exaggerated sodium appetite later in life.

Effects of a post-weaning n-3 polyunsaturated fatty acid deficient diet on spatial memory processes in rats

Effects of a post-weaning n-3 polyunsaturated fatty acid deficient diet on spatial memory processes in rats

Synergistic effects of stress and omega-3 fatty acid deprivation on emotional response and brain lipid composition in adult rats

The aim was to determine the consequences of multi-generational n-3 polyunsaturated fatty acids (PUFA) deficiency on emotional response in rats subjected to maternal separation (MS) as chronic early life stress. Pups fed a control or an n-3 PUFA deficient diet were daily separated for 2 weeks before weaning. In adult rats, reward response was assessed by sucrose consumption and reactivity to novelty using openfield test. Both n-3 PUFA deficiency and MS increased reward response and impulsivity. Moreover, nutritional deficiency and stress acted in synergy to elevate sucrose intake by 80%, compared to control conditions. n-3 PUFA deprivation induced a depletion of docosahexanoeic acid of brain membranes by 70% compensated by increase in 22:5 n-6 and arachidonic acid (AA) levels. The diet-induced AA increase was, however, significantly higher in MS rats. This suggests that n-3 PUFA deficit could be an environmental risk increasing vulnerability to depressive-like response induced by chronic stress.

Reduced numbers of dopamine neurons in the substantia nigra pars compacta and ventral tegmental area of rats fed an n-3 polyunsaturated fatty acid-deficient diet: A stereological study

Inadequate dietary n-3 polyunsaturated fatty acid (PUFA) content is associated with altered function of the CNS dopamine systems. In this study, the effects of dietary n-3 PUFA content were determined on dopamine cell number and morphology. Adult (postnatal day 70), male, Long-Evans rats were raised from conception on diets containing adequate (control) or negligible n-3 PUFAs. The number and morphology of tyrosine hydroxylase-positive cells in the substantia nigra pars compacta and ventral tegmental area were determined stereologically. The number of tyrosine hydroxylase-positive cells in rats fed the n-3 PUFA-deficient diet was 33.9% lower in the substantia nigra pars compacta and 33.7% lower in the ventral tegmental area than in those fed the control diet (P<0.05); however, the volume of tyrosine hydroxylase-positive cell bodies was not different between diet groups in either brain region. Rats fed the n-3 PUFA-deficient diet also exhibited dendritic depletion and isolation of tyrosine hydroxylase-positive cells compared to rats fed the control diet, which had clustering of tyrosine hydroxylase-positive cells and extensive dendritic arborization. These findings support a role for n-3 PUFAs in the survival of dopamine neurons and suggest that altered dopamine cell number, as well as function, contributes to the behavioral effects observed in rats raised on n-3 PUFA-deficient diets.

Effects of a n-3 PUFA deficient diet on the expression of retinoid nuclear receptors, neurogranin and neuromodulin in rat brain

A lot of studies performed in rodents revealed that n-3 polyunsaturated fatty acid (PUFA) deficient diets could induce deficits of learning capacities but the mechanisms involved are not well known. Retinoic acid (RA) and its nuclear receptors (RAR and RXR) play a central role in the maintenance of cognitive processes and synaptic plasticity via its action on target genes that are neurogranin (RC3) and neuromodulin (GAP43). Given some interferences were described between the retinoid and fatty acid signaling pathways, we investigated the effects of a _α-linolenic acid (18: 3 n-3) deficient diet on retinoic acid nuclear receptors (RAR, and RXR), on GAP43 and RC3, and on blood and brain fatty acid composition in rats at three times of diet: 3, 9 and 18 weeks. In blood and brain of these animals, we observed a severe n-3 PUFA deficit (18:3 n-3, 20:5 n-3 and particularly 22:6 n-3) associated with an increase in the n-6 PUFA content (mainly 22:5 n-6). Real-time PCR and western blot analysis allowed us to note that retinoid signaling, GAP43 and RC3 expression were affected in the striatum of the n-3 PUFA deprived rats.

