The joint effects of small dense low-density lipoprotein cholesterol (sd-LDL-C) and ambient PM2.5 exposure on stroke risk remain unclear. This longitudinal cohort study included 6457 stroke-free participants from the China Health and Retirement Longitudinal Study (2011-2020). PM2.5 exposure was estimated from the ChinaHighPM2.5 dataset. Cox regression models assessed hazard ratios (HR) with 95% confidence intervals (CI). K-means trajectory analysis identified sd-LDL-C risk groups. The restricted cubic spline examined the dose-response relationship. During a median 9-year follow-up, 710 stroke cases occurred. Both sd-LDL-C (HR per 1-SD: 1.116, 95% CI: 1.018-1.224) and PM2.5 (HR per 1-SD: 1.321, 95% CI: 1.222-1.428) independently predicted stroke risk. Significant multiplicative interaction was detected (p = 0.037). Combined high sd-LDL-C and high PM2.5 exposure conferred the greatest risk (HR: 1.713, 95% CI: 1.335-2.198) versus double-low exposure. Sustained high sd-LDL-C trajectory increased stroke risk by 36% (HR: 1.361, 95% CI: 1.086-1.706). Cumulative sd-LDL-C (cu-sd-LDL-C) exposure showed dose-dependent associations (Q4 vs. Q1: HR = 1.580, 95% CI: 1.115-2.239). Baseline sd-LDL-C (p = 0.009), annual average PM2.5 (p < 0.001), and cu-sd-LDL-C exposure (p = 0.037) all showed significant nonlinear relationship with incident stroke. sd-LDL-C demonstrated superior predictive ability over conventional LDL-C (AUC: 0.578 vs. 0.534, p < 0.001). Long-term elevated sd-LDL-C and PM2.5 exposure were independently associated with incident stroke risk, and participants with dual-high exposure showed the highest risk. sd-LDL-C outperforms LDL-C in stroke prediction, supporting its integration into risk assessment strategies and the importance of simultaneous lipid and pollution control.
Despite notable medical advancements, the continuous development of novel cancer therapies remains imperative. In this study, we aimed to evaluate the anticancer activity of liposomes prepared solely from nonnatural myristoylated (saturated C14 chains) or natural cardiolipin to develop a cancer therapies strategy. We calculated IC50 values using a cell proliferation inhibition assay and investigated the underlying mechanisms in cells exhibiting high inhibitory activity using Western blotting and flow cytometry. Calculation of the IC50 revealed that liposomes prepared solely with natural cardiolipin exhibited low toxicity to normal cells (> 100 μM) and showed the strongest toxicity against cancer cells, specifically KMS-12-PE (multiple myeloma cells) (23.5 ± 11.4 μM) among various cancer cells. In contrast, liposomes prepared solely with myristoylated cardiolipin exhibited weak anticancer activity. Furthermore, the mechanism of anticancer activity was evaluated using immunoblotting and flow cytometry. After administration of natural cardiolipin liposomes, CASPASE-3 cleavage was confirmed in KMS-12-PE cells, and the annexin V-positive rate was higher than in the liposome-free control group, suggesting apoptosis induction. These results indicate that natural cardiolipin is nontoxic to normal cells and possesses anticancer activity. This study demonstrated that liposomes formulated with cardiolipin can induce anticancer activity independently. This new finding is considered a foundation for future therapeutic strategies.
In atherosclerosis (AS), the conversion of vascular smooth muscle cells (VSMCs) to a macrophage-like phenotype is a key contributor to plaque instability. Although retinoic acid receptor responder 2 (RARRES2) has been identified as an adipokine implicated in inflammation and metabolism, its role in VSMC phenotypic transformation remains unknown. This study aimed to investigate whether RARRES2 regulates the macrophage-like transformation and dysfunction of VSMCs. In the in vitro AS model, RARRES2 expression was significantly upregulated. Knockdown of RARRES2 inhibited VSMC proliferation and migration, reduced the secretion of inflammatory factors, decreased lipid accumulation, and the number of CD68-positive cells, and suppressed the activation of key proteins in the NF-κB/NLRP3 pathway. In the AS model, RARRES2 expression was found to be significantly upregulated. Knockdown of RARRES2 inhibited the proliferation and migration of VSMCs, reduced the secretion of TNF-α, IL-6, IL-1β, and MMP-2, reduced lipid accumulation, decreased the number of CD68-positive cells (indicating an acquisition of partial macrophage-like features, though further lineage markers are needed to confirm full partial macrophage-like phenotype), and inhibited the activation of key proteins (p-p65, NLRP3, ASC) in the NF-κB/NLRP3 pathway. RARRES2 knockdown suppresses NF-κB/NLRP3 signaling and attenuates macrophage-like transformation, inflammatory responses, and lipid accumulation in VSMCs, suggesting that RARRES2 may represent a potential therapeutic target for AS.
