Search Results (115)

This study reports the development of a sustainable biocatalyst system for free fatty acid (FFA) production from cocoa bean shell (CBS) oil using Burkholderia cepacia lipase (BCL). CBS was explored as both a support material and a reaction substrate. Six immobilized systems were prepared using organic (CBS), inorganic (silica), and hybrid (CBS–silica) supports via physical adsorption or covalent binding. Among them, the covalently immobilized enzyme on CBS (ORG-CB) showed the most balanced performance, achieving a catalytic efficiency (Ke) of 0.063 mM⁻¹·min⁻¹ (18.6% of the free enzyme), broad pH–temperature tolerance, and over 50% activity retention after eight reuse cycles. Thermodynamic analysis confirmed enhanced thermal resistance for ORG-CB (Ed = 32.3 kJ mol⁻¹; ΔH‡ = 29.7 kJ mol⁻¹), while kinetic evaluation revealed that its thermal deactivation occurred faster than for the free enzyme under prolonged heating. In application trials, ORG-CB reached 60.1% FFA conversion from CBS oil, outperforming the free enzyme (49.9%). These findings validate CBS as a dual-function material for enzyme immobilization and valorization of agro-industrial waste. The results also reinforce the impact of immobilization chemistry and support composition on the operational and thermal performance of biocatalysts, contributing to the advancement of green chemistry strategies in enzyme-based processing. Full article

Lipids play vital roles in insect physiology, functioning as energy reserves, membrane constituents, and cuticular protectants. However, few studies have examined the anatomical distribution of lipids in blood-feeding Diptera and compared the compositions of the cuticular and internal compartments. This study analyzes the qualitative and quantitative profiles of free fatty acids (FFAs) in the female Tabanus bovinus, a hematophagous horsefly species, across different anatomical regions, including the head, wings, legs, thorax, and abdomen. The surface and internal lipid fractions were isolated using petroleum ether/dichloromethane extraction followed by sonication. GC-MS revealed the presence of 21 FFAs, including 16 saturated (C7:0, C8:0, C9:0, C10:0, C11:0, C12:0, C13:0, C14:0, C15:0, C16:0, C17:0, C18:0, C19:0, C20:0, C22:0, C24:0) and five unsaturated (C16:1, C18:2, C18:1, C20:5, C20:4). The head and wings showed the highest concentrations of cuticular FFAs. At the same time, internal lipid stores were most prominent in the thorax and abdomen (but four times lower than in the head cuticle), reflecting their role in energy storage and reproduction. All cuticular and internal extracts were dominated by C16:0, C18:0, and C18:1. Notably, several FFAs were undetected in specific compartments: C10:0 from inside the head, C11:0 and C13:0 from inside all examined body parts, C19:0 was absent from inside the head, wings and legs, while C20:5 and C20:4 were absent from both the cuticular and internal lipid pools of the wings. Interestingly, our analysis of the cuticle on the thorax and abdomen together revealed that both C13:0 and C19:0 were present only on the dorsal side, i.e., absent from the ventral side. These absences suggest a selective lipid metabolism tailored to the functional and ecological demands of T. bovinus females. Our findings suggest that the absence of specific compounds from individual body parts may serve as an indicator of physiological specialization. This work provides new insights into lipid compartmentalization in Tabanidae and offers a framework for future comparative and ecological lipidomics studies in insects. Full article

