Lipidology

Lipids play a central role in poultry nutrition by modulating energy utilization, nutrient digestibility, and metabolic processes related to lipid absorption and deposition. This review synthesizes current knowledge on the main dietary lipid sources used in poultry nutrition and their effects on performance, lipid metabolism, and egg yolk fatty acid composition. Conventional lipid sources, including vegetable oils and animal fats, differ in fatty acid profile, degree of saturation, and digestibility, which directly influence metabolic efficiency and productive responses. In addition, the strategic use of lipid sources enables the modulation of fatty acid profiles in poultry products, particularly through the enrichment of polyunsaturated fatty acids such as omega-3. These effects are associated with mechanisms involving lipid digestion, absorption, and hepatic lipoprotein synthesis, which regulate fatty acid deposition in tissues and egg yolks. However, responses to dietary lipids are influenced by factors such as inclusion level, oxidative stability, and lipid composition. Overall, dietary lipid manipulation represents an effective strategy to optimize production efficiency and enhance the nutritional quality of poultry-derived foods. Full article

Background/Objectives: Sebocytes, the primary cell type in sebaceous glands (SGs), produce a lipid mixture called sebum that is released onto the skin surface and is required for skin homeostasis. The lipid receptor Peroxisome Proliferator-Activated Receptor gamma (PPARγ) regulates sebocyte proliferation and lipid synthesis and is involved in acne development. As inhibition of PPARγ has been shown to reduce insulin-induced lipogenesis and Akt/mTOR signalling in SZ95 sebocytes, we here investigated the effects of PPARγ deletion on lipid homeostasis and autophagic stress responses and how the secretomes affect dermal fibroblasts. Methods: SZ95 sebocytes wildtype (WT) and PPARγ knockout (KO) were shifted to low serum and EGF-deficient conditions permissive for autophagy. Untargeted and targeted HPLC-MS/MS analyses were used to analyze native and oxidized lipids, respectively. Protein levels of LC3I/II and p62 were assessed using immunoblots and immunofluorescence microscopy to investigate the autophagic flux. Dermal fibroblasts were exposed to conditioned media. Results: In low serum culture media, KO SZ95 sebocytes displayed significantly altered levels of 23 lipid classes. We observed a significant increase in ether-linked fatty acids as components of complex lipids and detected elevated levels of phospholipid hydroperoxides and aldehydolipids in the KO sebocytes. KO SZ95 sebocytes failed to show the typical responses to lipoxidative stress, such as elevated p62 crosslinking or inclusion body formation, and had reduced LC3II/I ratios as compared to WT cells. PPARγ KO conditioned media promoted a trend towards an inflammatory fibroblast phenotype. Conclusions: These findings suggest that PPARγ in sebocytes may alter the lipidome, elevate redox stress, and affect the autophagic machinery, which could cause accumulation of oxidized lipids and other potentially harmful compounds in sebocytes. Full article

Background/Objectives: Microalgae are gaining increasing attention as sustainable sources of dietary lipids and other bioactive compounds; however, the relationship between microalgae lipid composition and physiological outcomes in vivo remains insufficiently understood. This study aimed to characterize antioxidant activity, total lipid content and fatty acid (FA) profiles of selected freshwater microalgae and to evaluate their dietary impact using Drosophila melanogaster as a whole-organism model. Methods: Four freshwater microalgal species (Chlorella vulgaris, Nannochloris limnetica, Scenedesmus communis, and Tetradesmus obliquus) were cultivated separately in 3N-BBM+V medium under controlled laboratory conditions. DPPH, FRAP and TPC were measured in microalgae methanolic extracts. Total lipids were extracted using a modified Breuer method and quantified gravimetrically. FA profiles were determined as fatty acid methyl esters by GC-FID. Freeze-dried microalgal biomass (3 mg/mL) was incorporated into standard D. melanogaster diet. Lifespan and body mass were assessed separately in females and males, as well as fecundity in general. Results: Total lipid content ranged from 17.3% to 28.1% of dry weight, with FA profiles dominated by C16 saturated, monounsaturated (omega-9), and omega-6 polyunsaturated fatty acids. Correlation analysis indicates that antioxidant properties of the studied microalgae are more closely linked to lipid fractions than to phenolic content. Dietary supplementation with microalgal biomass of three out of four microalgal species significantly extended median lifespan, particularly in males, without adverse effects on body mass or fecundity. Conclusions: These findings indicate that freshwater microalgae can serve as a physiologically safe dietary lipid source. D. melanogaster represents a suitable in vivo model for screening the nutritional potential of microalgal lipids. Full article