This review explores how the fatty acid (FA) profile of the Amazonian Rhynchophorus palmarum larva (Chontacuro), traditionally eaten for respiratory ailments, might biochemically mitigate viral respiratory infections. During metamorphosis, this insect utilizes its unique FA matrix to survive severe, self-inflicted oxidative and inflammatory tissue stress. The authors hypothesize that when consumed by humans, these insect lipids undergo chylomicron-mediated lymphatic transport. This pathway bypasses initial liver metabolism, delivering unsaturated FAs directly to the pulmonary microvasculature and alveolar macrophages in the lungs. Once there, the FAs are proposed to act via two main mechanisms: One is inflammation resolution, where the ω-3 fraction is hypothesized to be metabolized via the 15-LOX enzyme pathway into Specialized Pro-Resolving Mediators (SPMs) and activate PPAR-α, potentially shifting the immune response from chronic inflammation toward active tissue repair. The other is viral sabotage: The highly unsaturated fats increase cell membrane fluidity, destabilizing the "lipid rafts" that viruses rely on for cellular entry and assembly. While in vitro and in silico models suggest a synergistic "cocktail effect" that primes and then resolves the immune response, the authors note that direct human clinical evidence is currently lacking.
Insufficient physical activity, poor dietary practices, escalating stress levels, and environmental factors are all contributors to the swift rise in obesity, type 2 diabetes mellitus (T2DM), and hypothyroidism worldwide. This study aimed to assess the effects of obesity on lipid profiles, glycemic control, and thyroid function in individuals with T2DM and hypothyroidism. The study included 154 participants: 100 T2DM patients with hypothyroidism and 54 healthy controls. Anthropometric measurements were collected, and biochemical tests, including fasting blood glucose (FBG), hemoglobin A1c (HbA1c), lipid profiles, and thyroid hormone levels; thyroid-stimulating hormone (TSH), free thyroxine (FT4), and free triiodothyronine (FT3) were performed. The groups differed significantly (p < 0.05) in age, body mass index (BMI), FBG, HbA1c, TSH, FT3, total cholesterol, and triglycerides. Compared to patients without obesity and controls, diabetic patients with obesity showed higher levels of FBG, HbA1c, cholesterol, triglycerides, and more notable changes in thyroid hormones. Age, FBG, HbA1c, and total cholesterol were found to be significant predictors of obesity by receiver operating characteristic (ROC) curve analysis. The results demonstrate that people suffering from coexisting diabetes, hypothyroidism, and obesity present compromised glycemic control, lipid profile alterations, and thyroid dysfunction. This identifies a metabolic assessment as a primary tool in the management of obese diabetics.
Climate change is expected to alter the phytoplankton production of n-3 long-chain polyunsaturated fatty acids (n-3 LC PUFA), including DHA (docosahexaenoic acid), impacting their transfer toward marine consumers. European sardine (Sardina pilchardus) is a major source of n-3 LC PUFA for human populations and is considered to be unable to synthesize sufficient quantities of n-3 LC PUFA to meet their physiological needs. This study aimed to understand the effect of a dietary DHA deficiency on the n-3 LC PUFA metabolism of sardine by investigating their fatty acid composition in three tissues (muscle, brain, and liver) and the hepatic expression of genes involved in the LC PUFA synthesis pathway. Wild-caught fish were fed either a DHA-deficient diet or a control diet for 2 months. The dietary DHA deficiency led to a lower DHA content in muscle reserves and liver membranes but did not change the brain fatty acid composition in sardines. In both dietary groups, the hepatic expressions of genes encoding elongase (elovl2, elovl5) and desaturase (fads2) enzymes were similar, but the expression levels of elovl2 and fads2 were negatively correlated to the DHA percentage in hepatic reserve lipids. The relative expressions of elovl5 and fads2 genes were positively correlated but only in DHA-deficient individuals. Besides, the individuals fed the DHA-deficient diet showed a higher expression of the phospholipase A2 gene (pla2g12b), suggesting a mobilization of n-3 LC PUFA from phospholipids. These results may suggest the activation of compensatory mechanisms at the molecular level in sardines to offset the dietary DHA deficiency.