Squalane (SQ, a saturated, sebum-mimetic hydrocarbon), oleic acid (OA, a monounsaturated fatty acid), and linoleic acid (LA, a polyunsaturated essential fatty acid) belong to the category of “lipids and fats” in cosmetic materials, and are widely employed as skin-conditioning emollients. However, they present differences in UV stress. In this study, we compared their effects on UV-induced oxidative damage, inflammation, and lipid metabolism using a mouse model and human sebaceous gland cells (SZ95). Results showed that 10% SQ did not worsen oxidative damage or inflammation after 6 weeks of UV exposure. In contrast, the 5% and 10% OA/LA groups showed increased skin wrinkling (p < 0.01), epidermal thickening (p < 0.05), and sebaceous gland atrophy. Transcriptome analysis indicated OA/LA upregulated arachidonic acid-related cytokine pathways (PTGS2/IL-1β; p < 0.001). In SZ95 cells, 0.006% OA/LA significantly increased lipid droplet formation (p < 0.001), free fatty acid (FFA) levels (p < 0.001), and pro-inflammatory gene expression (p < 0.001). Conversely, SQ neither promoted lipid droplet/FFA secretion nor induced oxidative stress. These findings suggest that high concentrations of unsaturated fatty acids in skincare may worsen lipid dysregulation and inflammation, while formulations based on saturated hydrocarbons like SQ could provide superior photoaging management by stabilizing skin barrier function. Full article

The advancement of modern lifestyles has precipitated excessive consumption of energy-dense foods, driving the escalating global burden of lipid metabolism dysregulation-related pathologies—including obesity, type 2 diabetes mellitus (T2DM), non-alcoholic fatty liver disease (NAFLD), and cardiovascular disorders—which collectively pose a formidable challenge to global public health systems. The almond hull, as a by-product of almond processing, is rich in polyphenolic compounds with demonstrated antioxidant, anti-inflammatory, and lipid-lowering potential, though its precise hypo-lipidemic mechanisms remain elusive. In this study, polyphenols were extracted from almond hulls using 50% ethanol with ultrasound-assisted extraction, followed by preliminary purification via solvent partitioning. The ethyl acetate fraction was analyzed by liquid chromatography–mass spectrometry (LC-MS). Network pharmacology and molecular docking were employed to investigate the interactions between key bioactive constituents (e.g., quercetin, baicalein, and kaempferol) and targets in lipid metabolism-related pathways. Molecular dynamics (MD) simulations further evaluated the stability of the lowest-energy complexes. Results revealed that the ethyl acetate fraction exhibited potent pancreatic lipase inhibitory activity (IC50 = 204.2 µg/mL). At 0.1 mg/mL after 24 h treatment, it significantly reduced free fatty acids (FFAs)-induced intracellular triglyceride accumulation (p < 0.01) and enhanced cellular antioxidant capacity. Network pharmacology and in vitro studies suggest almond hull extract modulates PI3K-AKT signaling and improves insulin resistance, demonstrating lipid-lowering effects. These findings support its potential in functional foods and pharmaceuticals, though further in vivo validation and mechanistic investigations are required. Full article

Background/Objectives: Metabolic syndrome (MetS) is a complex, multifaceted disorder with significant socioeconomic and public health consequences, increasingly acknowledged as a global epidemic. Fibroblast growth factor 21 (FGF-21) is known to play a vital role in metabolic regulation; however, the precise roles and interactions of free fatty acids (FFAs) and insulin in influencing FGF-21 activity under both normal and pathological conditions are not yet fully understood. Meteorin-like protein (Metrnl) is a newly identified adipokine that appears to have the potential to regulate metabolic inflammation, which is a critical pathological factor in obesity and insulin resistance. Additionally, nesfatin-1, which is widely expressed in both central and peripheral tissues, is thought to be involved in various physiological functions beyond appetite control, such as glucose homeostasis, stress response, and cardiovascular health. Recent studies have indicated that sortilin may play a role in the pathophysiology of several metabolic disorders, including type 2 diabetes mellitus. Methods: This investigation was a cross-sectional study involving 200 individuals with obesity, which included both metabolically healthy obese participants and those experiencing obesity along with glycemic disorders. Serum levels of FGF-21, sortilin, Metrnl, and nesfatin-1 were measured using standardized enzyme-linked immunosorbent assay (ELISA) techniques. Results: The results indicated that FGF-21 levels were significantly elevated in patients with metabolic syndrome (p < 0.001), as well as those with insulin resistance (p = 0.009) and dyslipidemia (p = 0.03). Serum Metrnl levels were notably elevated in individuals meeting the criteria for insulin resistance, with a statistical significance of p < 0.001. Additionally, patients experiencing carbohydrate metabolism disorders exhibited significantly higher serum sortilin levels compared to those with normal blood glucose levels, with a p-value of 0.003. Conclusions: This research highlights FGF-21, Metrnl, nesfatin-1, and sortilin as potential biomarkers involved in the development of critical aspects of metabolic syndrome. Full article