Micro- and nanoplastics (MNPs) are increasingly recognized as frequent environmental pollutants with growing evidence of tissue-specific lipid disruption in exposed organisms. MNP exposure is unavoidable and has attracted global attention due to its potential public health and ecological security risks. Unlike earlier studies that emphasize oxidative stress and inflammation, recent findings show that lipids are among the earliest and most sensitive molecular targets of MNP exposure. Lipidomics investigations across animal models reveal consistent patterns of lipidome remodeling, including altered phospholipid composition, disrupted sphingolipid balance, increased neutral-lipid storage, and mitochondrial lipid damage in metabolically active tissues such as the liver, kidney, lung, adipose tissue, and brain. Mechanistically, MNPs perturb membrane bilayer organization, induce MUFA and PUFA peroxidation, and destabilize lysosomal and mitochondrial function. These alterations trigger cardiolipin oxidation, ceramide accumulation, lipid droplet biogenesis, and impaired lipophagy, which collectively promote metabolic stress, energy imbalance, and neurotoxic or hepatotoxic phenotypes. Despite the growing number of tissue-specific studies, a major gap remains in understanding systemic MNP toxicity. The present review uniquely emphasizes tissue-resolved lipidomic signatures to identify convergent pathways of lipid disruption and proposes a conceptual framework, the “Lipid–Stress Axis”, to explain how localized lipidome perturbations may propagate into broader physiological dysfunction. By integrating lipidomics with metabolomics, imaging, and systems-biology approaches, we highlight key lipid-based biomarkers, mechanistic insights, and research needs essential for improving risk assessment and developing mitigation strategies against MNP-induced lipid dysregulation. Full article

Background/Objectives: Palmitic acid (PA), the most abundant saturated fatty acid in circulation, is elevated in obese individuals and has been implicated in promoting inflammation. However, its effects on inflammatory cytokine production in microglial cells and the involvement of cell surface receptors remain poorly characterized. Methods: In this study, we treated BV2 murine microglial cells with 200 µM PA or bovine serum albumin (BSA) control for 24 h and assessed IL-1β expression using semi-quantitative RT-PCR and/or ELISA. The roles of toll-like receptor (TLR)-2, TLR-4, G-protein-coupled receptor (GPR) 40, and GPR120 were investigated using siRNA knockdown and/or pharmacological inhibition. Results: Our studies found that PA treatment significantly increased IL-1β production as well as the mRNA expression of TLR-2, TLR-4, GPR40, and GPR120 compared to BSA controls. IL-1β expression correlated positively with TLR-2, TLR-4, and GPR40 levels. RNAi silencing of TLR-2, TLR-4, or GPR40 substantially diminished IL-1β expression in cells exposed to both BSA and PA. In contrast, neither RNAi silencing nor pharmacological inhibition of GPR120 suppressed IL-1β expression, suggesting that GPR120 may not mediate PA-induced inflammation. Conclusions: Our studies suggest that PA-induced production of IL-1β may be mediated via TLR-2, TLR-4, and GPR40, and that these cell surface receptors may serve as important molecular links between saturated fatty acids (SFAs) and neuroinflammation. Full article

