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Vaccenic acid (trans-11-C₁₈:₁) chemically resembles elaidic acid (trans-9-C₁₈:₁) which is assumed to increase the risk of cardiovascular diseases, and thus could exert similar effects. Possible different oxidation rates of vaccenic versus elaidic acid were checked in muscles and liver, and through related gene expression in normal rat liver cells. In hepatic mitochondria, carnitine palmitoyltransferase (CPT) I exhibited comparable activity rates with both trans-isomers. CPT II activity was 30% greater (P < 0.05) with vaccenic than with elaidic acid as nonesterified fatty acids (NEFAs) or acyl-CoAs. Activity of the first β-oxidation step was similar between the isomers in all the tissue slices and liver extracts assayed. Respiration rates were comparable with both trans-isomers as NEFAs in various liver extracts, but were 30% greater (P < 0.05) with vaccenoyl-CoA than with elaidoyl-CoA in liver mitochondria. Vaccenic acid was oxidised 25% more (P < 0.05) by liver peroxisomes than elaidic acid. In hepatocytes cultured with trans- and corresponding cis-C₁₈:₁ isomers, gene expression of CPT I, hydroxyacyl-CoA dehydrogenase and hydroxymethylglutaryl-CoA synthase was at least 100% increased (P < 0.05), but was unchanged with vaccenic acid, relative to controls. In conclusion, the position and geometry of the double bonds in acyl chains are suggested to confer on vaccenic and elaidic acid specific biochemical properties that might differently affect their fates in tissues.

Numerous studies have shown that high olive oil intake reduces blood pressure (BP). These positive effects of olive oil have frequently been ascribed to its minor components, such as α-tocopherol, polyphenols, and other phenolic compounds that are not present in other oils. However, in this study we demonstrate that the hypotensive effect of olive oil is caused by its high oleic acid (OA) content ([almost equal to]70-80%). We propose that olive oil intake increases OA levels in membranes, which regulates membrane lipid structure (HII phase propensity) in such a way as to control G protein-mediated signaling, causing a reduction in BP. This effect is in part caused by its regulatory action on G protein-associated cascades that regulate adenylyl cyclase and phospholipase C. In turn, the OA analogues, elaidic and stearic acids, had no hypotensive activity, indicating that the molecular mechanisms that link membrane lipid structure and BP regulation are very specific. Similarly, soybean oil (with low OA content) did not reduce BP. This study demonstrates that olive oil induces its hypotensive effects through the action of OA.

Background: The aim of this study is to determine the correlations between dietary fatty acid (FA) intakes and plasma phospholipid (PL) FA levels in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. Methods: The dietary intake of 60 individual FAs was estimated using centre-specific validated dietary questionnaires. Plasma PL FA concentrations of these FAs were measured in non-fasting venous plasma samples in nested case-control studies within the EPIC cohort (n = 4923, using only non-cases). Spearman rank correlations were calculated to determine associations between FA intakes and plasma PL FA levels. Results: Correlations between FA intakes and circulating levels were low to moderately high (−0.233 and 0.554). Moderate positive correlations were found for total long-chain n-3 poly-unsaturated FA (PUFA) (r = 0.354) with the highest (r = 0.406) for n-3 PUFA docosahexaenoic acid (DHA). Moderate positive correlations were also found for the non-endogenously synthesized trans-FA (r = 0.461 for total trans-FA C16-18; r = 0.479 for industrial trans-FA (elaidic acid)). Conclusions: Our findings indicate that dietary FA intakes might influence the plasma PL FA status to a certain extent for several specific FAs. The stronger positive correlations for health-enhancing long-chain PUFAs and the health-deteriorating trans-FA that are not endogenously produced are valuable for future cancer prevention public health interventions.

BACKGROUND: Aedes aegypti and Aedes albopictus and Culex pipiens pallens mosquitoes transmit dengue fever and West Nile virus diseases, respectively. This study was conducted to determine the toxicity and mechanism of action of four flavonoids and two fatty acids from Millettia pinnata (Fabaceae) seed as well as six pure fatty acids and four fatty acid esters toward third instar larvae from insecticide-susceptible C. pipiens pallens and A. aegypti as well as wild A. albopictus. Efficacy of 12 experimental liquid formulations containing M. pinnata seed methanol extract and hydrodistillate (0.5–10.0% liquids) was also assessed. METHODS: The contact toxicities of all compounds and 12 formulations were compared with those of two larvicides, temephos and fenthion and the commercial temephos 200 g/L emulsifiable concentrate (EC). The possible mode of larvicidal action of the constituents was elucidated using biochemical methods. Larval mortality and cAMP level were analyzed by the Bonferroni multiple-comparison method. RESULTS: Potent toxicity was produced by karanjin, oleic acid, karanjachromene, linoleic acid, linolenic acid, pongamol, pongarotene, and elaidic acid toward C. pipiens pallens larvae (24 h LC₅₀, 14.61–28.22 mg/L) and A. aegypti larvae (16.13–37.61 mg/L). Against wild A. albopictus larvae, oleic acid (LC₅₀, 18.79 mg/L) and karanjin (35.26 mg/L) exhibited potent toxicity. All constituents were less toxic than either temephos or fenthion. Structure–activity relationship indicates that the degree of saturation, the side chain length, and the geometric isomerism of fatty acids appear to play a role in determining the fatty acid toxicity. Acetylcholinesterase (AChE) is the main site of action of the flavonoids, oleic acid, and palmitic acid. The mechanism of larvicidal action of elaidic acid, arachidic acid, and behenic acid might be due to interference with the octopaminergic system. Linoleic acid and linolenic acid might act on both AChE and octopaminergic receptor. M. pinnata seed extract or hydrodistillate applied as 10% liquid provided 100% mortality toward the three mosquito species larvae and the efficacy of the liquids was comparable to that of temephos 200 g/L EC. CONCLUSION: Further studies will warrant possible applications of M. pinnata seed-derived products as potential larvicides for the control of mosquito populations.

