BACKGROUND:Pathogenic mechanisms involved in arterial hypertension (HT) promote the atherosclerosis development. Fatty acids (FAs) could modulate these processes. We investigated the association between dietary and serum FAs and early atherosclerosis development and their correlation with serum vascular inflammation markers in HT. METHODS:96 patients were included. Dietary information was collected through a validated food frequency questionnaire. Serum FAs were detected by gas chromatography. High-sensitivity C-reactive protein (hs-CRP), interleukin 6 (IL-6) and fibrinogen serum were determined by immunoturbidimetry, enzyme immunoassay and Clauss method, respectively. Carotid intima media-thickness (cIMT) was determined by ultrasound. Multivariate linear regression models were applied. RESULTS:Patients showed an adverse health profile, with high caloric intake (3113 ± 1477 kcal/day), LDL cholesterol (126.0 ± 35.1 mg/dL), and overweight (BMI 31.1 ± 5.5 kg/t2), and also an inflam-matory process, characterised by higher hs-CRP (3.9 ± 2.7 mg/L) and fibrinogen (433.4 ± 84.6 mg/dL) concentrations. We found significant inverse correlations between dietary monounsaturated FAs (MUFAs), serum omega-3 polyunsaturated FAs (n-3 PUFAs), and hs-CRP (β = -3.59, [95% CI -6.87 to -0.32], p = 0.03 and β = -0.70, [95% CI -1.42-0.01], p = 0.05, respectively), significant positive associations between dietary MUFAs, serum saturated FAs (SFAs) and cIMT (β = 81.96, [95% CI 33.42-130.50], p = 0.002 and β = 36.71, [95% CI 6.34-67.08], p = 0.02, respectively), and significant inverse correlations between serum omega-6 polyunsaturated FAs (n-6 PUFAs) and cIMT (β = -91.44, [95% CI -168.01 to -14.88], p = 0.02 and β = -41.01, [95% CI -70.73-11.28], p = 0.01). CONCLUSIONS:Serum n-3 PUFAs modulate hs-CRP levels, while n-6 PUFAs suggest antiatherosclerotic properties in HT. The ambiguous impact of MUFAs requires comprehensive research.

Linoleic acid (ω-6 LA) and α-linolenic acid (ω-3 ALA) are essential fatty acids (EFA) for human beings. They must be consumed through diet and then extensively metabolized, a process that plays a fundamental role in health and eventually in disease prevention. Given the numerous changes depending on age and sex, EFA metabolic adaptations require further investigations along the women’s life cycle, from onset to decline of the reproductive age. Thus, this review explains women’s life cycle stages and their involvement in diet intake, digestion and absorption, the role of microbiota, metabolism, bioavailability, and EFA fate and major metabolites. This knowledge is crucial to promoting lipid homeostasis according to female physiology through well-directed health strategies. Concerning this, the promotion of breastfeeding, nutrition, and physical activity is cardinal to counteract ALA deficiency, LA/ALA imbalance, and the release of unhealthy derivatives. These perturbations arise after menopause that compromise both lipogenic and lipolytic pathways. The close interplay of diet, age, female organism, and microbiota also plays a central role in regulating lipid metabolism. Consequently, future studies are encouraged to propose efficient interventions for each stage of women's cycle. In this sense, plant-derived foods and products are promising to be included in women’s nutrition to improve EFA metabolism.

Metabolic syndrome (MS) is a global health problem. Dietary factors, especially fatty acids, may affect MS pathology. However, the associations between omega-3 polyunsaturated fatty acids (n-3 PUFAs) and MS risk demonstrate inconsistent results. To clarify the relationship between dietary n-3 PUFA and endothelial function on MS, we carried out a systematic review. An electronic literature search based on controlled clinical trials (CCTs) between 2004 and 2020 was conducted. A total of 28 articles were included in the systematic review. Studies were analyzed according intervention type: dietary interventions (12 CCTs), dietary supplementation interventions (9 CCTs) and mixed interventions (7 CCTs). Studies with dietary interventions characterized by n-3 PUFAs increased by food source, such as Mediterranean and Nordic-style diets, reported significant reduction in systolic and diastolic blood pressure, and also in inflammatory endothelial biomarkers. The same effect was also observed in mixed interventions and in CCTs with n-3 PUFAs supplementation. Dietary interventions with n-3 PUFAs contributes to improved endothelial and cardiovascular health in SM and associated risk factors.