Background/Objectives: Lipid oxidation is a major factor limiting the shelf life and nutritional quality of edible vegetable oils. Enhancing the oxidative stability of extra virgin olive oil (EVOO) through natural antioxidants is of increasing interest to both industry and consumers. This study aimed to evaluate the impact of five plant-derived essential oils (orange, lemon, black pepper, oregano, and rosemary) incorporated at three concentrations (0.5, 1, and 2% w/w) on the oxidative stability, antioxidant capacity, and bioactive compound retention of EVOO. Methods: All fortified EVOO samples were stored at 60 °C for 28 days to simulate accelerated oxidation. A positive control containing 200 ppm of butylated hydroxytoluene (BHT) was included for comparison. Oxidative stability was assessed through peroxide value, TBARS, p-anisidine value, and conjugated dienes/trienes. Tocopherols, carotenoids, and chlorophylls were quantified, while radical scavenging activity was determined using Trolox-equivalent assays. Correlation analyses were performed to explore relationships between essential oil composition and antioxidant performance. Results: Among the tested essential oils, oregano at 2% demonstrated the strongest protective effect, reducing both primary and secondary oxidation products and yielding a Totox value (34.26) close to that of the BHT-enriched control (29.86) after 28 days. Regarding long-term radical scavenging capacity, rosemary at 1% concentration provided the closest activity to BHT (402.89 vs. 536.64 μM Trolox equivalents). Both oregano and rosemary enhanced the preservation of α-tocopherol, likely due to the activity of key constituents such as carvacrol and 1,8-cineole. Conclusions: The incorporation of selected essential oils, particularly oregano and rosemary, can effectively enhance the oxidative stability and antioxidant capacity of EVOO, supporting their potential use as natural alternatives to synthetic antioxidants. Full article

Background: n-3 Docosapentaenoic acid (DPA; 22:5 n-3) is increasingly viewed as a distinct long-chain omega-3 fatty acid with biological activities that are not fully captured by eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA). However, progress remains limited by restricted access to high-purity DPA: most commercial sources contain DPA as a minor component, and published isolation strategies often yield only enriched mixtures or require multi-step workflows that are difficult to scale in standard laboratories. Objectives: We aimed to establish a robust, laboratory-accessible purification workflow to obtain DPA ethyl ester at high purity while preserving oxidative quality. Methods: Candidate lipid sources were screened to select an optimal DPA-containing feedstock. Oils were stabilized with antioxidants and pre-fractionated by cold crystallization (−20 °C) to reduce saturated lipids and oxidation by-products. Preparative separation used a stacked C18 flash system (15 μm + 45 μm in series) operated isocratically (methanol/water 92:8, v/v) at 120 mL/min. Fractions were analyzed by GC and iteratively reinjected to progressively enrich the DPA window. Solvent was recovered by distillation and reused. Results: Omegavie^® 4020EE (5.4% n-3 DPA) was identified as the best starting material. Pretreatment eliminated detectable TBARS-derived malondialdehyde. The isocratic purification-loop strategy produced tens of grams of DPA ethyl ester at >98% purity (GC–FID) defined as n-3 DPA area% of total identified fatty acid methyl esters by GC–FID, with per-cycle DPA recovery of 91–95%, overall recovery of 76% from the starting DPA content, and >90% solvent recycling. The workflow is scalable at the gram-to-tens-of-grams level for research laboratories, although solvent burden and column maintenance remain practical constraints for larger-scale implementation. Identity and purity were confirmed by GC–MS and ^1H NMR, and oxidation indices remained low (peroxide value < 0.2 meq/kg; p-anisidine < 3). Conclusions: This scalable, solvent-conscious protocol enables reliable access to high-purity DPA and should be adaptable to other low-abundance polyunsaturated fatty acids. Full article

Background/Objectives: Metabolic alterations, including dyslipidemia, may influence tumor biology and treatment outcomes in neuroendocrine tumors. However, the clinical relevance of dyslipidemia and lipid-lowering therapy in bronchopulmonary neuroendocrine tumors (BP-NETs) treated with somatostatin analogues (SSAs) remains poorly defined. This translational proof-of-concept study evaluated progression-free survival (PFS) in patients with advanced BP-NETs receiving SSAs according to dyslipidemia and statin therapy and explored the effects of statin-SSA combination treatment in vitro. Methods: We retrospectively analyzed 24 patients with advanced well-differentiated BP-NETs treated with SSAs as first-line therapy. Fourteen patients (58.3%) had dyslipidemia, and 11 of them were receiving statins. In parallel, NCI-H727 cells were treated with atorvastatin (10 µM), lanreotide (5 or 10 µM), or their combination for 48–72 h. Cell viability, proliferation, cell death, apoptosis, DNA damage, and ATP production were assessed. Results: Median PFS was 22.5 months overall. A trend toward longer PFS was observed in non-dyslipidemic vs. dyslipidemic patients (70 vs. 36 months, p = 0.08). Among dyslipidemic patients, statin therapy was associated with a non-significant trend toward longer PFS compared with no statin therapy (36 vs. 18 months, p = 0.30). In vitro, combined atorvastatin–lanreotide treatment reduced cell viability and proliferation, increased cell death, enhanced cleaved caspase-3 and p-γH2AX expression, and reduced ATP production. Conclusions: These findings support the potential relevance of lipid metabolism modulation as an adjunct strategy in advanced BP-NETs while highlighting the need for larger prospective studies and dedicated biochemical investigation of the underlying lipid-related pathways. Full article