Docosahexaenoic acid synthesis from α-linolenic acid by rat brain is unaffected by dietary n-3 PUFA deprivation

Rates of conversion of alpha-linolenic acid (alpha-LNA, 18:3n-3) to docosahexaenoic acid (DHA, 22:6n-3) by the mammalian brain and the brain's ability to upregulate these rates during dietary deprivation of n-3 polyunsaturated fatty acids (PUFAs) are unknown. To answer these questions, we measured conversion coefficients and rates in post-weaning rats fed an n-3 PUFA deficient (0.2% alpha-LNA of total fatty acids, no DHA) or adequate (4.6% alpha-LNA, no DHA) diet for 15 weeks. Unanesthetized rats in each group were infused intravenously with [1-(14)C]alpha-LNA, and their arterial plasma and microwaved brains collected at 5 minutes were analyzed. The deficient compared with adequate diet reduced brain DHA by 37% and increased brain arachidonic (20:4n-6) and docosapentaenoic (22:5n-6) acids. Only 1% of plasma [1-(14)C]alpha-LNA entering brain was converted to DHA with the adequate diet, and conversion coefficients of alpha-LNA to DHA were unchanged by the deficient diet. In summary, the brain's ability to synthesize DHA from alpha-LNA is very low and is not altered by n-3 PUFA deprivation. Because the liver's reported ability is much higher, and can be upregulated by the deficient diet, DHA converted by the liver from circulating alphaLNA is the source of the brain's DHA when DHA is not in the diet.

Cerebral Asymmetry and Behavioral Lateralization in Rats Chronically Lacking n-3 Polyunsaturated Fatty Acids

Anatomic and functional brain lateralization underlies hemisphere specialization for cognitive and motor control, and deviations from the normal patterns of asymmetry appear to be related to behavioral deficits. Studies on n-3 polyunsaturated fatty acid (PUFA) deficiency and behavioral impairments led us to postulate that a chronic lack of n-3 PUFA can lead to changes in lateralized behavior by affecting structural or neurochemical patterns of asymmetry in motor-related brain structures. We compared the effects of a chronic n-3 PUFA deficient diet with a balanced diet on membrane phospholipid fatty acids composition and immunolabeling of choline acetyltransferase (ChAt), as a marker of cholinergic neurons, in left and right striatum of rats. Lateral motor behavior was assessed by rotation and paw preference. Control rats had an asymmetric PUFA distribution with a right behavioral preference, whereas ChAt density was symmetrical. In deficient rats, the cholinergic neuron density was 30% lower on the right side, associated with a loss of PUFA asymmetry and behavior laterality. They present higher rotation behavior, and significantly more of them failed the handedness test. These results indicate that a lack of n-3 PUFA is linked with a lateral behavior deficit, possibly leading to cognitive disturbances.

Polyunsaturated fatty acid deficiency reverses effects of alcohol on mitochondrial energy metabolism

Polyunsaturated fatty acids (PUFA) deficiency is common in patients with alcoholic liver disease. The suitability of reversing such deficiency remains controversial. The aim was to investigate the role played by PUFA deficiency in the occurrence of alcohol-related mitochondrial dysfunction. Wistar rats were fed either a control diet with or without alcohol (control and ethanol groups) or a PUFA deficient diet with or without alcohol (PUFA deficient and PUFA deficient+ethanol groups). After 6 weeks, liver mitochondria were isolated for energetic studies and fatty acid analysis. Mitochondria from ethanol fed rats showed a dramatic decrease in oxygen consumption rates and in cytochrome oxidase activity. PUFA deficiency showed an opposite picture. PUFA deficient+ethanol group roughly reach control values, regarding cytochrome oxidase activity and respiratory rates. The relationship between ATP synthesis and respiratory rate was shifted to the left in ethanol group and to the right in PUFA-deficient group. The plots of control and PUFA deficient+ethanol groups were overlapping. Phospholipid arachidonic over linoleic ratio closely correlated to cytochrome oxidase and oxygen uptake. PUFA deficiency reverses alcohol-related mitochondrial dysfunction via an increase in phospholipid arachidonic over linoleic ratio, which raises cytochrome oxidase activity. Such deficiency may be an adaptive mechanism.

