Effects Of Dietary Fatty Acids Research Articles

Differential Effects of Dietary Fatty Acids on Body Composition and Adiposity

Recent evidence has highlighted that fat accumulation, particularly abdominal fat distribution, is strongly associated with metabolic disturbance. It is also well-recognized that the metabolic responses to variations in macronutrients intake can affect body composition. Previous studies suggest that the quality of dietary fats can be considered as the main determinant of body-fat deposition, fat distribution, and body composition without altering the total body weight; however, the effects of dietary fats on body composition have controversial results. There is substantial evidence to suggest that saturated fatty acids are more obesogen than unsaturated fatty acids, and with the exception of some isomers like conjugate linoleic acid, most dietary trans fatty acids are adiposity enhancers, but there is no consensus on it yet. On the other hand, there is little evidence to indicate that higher intake of the n-3 and the n-6 polyunsaturated fatty acids can be beneficial in attenuating adiposity, and the effect of monounsaturated fatty acids on body composition is contradictory. Accordingly, the content of this review summarizes the current body of knowledge on the potential effects of the different types of dietary fatty acids on body composition and adiposity. It also refers to the putative mechanisms underlying this association and reflects on the controversy of this topic.

Dietary fat and obesity as modulators of breast cancer risk: Focus on DNA methylation.

Breast cancer (BC) is the most common cancer and second leading cause of cancer mortality in women worldwide. Validated biomarkers enhance efforts for early detection and treatment, which reduce the risk of mortality. Epigenetic signatures have been suggested as good biomarkers for early detection, prognosis and targeted therapy of BC. Here, we highlight studies documenting the modifying effects of dietary fatty acids and obesity on BC biomarkers associated with DNA methylation. We focus our analysis on changes elicited in writers of DNA methylation (i.e., DNA methyltransferases), global DNA methylation and gene-specific DNA methylation. To provide context, we precede this discussion with a review of the available evidence for an association between BC incidence and both dietary fat consumption and obesity. We also include a review of well-vetted BC biomarkers related to cytosine-guanine dinucleotides methylation and how they influence BC risk, prognosis, tumour characteristics and response to treatment. LINKED ARTICLES: This article is part of a themed section on The Pharmacology of Nutraceuticals. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v177.6/issuetoc.

Antioxidants, Dietary Fatty Acids, and Sperm: A Virtual Reality Applied Game for Scientific Dissemination.

Fatty acid (FA) profile appears to be critical to infertility, and the effects of dietary FAs on sperm FA content are a current focus of studies in the field of nutrition and reproduction. Starting from a validated “OXISTRESS” model in which modification of FA content results to influence reactive oxygen species, antioxidants, isoprostanes, cytokines, sperm kinetic, and acrosome reaction, we developed a virtual reality game where the player, in order to improve the health of some virtual spermatozoa, is called to take dietary choices and then discover their consequences on the main biological aspects. In the LabVR of the University of Siena, a team of VR environment designer and developer used Unity development engine to make the experience run on Oculus Quest and a wireless 6DOF (six degrees of freedom of movement in 3D space) VR Headset. In the game, the player is immersed in the epididymis and observes closer how dietary n-3 may change the sperm plasma membrane and consequently modify sperm traits. A simulation game in the virtual reality may represent a tool to give greater visibility to scientific data in the relevance of appropriate dietary habits in the human health.

The effects of dietary fatty acids in the physiological outcomes of maternal high-fat diet on offspring energy homeostasis in mice.