Background and AimsThe relationship between blood lipids and atrial fibrillation (AF) remains unclear. Nuclear magnetic resonance (NMR) spectroscopy enables the profiling of size-defined lipoproteins and their contained lipid components. This study aimed to analyze the genetic causal relationships between lipoproteins, NMR-measured lipids, and AF, providing insights into the prediction and treatment of AF. Methods and Results. Summary-level data on lipoprotein and lipid concentrations measured by NMR were obtained from the UK Biobank. Summary-level data on AF were sourced from the FinnGen project. Mendelian Randomization (MR) analysis using inverse-variance weighting was employed as the primary analytical method. Genetically predicted elevated low-density lipoprotein (LDL) cholesterol, LDL free cholesterol, LDL phospholipids, and LDL total lipids measured by NMR were associated with an increased risk of AF. MR analyses did not identify robust causal associations between lipids contained in high-density lipoproteins (HDL), intermediate-density lipoproteins (IDL), or very-low-density lipoproteins (VLDL) and AF. Among size-defined LDL particles, elevated lipids of large LDL (L-LDL) were strongly associated with increased risk of AF. Hypertension and coronary heart disease mediated these effects. Genetic variation alleles at ABCG5, LDLR, and PCSK9 genes, which reduce lipid levels, were associated with lower risk of AF. Conclusions Increased lipids contained in LDL were associated with elevated risk of AF. L-LDL particles exhibited a clear association with increased AF risk. LDL is identified as a critical lipoprotein for predicting and treating AF.
Tocotrienols (T3), vitamin E analogues with potent antioxidant and therapeutic properties, have attracted increasing scientific interest. However, their clinical translation is hindered by poor and variable oral bioavailability. This limitation arises from their low aqueous solubility, rapid elimination, chemical instability and weak affinity for α-tocopherol transfer protein, which restricts systemic retention and tissue distribution. The intestinal absorption of T3 is a saturable, concentration-dependent process mediated primarily by Niemann-Pick C1-like 1 and, to a lesser extent, scavenger receptor class B type 1. This review outlines the pharmacokinetics of T3 and critically examines recent advances in oral delivery systems aimed at improving bioavailability. While existing approaches offer improvement in bioavailability, intrinsic absorption barriers remain a challenge. Future progress requires integrating both physicochemical and biological strategies, focusing on modulating intestinal transporters and controlling the release kinetics to mitigate local saturation. Such next-generation formulations may enable consistent absorption, prolonged circulation, and enhanced therapeutic efficacy of T3.
Randomized trial evidence firmly establishes that lowering LDL-C reduces atherosclerotic cardiovascular disease. However, observational studies consistently report U-shaped cholesterol-mortality associations, raising concerns about potential non-cardiovascular risks at very low levels. This narrative review (not systematic review; no PRISMA flow or formal search strategy) distinguishes observational associations from causal evidence, defines "very low cholesterol" as LDL-C < 70 mg/dL, and emphasizes patient context in personalized management for adults (not pediatrics). Epidemiologically, low cholesterol correlates with cancer, depression, hemorrhagic stroke, and infection, with biological plausibility involving membrane integrity, neurosteroid synthesis, vascular stability, and immune function. Yet these mechanisms remain speculative, and such associations are highly susceptible to reverse causation, whereby chronic illness itself lowers cholesterol. Critically, Mendelian randomization studies and meta-analyses of randomized controlled trials-including statin and PCSK9 inhibitor trials-have not demonstrated causal links between pharmacologically induced low LDL-C and these adverse outcomes. Mathematical models (quadratic, hormetic, biomechanical) are included as conceptual illustrations only and are not clinically validated. All mathematical models (quadratic, hormetic, Arrhenius, Hill, Laplace, CHI) presented herein are conceptual illustrations only, not clinically validated. They serve heuristic and hypothesis-generating purposes, not clinical prediction. For most high-risk patients, cardiovascular benefits clearly outweigh theoretical risks. However, subgroups such as the very elderly, frail individuals, or those with prior hemorrhagic stroke warrant individualized assessment guided by comorbidities, life expectancy, and treatment safety rather than cholesterol levels alone. Ultimately, observational signals do not challenge established LDL-C reduction benefits in high-risk populations; their primary value lies in reinforcing context-driven personalization at the margins of therapy.