Universal guidelines for the editing of scientific results in Spanish and English in the wide flelcls of Health Sciences, written In a concise, practica] and colloctuial way are given. Thls article is devoted to those professionals whose inain activities are the practical care of patients; however, having original results they lack enough practice and training in the cornplex editing process in order to send the manuscripts for consideration to the Editors of well qualifled, Indexed, journals. Some ways to make easy the wrlting of the clifferent sectlons of the rnanuscripts, appropriate verb tenses as well as explanation of the main bibliometrlc parameters as lmpact Factor are dlscussed. Others relevant issues, as authorship, letters to the editors and referees are also analysed.

Diabetic encephalopathy is a chronic complications of diabetes mellitus that affects the central nervous system. We evaluated the effect of ω3 and ω6 polyunsaturated fatty acids (PUFAs) supplementation plus the antioxidant agent nordihydroguaiaretic acid (NDGA) on the etiopathology of diabetic encephalopathy in eSS rats, a spontaneous model of type 2 diabetes.

Vision disorders are one of the most serious complications of diabetes mellitus (DM) affecting the quality of life of patients and eventually cause blindness. The ocular lesions in diabetes mellitus are located mainly in the blood vessels and retina layers. Different retina lesions could be grouped under the umbrella term of diabetic retinopathies (DMRP). We propose that one of the main causes in the etiopathogenesis of the DMRP consists of a progressive loss of the selective permeability of blood retinal barriers (BRB). The loss of selective permeability of blood retinal barriers will cause a progressive autoimmune process. Prolonged autoimmune injures in the retinal territory will triggers and maintains a low-grade chronic inflammation process, microvascular alterations, glial proliferation and subsequent fibrosis and worse, progressive apoptosis of the photoreceptor neurons. Patients with long-standing DM disturbances in retinal BRBs suffer of alterations in the enzymatic pathways of polyunsaturated fatty acids (PUFAs), increase release of free radicals and pro-inflammatory molecules and subsequently incremented levels of vascular endothelial growth factor. These facts can produce retinal edema and photoreceptor apoptosis. Experimental, clinical and epidemiological evidences showing that adequate metabolic and alimentary controls and constant practices of healthy life may avoid, retard or make less severe the appearance of DMRP. Considering the high demand for PUFAs ω3 by photoreceptor complexes of the retina, it seems advisable to take fish oil supplements (2 g per day). The cellular, subcellular and molecular basis of the propositions exposed above is developed in this article. Synthesizer drawings the most relevant findings of the ultrastructural pathology, as well as the main metabolic pathways of the PUFAs involved in balance and disbalanced conditions are provided.

El modelo animal de ratas eSS es una buena herramienta para el estudio de la historia natural de la DM y aportamos evidencias nuevas sobre marcadores de inflamacion cronica relacionados. La administracion de ω-3 suplementado con NDGA en las dosis utilizadas, disminuye los parametros inflamatorios, metabolicos y de estres oxidativo, pudiendo ser su combinacion una alternativa promisoria en la prevencion y tratamiento de la DM humana, sirviendo este estudio para motivarnos en ampliar nuestros resultados, investigando el efecto de ω-3 PUFA con y sin NDGA, a traves la alimentacion con dietas experimentales.

Abstract Retinoic acid (RA) and unsaturated fatty acids (UFA) are proposed as nutritional anticancer agents. Nonetheless, the activity of their combination on human breast cancer needs further study. Our aim was to evaluate this activity on the MCF-7 and ZR-75-1 cell lines treated with 1 µM RA and 50 µM of γ-linoleic (GLA, ω-6), eicosapentaenoic (EPA, ω-3), oleic (OA, ω-9), or eicosatrienoic (ETA, ω-9) acids. The following cellular responses were compared by ANOVA and Fisher test (P < 0.05): fatty acids, E-cadherin, actin (differentiation), conjugated dienes, γ-glutamyltranspeptidase activity (stress), and viability, which were correlated by partial least squares regression. Although both cell lines responded differentially, RA modified unsaturated fatty acids, increased differentiation, reduced γ-glutamyltranspeptidase, and viability. RA differentiating activity on ZR-75-1 was morphologically enhanced by UFA. Stress induction with γ-glutamyltranspeptidase decrease and conjugated dienes was promoted by ETA in MCF-7, and EPA and OA in ZR-75-1. RA-related reduced viability was potentiated by EPA and OA in both lines. GLA was less active. Therefore, unsaturated fatty acids (ω-3/ω-9) potentiated the multitarget retinoic acid activity against these human breast cancer cells.