The early-life origins of disease hypothesis has been applied to obesity research and modeled through overnutrition, usually with a high-fat diet (HFD). Since the obesity epidemic coincided with societal change in dietary fat consumption, rather than amount, manipulation of fatty acid (FA) profile is an under-investigated area of study. Additionally, the binding of FAs to nuclear receptors may have persistent intergenerational, extranutritive endocrinological effects that interact with the actions of reproductive steroids causing sex-dependent effects. To determine the role of FA type in the effects underlying maternal HFD, we fed wild-type C57BL6/J mating pairs, from preconception through lactation, a HFD with high saturated fat levels from coconut oil or high linoleic acid (LA) levels from vegetable oil. Male and female offspring body weight and food intake were measured weekly for 25 weeks. Assays for glucose metabolism, body composition, and calorimetry were performed at 25 weeks. Plasma metabolic peptides and liver mRNA were measured terminally. Obesity was primarily affected by adult rather than maternal diet in males, yet in females, maternal HFD potentiated the effects of adult HFD. Maternal HFD high in LA impaired glucose disposal in males weaned onto HFD and insulin sensitivity of females. Plasma leptin correlated with adiposity, but insulin and insulin receptor expression in the liver were altered by maternal LA in males. Our results suggest that maternal FA profile is most influential on offspring glucose metabolism and that adult diet is more important than maternal diet for obesity and other parameters of metabolic syndrome.

The effects of dietary fatty acids on bone, hematopoietic marrow and marrow adipose tissue in a murine model of senile osteoporosis

Purpose: Marrow adipose tissue (MAT) expansion and associated lipotoxicity are important drivers of age-related bone loss and hematopoietic bone marrow (HBM) atrophy. Fish oil and borage oil (rich in ω3 fatty acids) can partially prevent aged-related bone loss in SAMP8 mice. However, whether preservation of bone mass in this progeria model is associated with MAT volumes remains unknown.Results: MAT volume fraction (MAT%) showed a negative association with hematopoietic bone marrow (HBM%;r=-0.836, p<0.001) and bone (bone%;r=-0.344, p=0.013) volume fractions.Adjusting for multiple comparisons, bone% was higher and MAT% was lower in Fish oil (FO)-supplemented groups vs. controls (p<0.001). HBM% did not differ significantly between the four groups. However, in the group supplemented with FO, HBM comprised higher fractions and MAT constituted lower fractions of total marrow vs. controls (p<0.001).Conclusion: Feeding FO-enriched diet prevented age-related bone and HBM loss, by reducing MAT expansion. Our results further emphasize on the role(s) of MAT expansion in bone and HBM atrophy.Methods: SAMP8 mice (n>9 /group) were allocated into 4 categories and fed a control ration, FO-, sunflower oil (SFO)- and borage oil-enriched diets for lifetime. Femurs were scanned using microcomputed tomography (μCT) and bone, MAT, and HBM volumes were determined using an image analysis software.

Effects of dietary fatty acids on the reproduction of South American female catfish Rhamdia quelen (Quoy &amp; Gaimard, 1824)

The effects of a diet supplemented with 5% marine fish oil, 5% refined palm oil, 5% soybean oil, and a combination of the three on reproductive parameters of females Rhamdia quelen was investigated. Spawning was artificially induced to evaluate rates of fertilization, hatching and larvae normality. Fatty acid profiles of the diets, ovaries and oocytes were determined. A higher spawning rate (%) was observed for diets containing fish oil (78.65 ± 3.60) and palm oil (77.15 ± 3.97), followed by oil mix (65.46 ± 4.57). The diet containing soybean oil was associated with significantly lower fertilization (60.14 ± 5.66; P 0.05) were observed for all tested diets, whit 289.77 ± 23.90 (palm oil) until 323.31 ± 38.45 oocytes g -1 body weight (fish oil). The treatments were not shown to influence oocyte size, larval size or rate of larva deformity. Oocyte fatty acid composition was like that of gonads. Docosahexaenoic (DHA; C22:6 n-3) fatty acid was preferentially deposited in ovaries and oocytes. Ratios of n3/n6, DHA/EPA, EPA/ARA, did not affect the reproductive performance of females. Therefore, regarding female reproductive performance, the vegetable lipid sources tested are suitable for being used in R. quelen diet, and palm oil, in particular, is considered an excellent alternative to fish oil.

Modulation of endothelial cell responses and vascular function by dietary fatty acids.