Background/Objectives: Metabolic dysfunction-associated fatty liver disease (MAFLD) is a chronic hepatic condition marked by lipid buildup, lipotoxicity, and inflammation. Prior research indicates that 3,3′-Diindolemethane (DIM), a natural indole-type phytochemical that is abundant in brassicaceae vegetables, has been reported to reduce body weight and improve lipid metabolism in mice subjected to a high-fat diet (HFD). The aryl hydrocarbon receptor (AhR), a nuclear receptor implicated in lipid metabolism and immune regulation, serves as a functional receptor for DIM. However, the underlying signaling pathways that regulate MAFLD remain elusive. Our objective is to ascertain the beneficial impact of DIM on MAFLD and the associated mechanisms. Methods: Hematoxylin and eosin staining, together with Oil Red O staining, were utilized to assess the pathological changes and lipid deposition in the liver. Biochemical analysis was employed to measure levels of triglyceride (TG), total cholesterol (TC), free fatty acid (FFA), aspartate transaminase (AST), alanine transaminase (ALT), low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C). The cell survival rate of HepG2 cells treated with palmitic acid (PA) and DIM was assessed using the CCK-8 assay. Flow cytometry was employed to measure the fluorescence intensity emitted by lipid droplets within cells. Western blotting analysis was performed to assess AhR pathway and fatty acid transporter expression levels in hepatic tissue. Results: Our results showed that DIM significantly attenuated body weight gain and hepatic injury brought on by HFD, decreased lipid droplet accumulation in HepG2 cells, and effectively suppressed the phosphorylation of p38 MAPK and the protein expression levels of fatty acid transporters CD36 and FATP4. Conclusions: DIM reduced lipid accumulation by activating AhR and suppressing p38 MAPK phosphorylation, thereby inhibiting fatty acid transport and inflammatory responses. These findings suggest that DIM may represent a promising therapeutic candidate for MAFLD, warranting further exploration for clinical applications. Full article

In this study, we systematically investigated the mechanisms of the antioxidation and anti-lipid accumulation effects of antioxidant peptides from Litsea cubeba on a free fatty acid (FFA)-induced NAFLD model of HepG2 cells. The NAFLD cell model was constructed by inducing the HepG2 hepatocellular carcinoma cell line with 0.5 mmol/L FFAs, and AQRDAGLL, QEGPFVR, and DVPPPRGPL were given to the culture to study their lipid-lowering and antioxidant activities on NAFLD cells. The lipid-lowering activities of the three antioxidant peptides were evaluated by Oil Red O staining and TG and TC content assays, and the results showed that all three peptides had strong ameliorating effects on FFA-induced lipid accumulation in NAFLD cells. The intracellular antioxidant protease (CAT, GSH, and SOD) activity levels and lipid peroxidation (MDA) content were measured and intracellular ROS levels were detected. The results showed that after intervention with the antioxidant peptides, the intracellular ROS levels in the NAFLD model cells were significantly reduced, the SOD and CAT activities were increased, the GSH content was elevated, and the MDA content was reduced, which indicated that AQRDAGLL, QEGPFVR, and DVPPPRGPL were able to inhibit the oxidative stress of the cells effectively and to achieve the effect of intervening in NAFLD. JC-1 fluorescence staining experiments showed that the mitochondrial membrane potential function of NAFLD cells was restored under the effect of the antioxidant peptides. Molecular dynamics simulations revealed that the main driving force between QEGPFVR and Keap1 protein was van der Waals forces, ΔG = −62.11 kcal/mol, which indicated that QEGPFVR was capable of spontaneously binding to Keap1 protein. Full article