Energy thriftiness and metabolic adaptations have had a crucial role in the emergence and spreading of the Homo lineage in the world. A higher-energy demand was required not only for the growing body mass, encephalization and human proliferation, but also for the survival adaptations to the environmental stresses. Because lean body mass lacks the energy-storage capacity required to supply the body’s demands, dedicated fat-storing cells originated. To feed such fat stores, the hominid evolution developed “meat-adaptive” genes to detect, digest and metabolize higher fat diets, and body-fat stores can be affected by lifestyle through hormonal-controlled daily energy balance. In energy surplus conditions, hypertrophy and hyperplasia of adipocytes can occur, with hypertrophic adipocyte signaling both a neo-adipocyte differentiation (leading to hyperplasia) and a local macrophage density (resident + infiltrated macrophages) for fat surplus scavenging. Adiposity-induced inflammation is caused by fat-overstored (hypertrophied) adipocytes that may operate as an overactive endocrine organ secreting an array of pro-inflammatory adipokines that, in combination with resident-macrophage activity and infiltrated blood-recruited, monocyte-derived macrophages, amplify the inflammatory process by spurting pro-inflammatory cytokines into the bloodstream. From an evolutionary perspective, obese humans represent a natural selection overexpressing the “thrifty” genes evolved for efficient food collection and fat deposition intended to help in survival in prolonged periods of famine. However, genetically speaking, obesity is a polygenic multifactorial disorder. Considering the rapidity of obesity-epidemic growth worldwide, epigenetic sets forth the key assumption of the mismatch between our human genome molded over thousands of generations, coping with the unprecedented dietary and physical conditions. Consequently, obesity would be due to our evolutionary-adapted polygenic-charge expressed by a deteriorated lifestyle characterized by high energy-dense food intake coupled with a reduction in caloric expenditure stemming from new mobility-reducing technologies. As a model of lifestyle change (LiSM), our 28-year on-going longitudinal study (“Moving for Health”) has shown effectiveness in the reduction not only of obesity but especially of its comorbidities, in a (10 week to 3 year) length-dependent LiSM. However, a disappointing progressive decrease in compliance with the study has been observed and attributed to the resistance of people to change their actual “obesogenic” lifestyle, basically represented by the individuals’ demand for labor-saving technologies and convenient, affordable, palatable foods. Full article

The field of immunometabolism highlights the intricate interplay between immunity and metabolism. The cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway is a central component of innate immunity that detects double-stranded DNA (dsDNA) from a range of sources, including pathogenic and host-derived DNA. It is now recognized that the cGAS-STING pathway has broad implications in a variety of human conditions including cancer, age-related diseases, and autoimmune disorders. Given the abundance and diversity of lipids across cellular compartments serving as structural components and signaling molecules, it is unsurprising that lipid metabolism influences the regulation of cGAS-STING signaling. Lipids can directly alter signaling protein dynamics through interactions within membrane compartments, while alterations in lipid metabolism can remodel multiple cell-intrinsic signaling cascades. Here, we summarize emerging concepts and recent discoveries that have advanced our understanding of how lipid metabolism and lipids regulate the cGAS-STING pathway. Full article