The aim of this study was to determine whether α-linolenic acid (ALA ω-3 fatty acid) enriched diet affects growth parameters when applied to a syngeneic model of mammary carcinoma.

Background and Aims. Evidence suggests that quantity and quality of dietary polyunsaturated fatty acids (PUFAs) play a role in the development of cancer. However, the mechanisms involved in this interaction(s) are not clear. Endocannabinoids are lipid metabolites known to have growth modulatory actions. We studied the effect of supplementation with PUFAs omega-6 and omega-3 (essential fatty acids, EFAs), saturated and monoun-saturated fatty acids (non-EFAs) on the growth of tumor cells and modifications in their endocannabinoid content.Methods. Cell cultures of human glioblastoma (T98G) and breast cancer (MCF7) were supplemented with 50 or 100 mmol EFAs and non-EFAs for 72 h. Cell proliferation was then determined by MTT, anandamide (AEA) levels by HPLC, total fatty acids profiles by GLC, CB1 receptor expression by WB and FAAH activity by spectrophotometric method.Results. Fatty acids profile reflected the incorporation of the lipids supplemented in each assay. Arachidonic acid (EFA omega-6) supplementation increased AEA levels and inhibited the growth of T98G, whereas palmitic acid (non-EFA) enhanced their proliferation. In breast cancer (MCF7) cells, eicosapentaenoic acid (EFA omega-3) reduced and oleic acid (non-EFA) enhanced their proliferation. CB1 expression was higher in T98G and no differences were observed in FAAH activity.Conclusions. The growth of tumor cells can be differentially modulated by fatty acids and, at least in part, can be attributed to their ability to act on the components of the endocannabinoid system. (c) 2017 IMSS. Published by Elsevier Inc.

Lung cancer is the leading cause of death by cancer, and is a major sanitary concern worldwide. Some nutrients, such as ω-9 fatty acids, have been proposed as anticancer agents. Thus, an olein-enriched diet was assayed in a murine model of lung adenocarcinoma (LAC-1) to evaluate neoplastic and paraneoplastic evolution in BALB/c mice. The organic assimilation of dietary fatty acids was confirmed in liver by gas chromatography. This experimental oleic acid-containing diet increased animal survival and tumour latency (analysed by the Kaplan-Meier method), improving neoplastic evolution and general status, with weak effects on the paraneoplastic syndrome (thymus atrophy, splenomegaly, splenocyte response to mitogen, blood anaemia, and leucocytosis). Tumour lipid oxidation was not involved. Thus, diet enrichment with olein, a natural source of the ω-9 oleic acid, significantly delayed progression of LAC-1 and increased tumour latency and mice survival. These results support its use in nutritional management of cancer, with further studies being encouraged.

Numerous reports have demonstrated a tumor inhibitory effect of polyunsaturated fatty acids (PUFAs). However, the molecular mechanisms modulating this phenomenon are in part poorly understood. Here, we provide evidence of a novel antitumoral mechanism of the PUFA arachidonic acid (AA). In vivo and in vitro experiments showed that AA treatment decreased tumor growth and metastasis and increased apoptosis. Molecular analysis of this effect showed significantly reduced expression of a subset of antiapoptotic proteins, including BCL2, BFL1/A1, and 4-1BB, in AA-treated cells. We demonstrated that down-regulation of the transcription factor glioma-associated protein 1 (GLI1) in AA-treated cells is the underlying mechanism controlling BCL2, BFL1/A1, and 4-1BB expression. Using luciferase reporters, chromatin immunoprecipitation, and expression studies, we found that GLI1 binds to the promoter of these antiapoptotic molecules and regulates their expression and promoter activity. We provide evidence that AA-induced apoptosis and down-regulation of antiapoptotic genes can be inhibited by overexpressing GLI1 in AA-sensitive cells. Conversely, inhibition of GLI1 mimics AA treatments, leading to decreased tumor growth, cell viability, and expression of antiapoptotic molecules. Further characterization showed that AA represses GLI1 expression by stimulating nuclear translocation of NFATc1, which then binds the GLI1 promoter and represses its transcription. AA was shown to increase reactive oxygen species. Treatment with antioxidants impaired the AA-induced apoptosis and down-regulation of GLI1 and NFATc1 activation, indicating that NFATc1 activation and GLI1 repression require the generation of reactive oxygen species. Collectively, these results define a novel mechanism underlying AA antitumoral functions that may serve as a foundation for future PUFA-based therapeutic approaches.