Healthy and functional endothelial cells play important roles in maintaining vascular homeostasis, whereas endothelial dysfunction initiates and exacerbates vascular disease progression. Interventional studies with dietary fatty acids have shown that these molecules have varying effects on vascular function. It is hypothesized that the actions of dietary fatty acids on vascular function may be mediated in part through endothelial cells. This review summarizes the results of studies that have examined the acute and chronic effects of dietary fatty acids on endothelial function and vascular properties in humans, as well as the potential mechanisms by which n-3 polyunsaturated fatty acids regulate endothelial function. Altogether, this article provides an extensive review of how fatty acids contribute to vascular function through their ability to modulate endothelial cells and discusses relationships between dietary fatty acids and endothelial cells in the context of vascular dysfunction.

Dietary Fatty Acids Amplify Inflammatory Responses to Infection through p38 MAPK Signaling.

Obesity is an important risk factor for severe asthma exacerbations, which are mainly caused by respiratory infections. Dietary fatty acids, which are increased systemically in obese patients and are further increased after high-fat meals, affect the innate immune system and may contribute to dysfunctional immune responses to respiratory infection. In this study we investigated the effects of dietary fatty acids on immune responses to respiratory infection in pulmonary fibroblasts and a bronchial epithelial cell line (BEAS-2B). Cells were challenged with BSA-conjugated fatty acids (ω-6 polyunsaturated fatty acids [PUFAs], ω-3 PUFAs, or saturated fatty acids [SFAs]) +/- the viral mimic polyinosinic:polycytidylic acid (poly[I:C]) or bacterial compound lipoteichoic acid (LTA), and release of proinflammatory cytokines was measured. In both cell types, challenge with arachidonic acid (AA) (ω-6 PUFA) and poly(I:C) or LTA led to substantially greater IL-6 and CXCL8 release than either challenge alone, demonstrating synergy. In epithelial cells, palmitic acid (SFA) combined with poly(I:C) also led to greater IL-6 release. The underlying signaling pathways of AA and poly(I:C)- or LTA-induced cytokine release were examined using specific signaling inhibitors and IB. Cytokine production in pulmonary fibroblasts was prostaglandin dependent, and synergistic upregulation occurred via p38 mitogen-activated protein kinase signaling, whereas cytokine production in bronchial epithelial cell lines was mainly mediated through JNK and p38 mitogen-activated protein kinase signaling. We confirmed these findings using rhinovirus infection, demonstrating that AA enhances rhinovirus-induced cytokine release. This study suggests that during respiratory infection, increased levels of dietary ω-6 PUFAs and SFAs may lead to more severe airway inflammation and may contribute to and/or increase the severity of asthma exacerbations.

A high-fat diet induces rapid changes in the mouse hypothalamic proteome

BackgroundProlonged over-consumption of a high-fat diet (HFD) commonly leads to obesity and insulin resistance. However, even 3 days of HFD consumption has been linked to inflammation within the key homeostatic brain region, the hypothalamus.MethodsMice were fed either a low-fat diet (LFD) or HFD containing 10% or 60% (Kcal) respectively from fat for 3 days. Mice were weighed, food intake measured and glucose tolerance calculated using intraperitoneal glucose tolerance tests (IPGTT). Proteomic analysis was carried out to determine if hypothalamic proteins were changed by a HFD. The direct effects of dietary fatty acids on mitochondrial morphology and on one of the proteins most changed by a HFD, dihydropyrimidinase-related protein 2 (DRP-2) a microtubule-associated protein which regulates microtubule dynamics, were also tested in mHypoE-N42 (N42) neuronal cells challenged with palmitic acid (PA) and oleic acid (OA).ResultsMice on the HFD, as expected, showed increased adiposity and glucose intolerance. Hypothalamic proteomic analysis revealed changes in 104 spots after 3 days on HFD, which, when identified by LC/MS/MS, were found to represent 78 proteins mainly associated with cytoskeleton and synaptic plasticity, stress response, glucose metabolism and mitochondrial function. Over half of the changed proteins have also been reported to be changed in neurodegenerative conditions such as Alzheimer’s disease. Also,in N42 neurons mitochondrial morphology and DRP-2 levels were altered by PA but not by OA.ConclusionThese results demonstrate that within 3 days, there is a relatively large effect of HFD on the hypothalamic proteome indicative of cellular stress, altered synaptic plasticity and mitochondrial function, but not inflammation. Changes in N42 cells show an effect of PA but not OA on DRP-2 and on mitochondrial morphology indicating that long-chain saturated fatty acids damage neuronal function.