Background: Familial hypercholesterolaemia (FH) is an inherited condition that substantially increases the risk of premature atherosclerotic cardiovascular disease (ASCVD). Despite effective therapies, many affected individuals remain undiagnosed. Incorporation of FH testing into newborn screening (NBS) is a potential strategy to increase detection. This study explores the attitudes of expectant parents toward NBS for FH. Methods: Expectant parents attending Obstetrics and/or Obstetric Medicine clinics at a tertiary referral centre were invited to participate in a semi-structured interview in person or via telephone. The interview explored views on screening children for FH in general, preferred timing of screening, opinions on integrating FH screening into routine NBS, acceptability of genetic testing in children and newborns, willingness to engage in family screening and any potential impact on participation in routine NBS programmes. Participants were also invited to discuss concerns and benefits. Results: All participants (n = 22) supported screening children for FH with the majority (n = 19, 86%) preferring screening during the newborn period, and all but one (n = 21, 95%) supporting adding FH to routine NBS. All participants (n = 22, 100%) considered genetic testing for FH acceptable for children, 21 (95%) considered it acceptable for newborns. All participants would partake in extended family screening and none indicated that including FH genetic testing would reduce their willingness to engage in routine NBS. Concerns raised by participants included administering lipid-lowering therapy to children and potential post-diagnosis stress and anxiety. All participants reported that a diagnosis would not affect parent–child bonding. Key perceived benefits raised by participants included early diagnosis and prevention of heart disease, family screening, and broader health system and community advantages. Conclusions: Expectant parents demonstrated strong support for FH NBS and indicated no negative impact on uptake of routine NBS. Further work is needed to address parental concerns and guide implementation strategies. Full article

Background: Proprotein convertase subtilisin/kexin type 9 (PCSK9) promotes low-density lipoprotein receptor degradation and thereby regulates plasma LDL cholesterol levels. Although PCSK9 is primarily produced by the liver, it has been detected in platelets; however, the origin and functional relevance of platelet-associated PCSK9 remain unclear. Methods: Washed platelets (WPs) were isolated from normolipidemic subjects. Endogenous platelet PCSK9 content was quantified by ELISA, and PCSK9 molecular forms were assessed by immunoblotting. The WPs were incubated with recombinant PCSK9 (recPCSK9), and platelet aggregation in response to arachidonic acid (AA) or thrombin (Thr) was evaluated. The effects of LDL- or HDL-bound PCSK9 on platelet aggregation were also examined. Results: Platelets from normolipidemic subjects contained measurable amounts of PCSK9 (0.84 ± 0.27 ng/mg protein), which increased to 2.91 ± 0.53 ng/mg protein following incubation with recPCSK9. Exposure to recPCSK9 significantly enhanced AA- and Thr-induced platelet aggregation. In contrast, LDL and HDL inhibited platelet aggregation independently of their PCSK9 content. Conclusions: Human platelets contain endogenous PCSK9 and can accumulate additional PCSK9 from the extracellular environment. Exogenous PCSK9 enhances platelet aggregation, supporting a potential prothrombotic role for circulating PCSK9 even in normolipidemic individuals. These findings provide new insight into the complex interplay between PCSK9, lipoproteins, and platelet function. Full article

Atherosclerosis is a progressive cardiovascular disease characterized by lipid accumulation, oxidative stress, and inflammation within the arterial walls. Environmental pollutants, including particulate matter (PM), diesel exhaust particles (DEPs), and heavy metals, contribute directly to the initiation and progression of arterial plaques by promoting LDL oxidation, endothelial dysfunction, foam cell formation, and vascular inflammation, whilst high-density lipoprotein (HDL) provides protective effects. This review examines the mechanistic links between environmental exposures, lipid dysregulation, and plaque formation, highlighting how both gaseous and particulate pollutants and toxic and essential metals, as well as endocrine disrupting chemicals, influence atherosclerotic risk. Potential antioxidant and lifestyle interventions to mitigate these pollutant-driven effects are also discussed. Full article