Age-related macular degeneration (AMD) is a leading cause of irreversible vision loss in the elderly, and it is characterized by oxidative stress, lipid dysregulation, and dysfunction of the retinal pigment epithelium (RPE). A hallmark of AMD is the presence of drusen, extracellular deposits rich in lipids, proteins, and cellular debris, which are secreted by the RPE. These deposits impair RPE function, promote chronic inflammation, and accelerate disease progression. Despite advancements in understanding AMD pathogenesis, therapeutic strategies targeting lipid dysregulation and oxidative damage in RPE cells remain limited. This study evaluated the effects of liraglutide, a glucagon-like peptide-1 receptor agonist (GLP-1RA), on free fatty acid (FFA)-induced damage in ARPE-19 cells, a widely used in vitro model of RPE dysfunction. FFA treatment induced lipid droplet accumulation, oxidative stress, and epithelial–mesenchymal transition (EMT), which are processes implicated in AMD progression. Liraglutide significantly reduced lipid droplet accumulation, mitigated oxidative stress, and suppressed EMT, as demonstrated by high-content imaging, immunocytochemistry, and molecular assays. Mechanistic analyses revealed that liraglutide activates AMP-activated protein kinase (AMPK), enhancing lipophagy and restoring lipid homeostasis. Furthermore, liraglutide influenced exosome secretion, altering paracrine signaling and reducing EMT markers in neighboring cells. These findings underscore liraglutide’s potential to address critical mechanisms underlying AMD pathogenesis, including lipid dysregulation, oxidative stress, and EMT. This study provides foundational evidence supporting the development of GLP-1 receptor agonists as targeted therapies for AMD. Full article

(1) Background: Hepatic lipid accumulation is the initial factor in metabolic-associated fatty liver disease (MAFLD) in type 2 diabetics, leading to accelerated liver damage. The NOD-like receptor protein 3 (NLRP3) inflammasome plays a critical role in this process. Dapansutrile (DAPA) is a novel NLRP3 inflammasome inhibitor; however, its effect on ectopic lipid accumulation in the liver remains unclear. This study aimed to investigate the therapeutic effect of DAPA on hepatic lipid accumulation in a diabetic mouse model and its potential mechanisms. (2) Methods: The effects of DAPA on hepatic ectopic lipid deposition and liver function under metabolic stress were evaluated in vivo using db/db and high-fat diet (HFD) + streptozotocin (STZ) mouse models. Additionally, the role and mechanism of DAPA in cellular lipid deposition, mitochondrial oxidative stress, and inflammation were assessed in HepG2 cells treated with free fatty acids (FFA) and DAPA. (3) Results: Our findings indicated that DAPA treatment improved glucose and lipid metabolism in diabetic mice, particularly addressing liver heterotopic lipid deposition and insulin resistance. DAPA treatment also ameliorated lipid accumulation and mitochondrial-related functions and inflammation in HepG2 cells through the NLRP3-Caspase-1 signaling axis. (4) Conclusions: Targeting NLRP3 with DAPA may represent a novel therapeutic approach for diabetes-related fatty liver diseases. Full article