Age-related changes in phospholipid fatty acid composition and monoaminergic neurotransmission in the hippocampus of rats fed a balanced or an n-3 polyunsaturated fatty acid-deficient diet

The influence of aging (2, 6, 12, and 24 months) on hippocampal lipid composition and neurochemical markers (endogenous noradrenaline, serotonin levels, monoamine oxidase (MOA) activities) was studied in rats fed a control or an n-3 polyunsaturated fatty acid (PUFA)-deficient diet. The n-3 PUFA deficiency reduced the 22:6 (n-3) level, compensated by the increase in 22:5 (n-6). However, the difference in 22:6 (n-3) content between control and deficient rats was less between 2 and 12 months and then became stable. There was an overall age-induced decrease in the major phospholipid classes phosphatidylethanolamine (PE), and phosphatidylcholine (PC) whereas the minor classes, phosphatidylinositol (PI), phosphatidylserine (PS), and sphingomyelin (SM), were greatly increased, regardless of diet. The n-3 PUFA deficiency induced a reduction in the PS level, concomitant with a higher level in MAO-B activity as compared to control rats at the age of 24 months. The age-related evolution of the MAO-B activity was parallel with that of noradrenaline levels in both dietary groups. The noradrenaline and serotonin levels were modified according to age but without effect of the n-3 PUFA deficiency. Results showed that the hippocampus sustained specific age-induced modifications in lipid composition and neurotransmission factors, often with a transition period between 6 and 12 months.

Lipids of arctic charr,Salvelinus alpinus (L.) II. Influence of dietary fatty acids on the elongation and desaturation of linoleic and linolenic acid

Arctic charr,Salvelinus alpinus L. were fed five test diets containing 0% or 1% of different polyunsaturated fatty acids (PUFA) for 93 days. The fish were injected intraperitoneally with (1-(14)C)-18:2(n-6) or (1-(14)C)-18:3(n-3), and the bioconversion to longer chain PUFA studied. The conversion rate in neutral lipids was slow, with most label found as the fatty acid injected, while extensive modification took place prior to or during incorporation into polar lipids. Linolenic acid was preferred over linoleic acid as substrate for elongation and desaturation regardless of diet. In polar lipids, the predominant products of (1-(14)C)-18:2(n-6) metabolism were generally 20:3(n-6) and 20:4(n-6), while 18:4(n-3), 20:5(n-3) and 22:6(n-3) were the major products of (1-(14)C)-18:3(n-3) metabolism. The lack of radioactivity in 22:5(n-6) suggests that Δ 4 desaturation is specific for (n-3) PUFA. Feeding the PUFA deficient diet reduced the Δ 5 desaturation compared to fish maintained on PUFA supplemented diets. The Δ 6 desaturation was only reduced in fish fed C18 PUFA and injected with (1-(14)C)-18:3(n-3). Longer chain C20 and C22 PUFA, particularly those of the (n-3) family, exerted some inhibition on the elongation and desaturation of injected fatty acids compared to those fed C18 PUFA. The incorporation of radiolabelled fatty acids into polar lipids of fish fed a commercial diet was very low, and the desaturation neglectible in both polar and neutral lipids, showing that Arctic charr under culture conditions do not convert short chain PUFA to longer chain metabolites.

Changes in the fatty acid composition of phospholipids from turbot ( Scophthalmus maximus) in relation to dietary polyunsaturated fatty acid deficiencies

1. 1. Young turbot (1–20 g) were maintained for not less than 14 weeks on three diets: (1) a control diet containing normal amounts of polyunsaturated fatty acids (PUFA); (2) a diet totally deficient in PUFA; (3) a diet deficient in the ( n-6) series of PUFA but containing ( n-3) PUFA. 2. 2. At 14 weeks the fatty acid compositions of the phospholipids from liver, gut, gills and muscle were analysed. Large changes in the amounts of PUFA in the phospholipids were found. 3. 3. Fish maintained on the totally PUFA deficient diet 2 had retained arachidonic acid, 20:4( n-6), and docosahexaenoic acid, 22:6( n-3), at the expense of eicosapentaenoic acid, 20:5(n-3). 4. 4. Fish maintained on the ( n-6) PUFA-deficient diet (3) contained decreased amounts of 20:4( n-6) and 22:6( n-3) while retaining 20:5( n-3). 5. 5. In all cases phosphatidylinositol had the lowest n-3 n-6 ratios. These results are discussed in terms of PUFA function.

Perinatal linoleate deprivation impairs learning and memory in adult rats

Rats receiving polyunsaturated fatty acid (PUFA) deficient diets during the perinatal period showed in adult age undisturbed acquisition of a footshock motivated brightness discrimination task, but a significant impairment of retention. The same effects on retention were obtained in rats receiving the PUFA deficient diet in adulthood, when the behavioral parameters were investigated at the end of the dietary treatment.