Lipids are a diverse group of hydrophobic molecules including fats, oils, phospholipids, and steroids that are vital for numerous biological functions including energy storage, cellular structure, and signaling whose composition and metabolism undergo profound transformations with age. These age-related shifts due to increased lipid peroxidation, disrupted cholesterol homeostasis, and altered membrane phospholipid content, actively contribute to progressive loss in cellular homeostasis and pathogenesis of major age-related diseases. This review explores the critical role of lipids: as master regulators of cellular signaling pathways, and as key drivers of chronic inflammation and metabolic dysfunction. Dysregulated lipid metabolism is central to cardiovascular disease which is driven by altered myocardial energy substrate utilization and lipoprotein dynamics. In neurodegenerative disorders like Alzheimer’s and Parkinson’s disease, disruptions in ceramide, cholesterol, and specialized pro-resolving lipid mediators fuel neuroinflammation and protein aggregation. Furthermore, we explore the dual role of dietary lipids, which can either exacerbate or mitigate age-related decline, highlighting the potential of personalized nutritional approaches and lipid-targeting therapeutics. By integrating the mechanisms of lipid signaling, inflammation, and metabolic regulation, this analysis highlights that lipids are not merely passive structural components but active drivers of the aging process, positioning lipid metabolism as a promising frontier for interventions aimed at promoting health span and combating age-related disease. Full article

Cardiovascular disease is the leading cause of mortality in insulin-resistant individuals, with metabolic cardiomyopathy preceding overt heart failure in a substantial proportion of patients with diabetes. Skeletal muscle accounts for approximately 40% of body mass and nearly 80% of insulin-stimulated glucose disposal, positioning it as a major determinant of systemic lipid flux. Dysregulation of lipid droplet dynamics, lipolysis, and fatty acid trafficking in skeletal muscle alters circulating lipid availability and promotes ectopic lipid deposition and mitochondrial stress in the myocardium. Intramyocellular lipid handling is governed by coordinated actions of lipid droplets, perilipin proteins (PLIN2 and PLIN3), adipose triglyceride lipase (ATGL), and diacylglycerol acyltransferases (DGAT1/2), which together regulate the rate and composition of fatty acid release into the circulation. Impaired coupling between intramyocellular lipid droplet turnover and mitochondrial oxidation in insulin-resistant muscle increases circulating free fatty acids, reducing cardiac oxidative capacity. In response, the myocardium undergoes mitochondrial lipid remodeling, including alterations in cardiolipin composition that impair cristae structure and electron transport chain efficiency. Excess lipid exposure activates apoptosis signal-regulating kinase-1 (ASK-1), promoting cardiomyocyte apoptosis and inflammatory signaling, while peroxisome proliferator-activated receptor gamma (PPARγ) modulates lipid uptake, storage, and mitochondrial oxidation in a context-dependent manner. This review integrates skeletal muscle–cardiac lipid crosstalk with ASK-1 and PPARγ signaling to define mechanisms linking peripheral insulin resistance to early myocardial dysfunction and to identify targets for intervention before irreversible cardiac remodeling develops. Full article

Chronic, low-grade inflammation is a characteristic of metabolic diseases like type 2 diabetes. Despite recommendations to select low- or non-fat dairy foods over full-fat dairy foods for metabolic health, recent research suggests potential anti-inflammatory benefits of dairy fat consumption. We aimed to compare the systemic inflammatory tone (i.e., circulating inflammatory biomarker concentrations and ex vivo peripheral blood mononuclear cell inflammatory responses) of individuals with prediabetes after consuming diets with full-fat (3.25%) or non-fat yogurt. We hypothesized that short-term consumption of three daily full-fat yogurt servings beneficially affects inflammatory tone. Thirteen participants aged 45–75 years completed an eight-week randomized, double-masked, controlled crossover study. The two, three-week experimental diets comprised three daily servings of full-fat or non-fat yogurt and were each preceded by a one-week run-in diet. Following each diet, circulating inflammatory biomarkers and cytokine concentrations in the supernatants of peripheral blood mononuclear cells under control or lipopolysaccharide-stimulated conditions were measured. Compared with non-fat yogurt intake, circulating immature granulocyte concentrations were lower following full-fat yogurt intake, but there were no other differences in leukocyte concentrations. Circulating concentrations of cytokines or other inflammatory markers did not differ by diet. Cell supernatant interleukin-1β concentrations were lower following the full-fat yogurt diet under unstimulated conditions but were not different between diets under stimulated conditions. There were no differences by diet in supernatant concentrations of other cytokines under unstimulated or stimulated conditions. Together, minimal differences in inflammatory tone were observed following the short-term consumption of three daily servings of full-fat or non-fat yogurt in individuals with prediabetes. Full article