Diabetes mellitus (DM) is a complex disease with alterations in metabolic and inflammatory markers. Stillman Salgado rats (eSS) spontaneously develop type 2 DM by middle age showing progressive impairment of glucose tolerance with hyperglycemia, hypertriglyceridemia and hyperinsulinemia. We analyzed the effects of supplementation of ω-3 and ω-6 polyunsaturated fatty acids (PUFAs) with or without nordihydroguaiaretic acid (NDGA) added, an antioxidant and lipoxygenase inhibitor, on metabolic and inflammatory parameters in eSS rats to evaluate whether they can delay development and/or prevent progression of DM.

Salt sensitivity (SS) is associated with increased cardiovascular risk in diabetic patients. This abnormal mechanism results in an increased renal oxydation and decreased urinary sodium excretion and if it is maintained over time can develop hypertension and its complications. Currently the Western diet has limited content of polyunsaturated fatty acids, with antioxidant capacity such as ecoisapentaneoico acid (EPA). Therefore we hypothesized that nutritional supplementation with EPA, prevents SS in DM rats by decreasing renal oxidative stress. Our objectives were; to asses SS of eSS diabetic rats and to investigate the ability of EPA to prevent SS in these rats. Methods Wistar rats were used as healthy controls. Type II diabetic rat group (eSS), 3 months old, were divided in 3 groups, diabetic control (eSS), eSS treated with arachidonic acid (pro‐oxidant)(2.5mg / ip, per month) (eSS + AA) and eSS treated with EPA (2.5mg / ip per month) (eSS + EPA). Animals were treated during 1 year, then placed in metabolic cages and subsequently underwent 2 experimental periods of 7 days each with normal sodium diet (0.4% NaCl)(NNaD) and high salt diet (4% NaCl)(HNaD). At the end of each period weight, systolic blood pressure (SBP), HbA1c, triglycerides (Trig), cholesterol (Chol), creatinine (Cre), kidney γ‐glutamyl transpeptidase activity (γGTP)​​, urinary protein excretion (U prot V). Results eSS rats had elevated HbA1c, Tri, Chol and reduced body weight vs. Wistar control group. Renal function was normal during the experimental period. The eSS + AA group also showed elevation of HbA1c, Trig, with no change in Cre and Chol. During NNaD SBP was 119 ± 3 mmHg and after HNaD 125 ± 1 mmHg (p <0.05). In contrast, EPA + eSS lowered HbA1c (5.6 ± 0.3% vs 7.0 ± 0.2%, p <0.05), Trig (175±1 mg/dl vs 245±12 mg/dl p <0.05), and increased body weight (424±11 g vs 511±22gr, p <0.05) vs eSS. EPA supplement prevented the increase of SBP during the HNaD (126±2 mmHg vs. 128±2 mmHg p> 0.5). eSS + AA did not differ from eSS group. No significant difference was observed in U prot V between groups. Urinary sodium excretion increased with HNAD. Renal interstitium γ‐GT activity in eSS group was 0.65±0.04 au and 0.61±0.02 au in eSS + AA group, while in EPA + eSS 0.5±0.03 (p <0.05). Conclusion The salt sentitive eSS rats have hypertriglyceridemia and elevated HbA1c. Nutritional supplementation with EPA prevented the salt sensitivity, the increased of HbA1c and triglycerides. These changes were associated with lower kidney γ‐GT ​​activity, suggesting that the EPA dietary supplement can be used in diabetic patients to prevent salt sensitivity and improve metabolic abnormalities.