Obesity impairs adipose tissue metabolism and dietary interventions capable of modulating these alterations remain insufficiently explored. To investigate depot-specific metabolic adaptations in subcutaneous (SAT) and epididymal adipose tissue (EAT) in response to chia oil supplementation. Male C57BL/6J mice received a control diet (C group) or a high-fat diet (H group) for 8 weeks, followed by 5 weeks of chia oil supplementation (1.5% w/w; 1.5 g/100 g diet; CC and HC groups). Exometabolomic profiling of SAT and EAT explants was performed using 1H-NMR, accompanied by targeted gene-expression analyses. Chia oil supplementation reduced adipocyte hypertrophy and improved glucose tolerance in obese mice without altering body or adipose tissue mass. Obesity markedly decreased l-histidine secretion in SAT and this effect was not modified by chia oil supplementation. In obese SAT, chia oil reduced l-valine and l-proline secretion and increased l-threonine levels, while it increased lactate secretion in obese EAT. Obesity did not significantly affect acetate secretion, although chia oil supplementation resulted in a depot-specific variation exclusively in the HC group. Correlation analysis revealed that chia oil modified metabolic interaction networks in both adipose depots. Chia oil supplementation induced depot-specific metabolic adjustments in SAT and EAT, highlighting the plasticity of adipose tissue and the potential of dietary lipids to modulate adipose metabolic networks.
The diagnosis of premature coronary heart disease (PCHD) continues to pose challenges. miR-302a-3p serves as a potential diagnostic marker. This study investigated the diagnostic value of the combination serum miR-302a-3p and LDL-C for PCHD. This study encompassed a total of 116 patients with coronary artery stenosis (CAS), 116 patients with PCHD, and 108 control subjects. The levels of miR-302a-3p, TNF, IL6, and IL1B were detected by RT-qPCR. ROC curves and logistic regression analysis were used to evaluate diagnostic value and risk factors for disease progression, respectively. In vitro models of HUVECs were established by treating the cells with ox-LDL. Cell proliferation and apoptosis were detected by CCK-8 and flow cytometry, respectively. SOD and MDA were assessed using commercial kits. Serum levels of miR-302a-3p and LDL-C were increased in both the CAS and PCHD groups. miR-302a-3p, LDL-C, Apo B-100, and Gensini scores are independent risk factors for the progression of CAS to PCHD. The AUC of the combined diagnostic model of miR-302a-3p and LDL-C for differentiating PCHD from the control group was 0.902, whereas the diagnostic value of miR-302a-3p alone was 0.885. In cellular experiments, inhibition of miR-302a-3p can mitigate the release of inflammatory factors and oxidative stress induced by ox-LDL. miR-302a-3p serves as an independent risk factor for PCHD. The combination of miR-302a-3p with LDL-C can significantly enhance the accuracy of diagnostic value. miR-302a-3p may participate in the pathological process of PCHD, and its function is related to inflammatory responses and oxidative stress.
The serum C-reactive protein-triglyceride glucose index (CTI) is a parameter integrating inflammation and insulin resistance, which are potential mechanisms for osteoarthritis (OA) or rheumatoid arthritis (RA). Our study aims to investigate its association with the risk of OA or RA. This study is based on cross-sectional data from the National Health and Nutrition Examination Survey (NHANES) 1999-2010, involving 6395 participants aged ≥ 20 years. Weighted logistic regression, restricted cubic splines (RCS), and subgroup analysis were employed to assess the relationship between CTI and OA, RA. After adjusting for confounding factors, CTI showed a significant positive correlation with the risk of OA (p < 0.05), and a non-linear relationship was observed (p = 0.0069). The risk of OA peaked when CTI reached 8.35 and gradually declined beyond this threshold. Subgroup analyses confirmed that this association consistently existed across different populations (all interaction p > 0.05). For RA, after adjustment for metabolic and lifestyle factors, the association between CTI and RA was not statistically significant (p > 0.05). There is a significant non-linear association between CTI and the risk of OA, suggesting that CTI may serve as a comprehensive indicator for assessing OA risk.