Thin-layer chromatography (TLC) remains a widely used, cost-effective and convenient method to separate small molecules, particularly in the field of natural products and (phospho)lipids. Despite advances in chromatographic methods such as high-performance liquid chromatography (HPLC), TLC retains several advantages, including simplicity and accessibility. However, a critical step is the visualization of the separated lipids on the TLC plate. Although the majority of the regularly used methods were established decades ago, there are still a number of potential pitfalls and widely unknown aspects. This review provides a concise overview about commonly used stationary phases and the solvent systems in TLC analysis of lipids. The main focus is on visualization techniques, spanning from non-specific, destructive (charring by semi-concentrated acids) to specific, non-destructive approaches (e.g., exposition to iodine to monitor unsaturated lipids). The advantages and disadvantages of the different methods will be critically discussed and frequently occurring problems highlighted. Furthermore, the combination of TLC with mass spectrometry (MS) detection will be introduced, covering both extraction-based electrospray ionization MS techniques as well as desorption techniques such as matrix-assisted laser desorption/ionization MS. MS detection, while generally more sensitive and offering molecular specificity, introduces higher technical and financial requirements compared to conventional staining. Nonetheless, the combination of TLC with MS holds significant potential for enhancing lipidomic workflows, particularly in complex biological samples. Full article

Background: In recent decades, interest has grown in the link between lipid metabolism and mental health. Omega-3 fatty acids (EPA and DHA) play a crucial role in brain function, neuroplasticity, and emotional regulation. Deficiency or an imbalanced omega-6/omega-3 ratio, typical of Western diets, has been associated with an increased risk of mood disorders, such as major depression and bipolar disorder. Objective: This review critically synthesizes neurobiological and clinical evidence on the role of omega-3s in mood disorders, assessing mechanisms, randomized controlled trials, and meta-analyses, with a focus on inflammatory biomarkers and their integration into a personalized psychiatry framework. Methods: A narrative review of epidemiological studies, randomized controlled trials (RCTs), meta-analyses, and experimental research was conducted, evaluating mechanistic pathways (synaptic, inflammatory, neuroplastic, and redox) and clinical moderators (particularly inflammatory markers and dietary lipid profiles). Results: Consistent evidence indicates that EPA-enriched formulations (≥60%) exert antidepressant effects, particularly in patients with elevated inflammatory markers (CRP, IL-6, TNF-α). In contrast, DHA-only preparations show limited efficacy, and outcomes vary depending on dietary omega-6/omega-3 balance. However, the literature remains heterogeneous in design, sample size, and biomarker stratification, which limits generalizability and contributes to conflicting findings across studies. Conclusions: While omega-3 fatty acids represent promising adjunctive interventions for mood disorders, methodological weaknesses and inconsistent formulations hinder definitive conclusions. Future research should prioritize biomarker-guided, precision-based approaches to clarify therapeutic efficacy and optimize clinical use. Full article

Background/Objectives: Long-chain fatty acids induce lipid droplet formation in several cell types including cancer cells. These lipid droplets have been shown to accumulate in various cancers and are dysregulated in many pathologies. Thus, this study was designed to examine the many unique long-chain fatty acids and their abilities to induce lipid droplet formation in cancer cells. Methods: HeLa human cervical cancer cells were incubated with individual fatty acids and live-stained for lipid droplets. This study analyzed four saturated, four monounsaturated, and nine polyunsaturated (4 omega-3, 4 omega-6, and 1 omega-9) fatty acids. This diversity of fatty acids was chosen to highlight any important non-uniform differences in the regulation of lipid droplet formation by unsaturated fatty acids. The area of the lipid droplets and the number of lipid droplets per cell were measured and compared between the different fatty acid conditions. Results: Unsaturated fatty acids induced lipid droplets differently compared to saturated fatty acids. Further, an inverse relationship was established between average area of lipid droplets and the average number of lipid droplets per cell. Finally, two perilipin genes (PLIN1/2) involved in lipid droplet formation were shown to have significantly higher expression with the two polyunsaturated fatty acids (alpha- and gamma-linolenic acid) versus the saturated fatty acid (stearic acid) condition. Conclusions: Together, different fatty acids produce structurally different lipid droplets. It will be important to further investigate the biochemistry and mechanistic differences in the formation of these lipid droplets under these specific long-chain fatty acid conditions. Full article