There is increasing evidence that dietary habits play a role in prostate cancer (PC) occurrence. Argentinean cancer risk studies require additional attention because of the singular dietary pattern of this population. A case-control study (147 PC cases, 300 controls) was conducted in Córdoba (Argentina) throughout 2008–2013. A principal component factor analysis was performed to identify dietary patterns. A mixed logistic regression model was applied, taking into account family history of cancer. Possible bias was evaluated by probabilistic bias analysis. Four dietary patterns were identified: Traditional (fatty red meats, offal, processed meat, starchy vegetables, added sugars and sweets, candies, fats, and vegetable oils), Prudent (nonstarchy vegetables, whole grains), Carbohydrate (sodas/juices and bakery products), and Cheese (cheeses). High adherence to the Traditional (OR 2.82, 95%CI: 1.569–5.099) and Carbohydrate Patterns (OR 2.14, 95%CI: 1.470–3.128) showed a promoting effect for PC, whereas the Prudent and Cheese Patterns were independent factors. PC occurrence was also associated with family history of PC. Bias adjusted ORs indicate that the validity of the present study is acceptable. High adherence to characteristic Argentinean dietary patterns was associated with increased PC risk. Our results incorporate original contributions to knowledge about scenarios in South American dietary patterns and PC occurrence.

Objective: The aim of this study was to determine the effects of some polyunsaturated fatty acids plus phytomelatonin from walnuts in the development of mammary gland adenocarcinoma.Methods: BALB/c mice were fed a semisynthetic diet supplemented with either 6% walnut oil and 8% walnut flour containing phytomelatonin (walnut diet: WD); or 6% corn oil plus commercial melatonin (melatonin diet: MD), or the control group (CD), which received only 6% of corn oil. Membrane fatty acids of tumor cells (TCs) were analyzed by gas liquid chromatography, cyclooxygenase (COX) and lipoxygenase (LOX) derivatives, and plasma melatonin by high-performance liquid chromatography; apoptosis and tumor-infiltrating lymphocytes by flow cytometry.Results: TCs from the MD and WD mice showed significant decreases in linoleic acid compared with the CD group (P < 0.05). Significantly lower levels of LOX-[13(S)-HODE] were found in TCs from the MD and WD group than in CD (P < 0.0001). COX-[12(S)-HHT] was lower and 12 LOX-[12(S)-HETE] was higher in TCs from the MD group than form the WD and CD arms (P < 0.05). Plasma melatonin, apoptosis, tumor infiltration, and survival time were significantly lower in CD mice than in MD and WD mice (P < 0.05).Conclusions: This study shows that melatonin, along with polyunsaturated fatty acids, exerts a selective inhibition of some COX and LOX activities and has a synergistic anti-tumor effect on a mammary gland adenocarcinoma model. Published by Elsevier Inc.

Arsenic (As) is used in the treatment of leukemia and breast cancer due to its oxidative cytotoxic action. However, it is also toxic to normal cells. One proposed anticancer mechanism induced by As might be nitrosative stress (NS). It is believed that antioxidant flavonoids in combination with As might reduce its toxic action on normal cells without interfering with its antitumor action. In the present study, we evaluated the antineoplastic potential of As on breast human cancer lines MCF-7 and ZR-75-1 treated with redox-modulating flavonoids, such as quercetin (Q) and silymarin (S). Even though both cell lines differed about their oxidative responsiveness, their viability was decreased by NS induction through γ-glutamyltranspeptidase inhibition. Arsenic triggered NS in both MCF-7 and ZR-75-1 cultures, with the formers more sensitive without recovering their pre-treatment capacity. ZR-75-1 cells maintained their antioxidant status, whereas MCF-7 ones treated with S, As, and As + Q did not. Silymarin did not interfere with the described As bioactivity. NS was an anticancer mechanism exerted by As depending on the redox cellular response that could be differentially modified by dietary antioxidants. Hence, it is worthwhile to consider the use of dietary antioxidants as adjuvant in cancer chemotherapy, especially when using As.