Abstract P287: Hypocholesterolemic Effect of Dietary Stearic Acid May Be Partly Mediated via Alterations in Fecal Bile Acid Metabolism

Introduction: Dietary fat quality has a significant impact on CVD risk. Among the saturated fatty acids (FA), we and others have documented that stearic (18:0) is unique because, unlike shorter chain FA (12:0, 14:0, 16:0), it does not raise plasma LDL-C levels, relative to monounsaturated FA, such as oleic acid (18:1). The mechanism(s) responsible for this effect are not fully elucidated. Hypothesis: We tested the hypothesis that the hypocholesterolemic effect of dietary 18:0 and 18:1 relative to 16:0 is mediated by alterations in fecal bile acid metabolism. Methods: Primary (cholic, chenodeoxycholic) and secondary bile acids (SBA: lithocholic [LA], deoxycholic [DCA]) were quantified in stool samples from a randomized controlled cross-over trial examining the effect of dietary FA on CVD risk factors. Subjects (N=20 postmenopausal women, 50-85 years, BMI 25-35kg/m 2 , LDL-C &gt;100mg/dL) consumed each diet for 35 days separated by a 2 week washout period. Diets provided 55%E carbohydrate, 15%E protein and 30%E fat with half of the fat provided by 16:0, 18:0 or 18:1, respectively. CVD risk factors (lipids, glucose, insulin, inflammatory markers) were measured using standard methodology. For fecal bile acids analysis, freeze dried samples were spiked with the corresponding deuterated internal standards, followed by an overnight extraction, purification and analysis using reversed-phase liquid chromatography coupled with electrospray ionization quadrupole time of flight mass spectrometry. Quantification was by isotopic dilution. Spearman correlation coefficients were calculated between bile acids and CVD risk factors. Results: Fecal total SBA levels were significantly lower after subjects consumed the 18:0 (4.5±3.9 umol/g) compared to the 18:1 (6.8±5.7 umol/g) diet, with intermediate levels after the 16:0 diet (5.2±3.6 umol/g). This was predominantly due to significantly lower LA, and to a lesser extent DCA levels. No detectable differences were observed in primary bile acids levels. Total, LA and DCA levels were positively correlated with insulin (r=0.38 to 0.45; p&lt;0.05), hsCRP (r=0.31 to 0.37, p&lt;0.02), TG (r=0.46 to 0.60; p&lt;0.001), VLDL-C (r=0.47 to 0.63; p&lt;0.001), TC/LDL-C (r=0.42 to 0.63; p&lt;0.001) and LDL-C/HDL-C (0.37 to 0.57; p&lt;0.001) ratios, and negatively with HDL-C (r= -0.51 to -0.44; p&lt;0.001) levels. LA levels were also positively correlated with LDL-C levels (r=0.33; p=0.011). Conclusion: These data suggest that the hypocholesterolemic effect of dietary 18:0 was not mediated by increased bile acid excretion as was observed with dietary 18:1. Instead, dietary 18:0 appears to have an inhibitory effect on hydrophobic SBA synthesis in the intestine, which in turn could reduce the efficiency of cholesterol solubilization and thus cholesterol absorption. Further studies on the effects of dietary 18:0 on gut microbiome populations involved in SBA synthesis are warranted.