High concentrations of free fatty acids (FFAs) caused by negative energy balance render the cow more prone to inflammatory diseases in part due to an imbalance in the types of immune cells and their specific functions. We previously demonstrated that ORAI calcium release-activated calcium modulator 1 (ORAI1) was associated with increased CD4⁺ Th17 content, but the precise mechanisms remain unclear. The purpose of this study was to evaluate the efficacy of FFAs on CD4⁺ T cell inflammatory response. High FFAs in dairy cows caused the transcript level of the pro-inflammatory factor IL-17A, plasma concentration of IL-17A, and amount of intracellular IL-17A to increase while the transcript levels and intracellular amount of the anti-inflammatory factor FOXP3 were downregulated. These changes indicated Th17/Treg imbalance and inflammation in dairy cows with high FFA. Moreover, ORAI1 and SDS abundance was elevated in dairy cows with high FFAs by transcriptomics, QPCR, and Western blot. Knockdown of SDS (siSDS) did not alter ORAI1 expression in CD4⁺ T cells from high-FFA cows, while it decreased the expression of inflammatory factors. Transfection of CD4⁺ T cells using siRNA knockdown for ORAI1 (siORAI1) revealed that SDS and inflammatory factor abundance decreased. Serine can be catabolized to pyruvate by the action of serine dehydratase (SDS). Data from this study suggested that high FFAs caused by negative energy balance after calving regulates the Th17/Treg balance via SDS, but SDS does not regulate ORAI1 abundance. The above data suggested a pro-inflammatory mechanism in CD4⁺ T cells regulated by the ORAI1-sensitive SDS pathway in early postpartum cows experiencing high-FFA conditions. Thus, targeting this pathway may represent a new therapeutic and interventional approach for preventing immune-related disorders around parturition. Full article

Melatonin is involved in various functions such as the timing of circadian rhythms, energy metabolism, and body mass gain in experimental animals. However, its effects on adipose tissue lipid metabolism are still unclear. This study analyzes the effects of melatonin on the relative gene expression of lipolytic proteins in rat mesenteric adipose tissue and free fatty acid (FFA) and glycerol plasma levels of male Wistar rats fed a high-fat (HFD) or maintenance diet. Four experimental groups were established: control, obese, and control or obese plus 2.3 mg/kg/day of melatonin in tap water. After 11 weeks, animals were sacrificed at different times throughout a 24 h cycle, and mesenteric adipose tissue and plasma samples were collected and analyzed. Cgi58, Perilipin, and Dgat1 gene expression, as well as FFA and glycerol concentrations, showed rhythm patterns in the control group. HFD disrupted those rhythm patterns and increased FFA and glycerol concentrations during the dark photoperiod. In both melatonin-treated groups, almost all analyzed genes showed circadian patterns. Notably, melatonin significantly prevented the increase in FFA levels during the dark photoperiod in obese rats (obese group: ~1100 mM vs. obese + melatonin group: ~600 μM, similar to control levels). However, the rhythmic pattern observed in control animals was not sustained. According to our results, melatonin could regulate circadian gene transcription of mesenteric adipose tissue lipolysis proteins. The effect of melatonin on preventing elevated FFA plasma levels associated with high-fat diet intake warrants further investigation. Full article

In this paper, the effect of soybean isolate protein (SPI) content on the physicochemical properties and oxidative stability of chitosan–sodium tripolyphosphate (CS-STPP)-loaded fish oil capsules was investigated. The SPI/CS-STTP capsules formed after the addition of different amounts of SPI were larger in size and more homogeneous in morphology than the CS-STPP capsules, and the SPI was encapsulated on the surface of the CS matrix, altering the surface properties and morphology of the particles. The study of different CS-to-SPI blend ratios (1:0, 3:1, 2:1, 1:1, 1:2) showed that the water content of the microcapsules increased from 49.79% to 53.27–64.99%, the fish oil loading increased from 17.06% to 18.31–24.89%, and the encapsulation rate increased from 89.42% to 93.90–96.14%. In addition, the addition of SPI reduced the maximum peroxide value from 445 to 264 meq/kg oil. In the simulated in vitro digestion experiments, the addition of various amounts of SPI resulted in a significantly lower percentage of final free fatty acid (FFA) release than observed for CS-STPP capsules alone. These changes observed in the properties may be due to structural differences between CS-STPP capsules and SPI/CS-STPP capsules. All the results confirm that the obtained capsules are promising for the development of functional foods and drugs. Full article