Dietary intervention provides a novel approach for cancer therapy. Elaidic acid (EA), which accounts for 80-90% of total trans fatty acids in foods, has recently been found to exert anti-tumor effects. However, the biological functions and underlying mechanisms of EA remain elusive in hepatocellular carcinoma (HCC). In this study, targeted fatty acid metabolomics demonstrated that among 44 types of fatty acids, the concentration of EA decreased most significantly when comparing plasma from HCC patients with plasma from healthy people. Through assays using HCC orthotopic and xenograft mouse models, we further revealed that dietary EA attenuates HCC growth. Notably, when gut microbiota was depleted using a cocktail of antibiotics, the anti-tumor effect of EA was diminished, confirming that EA suppresses HCC tumor growth by modulating gut microbiota. Mechanistically, analysis of 16S ribosomal RNA sequencing showed that dietary EA markedly increases the abundance of intestinal . Subsequent untargeted metabolomic sequencing analysis further demonstrated that dietary EA drives the production of -derived spermidine (SPD), which attenuates HCC growth as well as . The observed impact correlated with the phosphorylation of p38 MAPK and the upregulation of biomarkers pertinent to apoptosis and proliferation, including tumor protein 53, bcl-2-associated X protein, and cysteine-requiring aspartate protease 3. Taken together, our findings highlight the important role of intestinal -derived SPD in EA-mediated HCC suppression, thereby offering a promising dietary strategy for HCC treatment.

Endothelial dysfunction and inflammation are recognised factors in the development of atherosclerosis. Evidence suggests that intake of industrial trans fatty acids (TFAs) promotes endothelial dysfunction, while ruminant TFAs may have the opposite effect. The aim of this study was to compare the effects of elaidic acid (EA (18:1n-9t); an industrially produced TFA) and trans vaccenic acid (TVA (18:1n-7t); a natural TFA found in ruminant milk and meat) on inflammatory responses of endothelial cells (ECs). ECs (EA.hy926 cells) were cultured under standard conditions and exposed to TFAs (1 to 50 μM) for 48 h. Then, the cells were cultured for a further 6 or 24 h with tumour necrosis factor alpha (TNF-α, 1 ng/mL) as an inflammatory stimulant. ECs remained viable after treatments. TFAs were incorporated into ECs in a dose-dependent manner. Preincubation with EA (50 µM) increased production of MCP-1, RANTES, and IL-8 in response to TNF-α, while preincubation with TVA (1 µM) decreased production of ICAM-1 and RANTES in response to TNF-α. Preincubation with EA (50 µM) upregulated toll-like receptor 4 and cyclooxygenase 2 gene expression in response to TNF-α. In contrast, preincubation with TVA (1 µM) downregulated TNF-α induced nuclear factor kappa B subunit 1 gene expression. Preincubation of ECs with EA (50 µM) increased THP-1 monocyte adhesion. In contrast, preincubation of ECs with TVA (1 µM) reduced THP-1 monocyte adhesion, while preincubation of ECs with TVA (50 µM) decreased the level of surface expression of ICAM-1 seen following TNF-α stimulation. The results suggest that TVA has some anti-inflammatory properties, while EA enhances the response to an inflammatory stimulus. These findings suggest differential effects induced by the TFAs tested, fitting with the idea that industrial TFAs and ruminant TFAs can have different and perhaps opposing biological actions in an inflammatory context.