Assessment on the effects of dietary fatty acids on growth performance, body compositions, plasma lysozyme activity and sensorial quality of juvenile marble goby, Oxyeleotris marmorata

The present study aimed to evaluate the effects of dietary fatty acids on the growth performance, body compositions, plasma lysozyme activity and sensorial quality of juvenile marble goby. Four experimental diets were formulated to contain different dietary oleic acid (OA, 18:1n-9)/ linoleic acid (LA, 18:2n-6) ratios ranged from 0.5 to 2.4 by manipulating the dietary oil sources. Fish oil was the main oil source for control diet (FO), while the other three diets, 50% of the dietary lipid was contributed by plant oil in which soybean oil, canola oil and a mixture of soybean and canola oils were added at the expense of fish oil and expressed as SO, CO and SOCO respectively. The results showed that feed conversion ratio (FCR) of fish fed CO was significantly higher (P < 0.05) than fish fed FO and SO, indicating that high dietary OA adversely affected the feed utilization of fish which then resulted in inferior weight gain. On the other hand, dietary OA/ LA ratio did not significantly (P > 0.05) affect the whole body and fillet proximate compositions, and biological indices of fish except for hepatosomatix index (HSI) that was significantly higher in fish fed LA rich diets, SO and SOCO. Hepatic lipid of fish fed SOCO was significantly higher than that of other treatment group, although the dietary LA content in SOCO was lower than that in SO diet, suggesting that feeding fish with LA rich diet increased the HSI, and the interaction between fatty acids in the mixture of soybean and canola oils promoted the lipid accumulation in liver. Besides, high dietary LA positively affected the fillet sensorial quality. On the other hand, plasma lysozyme activity of the fish was increased with the increasing ratio of dietary omega-3 polyunsaturated fatty acids/ omega-6 polyunsaturated fatty acids.

Molecular effects of dietary fatty acids on brain insulin action and mitochondrial function.

The prevalence of obesity and its co-morbidities such as insulin resistance and type 2 diabetes are tightly linked to increased ingestion of palatable fat enriched food. Thus, it seems intuitive that the brain senses elevated amounts of fatty acids (FAs) and affects adaptive metabolic response, which is connected to mitochondrial function and insulin signaling. This review will address the effect of dietary FAs on brain insulin and mitochondrial function with a special emphasis on the impact of different FAs on brain function and metabolism.

Growth and metabolomic responses of Pacific white shrimp (Litopenaeus vannamei) to different dietary fatty acid sources and salinity levels

The outstanding benefits of and strong interest in the inland low-salinity culture of penaeid shrimp have led to the growth of this industry worldwide. This study aimed to explore the effects of dietary fatty acids on shrimp in low-salinity culture. Individuals of the marine white shrimp Litopenaeus vannamei were fed one of three diets (coconut oil, fish oil, or an equal mixture of both) of differing fatty acid profiles for eight weeks while being maintained at two different salinities (3 or 30 psu). Then, a GC-TOF/MS-based metabolomics analysis was performed to reveal the regulatory roles of fatty acids in shrimp growth, survival and osmoregulation at two salinities. The shrimp fed the mixed oil diet had higher weight gain and survival, and those fed the diet with only fish oil added exhibited higher unsaturated fatty acid levels in the gills and hepatopancreas irrespective of salinity. Na+/K+-ATPase and total ATPase activities were lowest in the shrimp fed the mixed oil diet at both salinities. When coconut oil was the only lipid source, shrimp tissues contained higher tyrosine, lysine and serine levels at 3 psu than at 30 psu. In contrast, the shrimp fed fish oil as the sole lipid source had higher glucose at 3 psu than at 30 psu. This study indicates that appropriate supplementation of dietary unsaturated and saturated fatty acids can improve shrimp osmoregulation capacity and thus promote shrimp growth and survival in low-salinity water.

Association of Dietary Fatty Acids with Blood Lipids is Modified by Physical Activity in Adolescents: Results from the GINIplus and LISA Birth Cohort Studies.