Obesity has emerged as a significant public health crisis, closely linked to the pathogenesis and progression of chronic kidney disease (CKD). This review explores the intricate relationship between obesity-induced lipid metabolism disorders and renal health. We discuss how excessive free fatty acids (FFAs) lead to lipid accumulation in renal tissues, resulting in cellular lipotoxicity, oxidative stress, and inflammation, ultimately contributing to renal injury. Key molecular mechanisms, including the roles of transcriptional regulators like PPARs and SREBP-1, are examined for their implications in lipid metabolism dysregulation. The review also highlights the impact of glomerular and tubular lipid overload on kidney pathology, emphasizing the roles of podocytes and tubular cells in maintaining kidney function. Various therapeutic strategies targeting lipid metabolism, including pharmacological agents such as statins and SGLT2 inhibitors, as well as lifestyle modifications, are discussed for their potential to mitigate CKD progression in obese individuals. Future research directions are suggested to better understand the mechanisms linking lipid metabolism to kidney disease and to develop personalized therapeutic approaches. Ultimately, addressing obesity-related lipid metabolism disorders may enhance kidney health and improve outcomes for individuals suffering from CKD. Full article

The digestion and absorption properties of 1,3-dipalmitoyl-2-oleoyl glycerol (POP)-rich lipids was evaluated using in vitro gastrointestinal digestion and a Caco-2 cell-mediated coupled model. Caco-2 cell viability and monolayer integrity were assessed by an MTT assay and transepithelial electrical resistance. The IC50 for bile salts, pancreatin, and free fatty acid (FFA) were 0.22 mM, 0.22 mg/mL, and 1.47 mM, respectively, and no cytotoxicity was observed for bovine serum albumin (0.01–0.20 mM) or triacylglycerol (1.00–10.00 mM). The in vitro-digested POP-rich lipid containing FFA > 2.95 mM caused the disruption of monolayer tight junctions in Caco-2 cells. The major triacylglycerols (TAG) of POP-rich lipids were POP (50.8%), POO (17.8%), POL/OPL/PLO (7.6%), PPO (7.1%), and PLP (6.8%). Following digestion and uptake into Caco-2 cells, the resynthesized TAGs included PPO (20.6%), PPP (15.9%), POO (14.0%), POL/OPL/PLO (12.2%), POP (10.9%), OOO (7.5%), OPO (7.0%), OOL/OLO (6.7%), PLP (3.1%), and PPL (2.2%). The secreted major TAGs were POL/OPL/PLO (50.8%), PPP (11.1%), and OOL/OLO (8.4%), indicating a diverse TAG profile in newly synthesized lipids. This study provides a coupled model for lowering cytotoxicity and maintaining the monolayer in Caco-2 cells, and for evaluating the digestion and absorption properties of functional lipids containing specific fatty acids incorporated into TAG. Full article

One of the pressing issues in regenerative medicine is the restoration of somatic nerve function after injury. In this study, extraction methods were used to obtain lipids from nervous tissue, followed by chromatographic separation, quantitative analysis via densitometry, and qualitative and quantitative analyses of the fatty acid composition through gas chromatography. The results showed that nerve cutting results in the accumulation of all forms of phosphoinositides and a decrease in diacylglycerol (DAG) levels in both the proximal and distal segments of the nerve conductor. This phenomenon is likely attributable to the inactivation of phosphoinositide-specific phospholipase C and the activation of lipolytic enzymes, particularly phospholipases A₁ and A₂, resulting in an increase in the amount of free fatty acids (FFAs). The intramuscular administration of insulin-like growth factor-1 (IGF-1) was associated with enhanced phosphoinositide metabolism, increased DAG levels, reduced FFA levels, and a redistribution of fatty acids within the studied lipid fractions. The registration method of action potentials demonstrated the restoration of nerve conduction in the proximal segment of somatic nerves following the introduction of IGF-1. This correlates with our findings regarding alterations in the lipid fraction composition of damaged nerve conductors in response to the drug’s effects. Most likely, IGF-1 exerts its effects through activation of the phosphoinositide-specific phospholipase C and phosphatidylinositol-3 kinase signaling pathways, which are necessary for axonal regeneration and the restoration of functioning damaged nerve conductors. Full article