Chronic hepatitis B (CHB) and non-alcoholic fatty liver disease (NAFLD) frequently coexist, and lipid metabolic dysregulation may represent a shared biological feature between these conditions. However, the molecular mechanisms linking these conditions remain poorly defined. Transcriptomic datasets of CHB and NAFLD were analyzed to identify differentially expressed genes, followed by weighted gene co-expression network analysis (WGCNA), functional enrichment, and machine-learning-based feature selection. Gene set variation analysis (GSVA) was performed to assess pathway activity, and experimental validation was conducted in an FFA-induced steatosis model using HepG2 cells. Shared genes and lipid metabolism-related modules common to both CHB and NAFLD were identified. Functional enrichment revealed pathways associated with lipid metabolism and cellular stress regulation. Machine-learning analysis highlighted TRIM35 and MPP1 as potential key genes, which were further validated in vitro as upregulated in steatotic conditions. This integrative approach advances understanding of shared lipid metabolic features between CHB and NAFLD and suggests potential candidate genes for future investigation in disease diagnosis and therapy.
Lipid-soluble signaling molecule-related genes (LSMRGs) are critical in various tumors, but their role in gastric cancer (GC) prognosis and therapy remains unclear. Using transcriptomic data, this study analyzed LSMRG expression patterns, molecular subtypes, prognostic significance, and immune-microenvironment interactions in GC to identify new prognostic biomarkers and support precision medicine approaches. Using GC data from TCGA and GEO, LSMRGs from Genecard were analyzed. Unsupervised clustering defined LSMRG-based subtypes. Differentially expressed LSMRGs were identified by intersecting tumor-normal DEGs. A prognostic risk-score model was built via univariate Cox, LASSO, and multivariate Cox analyses, with model genes validated by qRT-PCR in cell lines. Comprehensive transcriptomic analyses included nomogram development, gene enrichment, immune infiltration, somatic mutations, and drug sensitivity. LSMRG-based clustering identified two patient subtypes with distinct survival and immunotherapy responses. From 83 differentially expressed LSMRGs, a 6-gene prognostic risk-score model was constructed, validated as an independent prognostic factor. Model gene expression was confirmed via qRT-PCR. The risk score accurately predicted 1-, 3-, and 5-year survival. High- and low-risk groups exhibited differential enrichment in pathways including neuroactive ligand-receptor interaction and hormone signaling. The high-risk group had a higher mutation burden, lower immune infiltration, and distinct drug sensitivity profiles compared to the low-risk group. This study delineates the expression landscape of LSMRGs in GC and clarifies their associations with molecular subtypes, prognosis, and immune regulation. The findings provide novel prognostic biomarkers and a molecular basis for targeting lipid-soluble signaling pathways in GC therapy.
Obesity induced by a high-calorie diet (HCD) results in the accumulation of ectopic fat in tissues not typically associated with lipid storage. This accumulation can cause lipotoxicity, a type of cellular stress triggered by the accumulation of lipid intermediates such as diacylglycerols (DAG) and ceramides (Cer) in nonadipose tissues like the liver. The accumulation of these bioactive lipids has been directly linked to the development of insulin resistance induced by a HCD. However, the specific molecular species of lipids associated with such metabolic abnormalities remain poorly defined. In this study, we conducted a systematic review and meta-analysis to consolidate current evidence on how HCDs alter the liver lipidome in rodents. A search was performed in PubMed to identify lipidomic studies on the livers of mice (C57Bl/6) and rats (Wistar and Sprague-Dawley) fed high-calorie diets. We assessed the effect size by calculating the standardized mean difference (SMD) using Hedges' g with a 95% confidence interval. A total of 18 studies were identified. The HCD had a significant effect on insulin resistance (HOMA-IR, p < 0.01) and significantly increased (p < 0.05) hepatic levels of Cer(18:0_18:0), Cer(18:1_18:0), Cer(18:1_20:0), Cer(18:2_20:0), and DAG(16:0_18:1) (p < 0.05). Furthermore, the HCD negatively affected three specific phosphatidylcholine (PC) species and four phosphatidylethanolamine (PE) species containing monounsaturated and polyunsaturated fatty acid chains. These findings may provide valuable insights for targeting the molecular mechanisms underlying tissue-specific insulin resistance, a significant condition in the context of obesity.