The role of consuming different types of fatty acids (FA) at the expense of carbohydrates (CHO), on the blood lipid profile of adolescents is largely unknown, as is the modulating effect of different levels of physical activity (PA). Children from the GINIplus and LISA birth cohorts, with complete data on dietary FA (assessed by food-frequency questionnaires), objectively-measured PA (assessed by accelerometers) and blood lipids (lipoprotein cholesterol and triglycerides) at age 15 years, were included (N = 837). Sex-stratified associations between dietary FA and blood lipids were assessed by linear regression in substitution models which represented isocaloric replacements of CHO with saturated FA (SFA), monounsaturated FA (MUFA), n-3 polyunsaturated FA (PUFA) or n-6 PUFA. To assess the interactions with PA, analyses were then performed stratified by tertiles of different PA levels (sedentary, lifestyle, moderate-to-vigorous (MVPA)). Both sexes presented a significant inverse association between MUFA and triglycerides, and females a direct association between n-3 PUFA and high-density lipoprotein. Stratifying by PA tertiles, associations were mainly restricted to participants with the lowest levels of lifestyle PA, or the highest time spent sedentary. The effects of dietary FA on the lipid profile vary in an activity-specific manner, emphasizing possible synergistic roles of diet and PA.

Dietary oleic acid-induced CD36 promotes cervical cancer cell growth and metastasis via up-regulation Src/ERK pathway

Epidemiological and experimental studies have revealed strong associations between dietary lipids and cancer risk. However, the molecular mechanisms underlying the effects of dietary fatty acids on the genesis and progression of cancer have been poorly explored. In this study, we found that a high olive oil diet stimulated cervical cancer (CC) carcinogenesis, and oleic acid (OA), the main lipid in olive oil, was associated with increased malignancy in HeLa cells. OA up-regulated the expression of CD36, which is the best characterized fatty acid transporter. Inhibiting CD36 prevented the tumor-promoting effects of OA, while overexpressing CD36 mimicked the effects of OA. Clinically, CD36 expression was positively correlated with tumor progression and poor prognosis in patients with CC. Furthermore, OA induced Src kinase and downstream ERK1/2 pathway activation in a CD36-dependent manner. Pretreatment of HeLa cells with an Src kinase inhibitor largely blocked the tumor-promoting effect of OA. Our findings suggest that dietary OA exerts a stimulatory effect on CC growth and metastasis, and CD36 might be a promising therapeutic target that acts against CC through an Src/ERK-dependent signaling pathway.

Effects of Dietary Fatty Acids in Pancreatic Beta Cell Metabolism, Implications in Homeostasis.

Fatty acids are involved in several metabolic processes, including the development of metabolic and cardiovascular diseases. In recent years a disease that has received escalated interest is type 2 diabetes (T2D). Many contributing factors including a high-caloric diet rich in dietary saturated fats have been broadly characterized as triggers of T2D. Insulin resistance resulting from a high saturated fat diet leads to alterations in lipid cellular intake and accumulation which generate lipotoxic conditions, a key phenomenon in the metabolism of β-cells. Alternatively, unsaturated fatty acids have been described to show opposite effects in pancreatic β-cells. The purpose of this work is to perform a critical analysis of the complex role of saturated and unsaturated fatty acids in β-cell metabolism. We discuss the diverse effects main dietary fatty acids have upon pancreatic β-cell metabolism as a key factor to maintain homeostasis by focusing in the cellular and molecular mechanisms involved in the development and progression of T2D. For instance, modifications in protein homeostasis as well as the intracellular management of lipid metabolism which are associated with inflammatory pathways. These conditions initiate critical metabolic rearrangements, that in turn have repercussions on insulin β-cell metabolism. This review allows an integral and broad understanding of different functions of fatty acids inside β-cells, being important metabolites for novel therapeutic targets in T2D treatment.

Butyrate and docosahexaenoic acid interact in alterations of specific lipid classes in differentiating colon cancer cells.