A spread was prepared using blends of virgin coconut oil (VCO), trans-free fat (TFF), whey powder, coconut fiber, emulsifiers, and flavors. Curcumin was added in micro quantities to provide a natural color. The samples formulated were tested for their spreadability, texture, and phase separation. The samples were analyzed for their physicochemical properties, such as color, texture, rheological characterization, and storage stability. The results showed that the formulated spread had moisture of 2.10%, protein of 9.23%, fat of 67.35%, ash of 4.56%, crude fiber of 11.2%, total carbohydrate 10.12%, and the values of peroxide, and percentage of free fatty acids were well below the acceptable levels during storage periods. The samples showed a phase separation after one month of storage at 38 °C. However, no separation was observed when stored at 4 °C and 27 °C. The spreads showed shear-thinning behavior, were solid at 4 °C, and were spreadable at 27 °C and flowy at 38 °C. DSC analysis indicated that the sample was solid below 9.63 °C and liquid over 20.57 °C. The spread was rich in lauric acid (26.01%), palmitic acid (28.26%), and trans fatty acid (Elaidic acid) was not detected. Based on the texture and sensory results, a 50:50 blend of VCO: TFF showed good spreadability. Sensorily, the products showed higher overall acceptability scores. The developed spread has an abundance of fiber, protein, and health-promoting factors from VCO.

The current study investigated the healing effects of polysaccharides and lipid extracts obtained from the cyanobacterium Cyanothece sp. on burn wounds in the rat model. This halophilic cyanobacterial species was originally isolated from Pink Lake (Lipar Lake) located on the margins of Oman Gulf, southeast Iran. A total of 40 white Wistar male rats were subjected to burn injuries and were allocated into four distinct experimental groups, each comprising 10 rats: the control group, standard group, polysaccharide group, and lipid group that were treated with Eucerin, Alpha ointment, Cyanothece sp. polysaccharide ointment (5% Eucerin-based), and Cyanothece sp. lipid ointment (5% Eucerin-based). The healing efficacy of the cyanobacterial components was evaluated by examining histopathological, morphological, hormonal, and inflammatory response changes in the rats. The cyanobacterial ointments, especially the lipid ointment, significantly enhanced wound healing by inducing cell proliferation, increasing blood vessel counts, wound closure rates, epithelial thickness, fibroblast numbers, and collagen density in the treated rats ( p <0.05). Furthermore, the ointment substantially reduced wound secretions and inflammatory markers, including tumor necrosis factor-alpha (TNFα), interleukins (IL)-2 and IL-8, neutrophil counts, C-reactive protein (CRP), cortisol, and adrenocorticotropic hormone (ACTH). GC-MS analysis identified fatty acid components in the extracted lipids, such as palmitic acid (31.98%), octadecanoic acid (12.86%), oleic acid (8.22%), palmitoleic acid (4.89%), α-linolenic (4.5%), elaidic acid (4.14%), and decanoic acid (3.31%) which are believed to contribute significantly to the wound repair process. Graphical Abstract

Industrially originated trans-fatty acids (I-tFAs), such as elaidic acid (EA), and ruminant trans-fatty acids (R-tFAs), such as trans-palmitoleic acid (TPA), may have opposite effects on metabolic health. The objective was to compare the effects of consuming 2–3% I-tFA or R-tFA on the gut microbiome and fecal metabolite profile in mice after 7 and 28 days. Forty C57BL/6 mice were assigned to one of the four prepared formulations: lecithin nanovesicles, lecithin nanovesicles with EA or TPA, or water. Fecal samples and animals’ weights were collected on days 0, 7, and 28. Fecal samples were used to determine gut microbiome profiles by 16S rRNA sequencing and metabolite concentrations by GC/MS. At 28 days, TPA intake decreased the abundance of Staphylococcus sp55 but increased Staphylococcus sp119. EA intake also increased the abundance of Staphylococcus sp119 but decreased Ruminococcaceae UCG-014, Lachnospiraceae, and Clostridium sensu stricto 1 at 28 days. Fecal short-chain fatty acids were increased after TPA while decreased after EA after 7 and 28 days. This study shows that TPA and EA modify the abundance of specific microbial taxa and fecal metabolite profiles in distinct ways.

Lymphoma defines a group of different diseases. This study examined pre-treatment plasma samples from 66 adult patients (aged 20–74) newly diagnosed with any lymphoma subtype, and 96 frequency matched population controls. We used gas chromatography-mass spectrometry (GC-MS) to compare the metabolic profile by case/control status and across the major lymphoma subtypes. We conducted univariate and multivariate analyses, and partial least square discriminant analysis (PLS-DA). When compared to the controls, statistically validated models were obtained for diffuse large B-cell lymphoma (DLBCL), chronic lymphocytic leukemia (CLL), multiple myeloma (MM), and Hodgkin lymphoma (HL), but not follicular lymphoma (FL). The metabolomic analysis highlighted interesting differences between lymphoma patients and population controls, allowing the discrimination between pathologic and healthy subjects: Important metabolites, such as hypoxanthine and elaidic acid, were more abundant in all lymphoma subtypes. The small sample size of the individual lymphoma subtypes prevented obtaining PLS-DA validated models, although specific peculiar features of each subtype were observed; for instance, fatty acids were most represented in MM and HL patients, while 2-aminoadipic acid, 2-aminoheptanedioic acid, erythritol, and threitol characterized DLBCL and CLL. Metabolomic analysis was able to highlight interesting differences between lymphoma patients and population controls, allowing the discrimination between pathologic and healthy subjects. Further studies are warranted to understand whether the peculiar metabolic patterns observed might serve as early biomarkers of lymphoma.