Hyperlipidemia or dyslipidemia is the term used for the increase in lipid levels in blood plasma, usually occurring due to a high-fat diet associated with a sedentary lifestyle. The increase in lipid levels can cause fatty infiltration in the liver known as hepatic steatosis, which can lead to inflammation, fibrosis, and necrosis consecutively. Melatonin is the hormone primarily responsible for regulating the circadian cycle, but it has antioxidant and anti-inflammatory properties and can also control lipid metabolism. Thus, the present research aimed to evaluate the effects of melatonin on the liver of hyperlipidemic rats. The animals were divided into control, tyloxapol, tyloxapol+melatonin. Hyperlipidemia was induced by applying tyloxapol at a dose of 400 mg/kg of body weight. Melatonin was administered simultaneously with tyloxapol in daily injections at a dose of 20 mg/kg. Sorological profiles for lipids, alkaline phosphatase, alanine aminotransferase, and aspartate aminotransferase, as well as liver histopathology and immunohistochemistry, were analyzed. Treatment with melatonin demonstrated an attenuating effect on the biochemical parameters of hyperlipidemic animals, reducing on average 80% the levels of triglycerides and very-low-density lipoprotein when compared to the tyloxapol group after 15 days of treatment, also showing a protective effect on the hepatic parenchyma that showed no changes. In addition, the administration of melatonin reduced the expression of proinflammatory cytokines and increased the expression of anti-inflammatory ones. The present study showed that melatonin administration has a protective effect on induction factors and the development of nonalcoholic fatty liver disease in Wistar rats with hyperlipidemia.
Ceramides (Cer) are bioactive lipids implicated in cardiovascular disease (CVD), yet their subtype-specific causal effects remain unclear. We performed a two-sample Mendelian randomization (MR) analysis using publicly available GWAS summary statistics to investigate the effects of C16:0-ceramide homologs (Cer16:0) and C24:1-ceramide homologs (Cer24:1) on six CVD outcomes. Instrumental variables were rigorously selected, and multiple MR methods were applied to ensure robust inference. Univariable MR identified a significant inverse association between Cer(d18:1/24:1) and heart failure (HF), which remained significant after false discovery rate correction. In contrast, the association for Cer(d17:1/16:0) did not remain significant after correction. No causal associations were observed for other CVD outcomes. When aggregating subtypes, genetically predicted higher total Cer16:0 levels were associated with increased HF risk, while no significant association was found for total Cer24:1. Multivariable MR further demonstrated that the protective effect of Cer(d18:1/24:1) on HF was robust, while estimates for C16 subtypes were attenuated and sensitive to model specification. In conclusion, our findings support a stable protective role of Cer(d18:1/24:1) in HF and highlight the complexity of subtype-specific effects among structurally related ceramides. These results underscore the importance of considering ceramide heterogeneity in cardiovascular research. Further studies are warranted to validate these findings and explore their clinical implications.
In this study, we report the first detection of a unique Delta 5,8,11,14,17-octadecapentaenoic acid (18:5n-1) in six diatom species (Thalassiosirales). The fatty acid was detected by GC-MS and GC-FID analyses using nonpolar capillary column SH-Rtx-5 ms (30 m & times; 0.25 mm, 0.25 mu m; Shimadzu, USA) and polar capillary column Supelcowax-10 (30 m & times; 0.25 mm, 0.25 mu m; Supelco, USA), respectively. Mass spectral analysis of 4,4-dimethyloxazoline (DMOX) derivative of this fatty acid indicated the presence of double bonds at Delta 5, 8, 11, and 14 positions, while the position of the terminal double bond (Delta 17) was inferred. The calculated and experimental equivalent chain lengths (ECL) were highly consistent, supporting the structural identification. To date, 18:5n-1 has not been described in diatoms, though previously detected in particulate organic matter samples and concentrated fish oil. The consistent occurrence of 18:5n-1 in the analyzed species suggests that it may represent a potential chemotaxonomic marker in diatoms, although its distribution across other diatom taxa remains to be established.
The impact of repeated heating of seed-based culinary oils on cardiometabolic health has not been well established. Heating oils to high temperatures (> 150°C) causes lipid peroxidation, thus generating potentially harmful compounds that may impair vascular function. This randomized, single-blind, crossover study investigated the acute effects of a high-fat meal containing either repeatedly heated (at 180°C, over 10 days, with 5 potato fries per day) sunflower oil-palm olein blend, compared with an unheated blend (containing 23.8% and 7.2% polar compounds respectively), on postprandial lipids and vascular function in 19 healthy male participants. Participants consumed each test meal on separate days, with measurements of flow-mediated dilation (FMD; primary outcome), arterial stiffness, plasma triacylglycerol (TAG), non-esterified fatty acid (NEFA), and glucose concentrations over 4 h. Postprandial vascular (FMD and arterial stiffness) responses as well as NEFA and glucose concentrations were comparable between meals. The postprandial TAG increase was lower after heated versus unheated oil (p < 0.001). These findings indicate that repeated heating of oil modifies postprandial lipaemia without acutely impairing vascular function. However, these short-term results do not address the potential cumulative effects of chronic, long-term consumption.