Docosahexaenoic acid (DHA) and sodium butyrate (NaBt) exhibit a number of interactive effects on colon cancer cell growth, differentiation, or apoptosis; however, the molecular mechanisms responsible for these interactions and their impact on cellular lipidome are still not fully clear. Here, we show that both dietary agents together induce dynamic alterations of lipid metabolism, specific cellular lipid classes, and fatty acid composition. In HT-29 cell line, a model of differentiating colon carcinoma cells, NaBt supported incorporation of free DHA into non-polar lipids and their accumulation in cytoplasmic lipid droplets. DHA itself was not incorporated into sphingolipids; however, it significantly altered representation of individual ceramide (Cer) classes, in particular in combination with NaBt (DHA/NaBt). We observed altered expression of enzymes involved in Cer metabolism in cells treated with NaBt or DHA/NaBt, and exogenous Cer 16:0 was found to promote induction of apoptosis in differentiating HT-29 cells. NaBt, together with DHA, increased n-3 fatty acid synthesis and attenuated metabolism of monounsaturated fatty acids. Finally, DHA and/or NaBt altered expression of proteins involved in synthesis of fatty acids, including elongase 5, stearoyl CoA desaturase 1, or fatty acid synthase, with NaBt increasing expression of caveolin-1 and CD36 transporter, which may further promote DHA incorporation and its impact on cellular lipidome. In conclusion, our results indicate that interactions of DHA and NaBt exert complex changes in cellular lipidome, which may contribute to the alterations of colon cancer cell differentiation/apoptotic responses. The present data extend our knowledge about the nature of interactive effects of dietary fatty acids.

Dietary Fatty Acid Composition Modulates Obesity and Interacts with Obesity-Related Genes.

The prevalence of obesity is skyrocketing worldwide. The scientific evidence has associated obesity risk with many independent factors including the quality of dietary fat and genetics. Dietary fat exists as the main focus of dietary guidelines targeting obesity reduction. To prevent/minimize the adipogenic effect of dietary fatty acids (FA), intakes of long-chain saturated- and trans-FA should be reduced and substituted with unsaturated FA. The optimal proportions of dietary unsaturated FA are yet to be defined, along with a particular emphasis on the need to achieve a balanced ratio of n-3:n-6 polyunsaturated FA and to increase monounsaturated FA consumption at the expense of saturated FA. However, inter-individual variability in weight loss in response to a dietary intervention is evident, which highlights the importance of exploring gene-nutrient interactions that can further modulate the risk for obesity development. The quality of dietary fat was found to modulate obesity development by interacting with genes involved in fatty acid metabolism, adipogenesis, and the endocannabinoid system. This review summarizes the current knowledge on the effect of the quality of dietary fat on obesity phenotype and obesity-related genes. The evidence is not only supporting the modulatory effect of fat quality on obesity development but also presenting a number of interactions between obesity-related genes and the quality of dietary fat. The identified gene-FA interaction may have a clinical importance and holds a promise for the possibility of using genetically targeted dietary interventions to reduce obesity risk in the future.

SUN-P302: Evaluating the Effects of Dietary Fatty Acid and Antioxidant Vitamin Intake on Metabolic Profile in Patients with Schizophrenia

SUN-P302: Evaluating the Effects of Dietary Fatty Acid and Antioxidant Vitamin Intake on Metabolic Profile in Patients with Schizophrenia

Dietary fatty acids modulate adipocyte TNFa production via regulation of its DNA promoter methylation levels

The factors regulating TNF alpha (TNFa) levels could be considered therapeutic targets against metabolic syndrome development. DNA methylation is a potent regulator of gene expression and may be associated with protein levels. In this study we investigate whether the effect of dietary fatty acids on TNFa released from adipocytes might be associated with modifications of the TNFa promoter DNA methylation status. A group of rats was assigned to three diets with a different composition of saturated, monounsaturated and polyunsaturated fatty acids. Samples of visceral adipose tissues were taken for adipocyte isolation, in which released TNFa levels were measured, and for methylation and expression studies. In addition, 3 T3-L1 cells were treated with palmitic, oleic and linoleic acids, with and without 5-Azacitydine (5-AZA). After treatments, cells and supernatants were included in the same analyses as rat samples. TNFa promoter methylation levels, gene expression and secretion were different according to the diets and fatty acid treatments associated with them. Cells treated with 5-AZA displayed higher TNFa levels than in the absence of 5-AZA, without differences between fatty acids. According to our results, dietary fatty acid regulation of adipocyte TNFa levels may be mediated by epigenetic modifications of the TNFa promoter DNA methylation levels.