오메가9 (올레산)

BACKGROUND: GPR3(G-protein-coupled receptor 3), an orphan G-protein-coupled receptor (GPCR) with constitutive Gs activity, is expressed in the brain, liver, ovary, and other tissues, regulating cell proliferation, differentiation, and apoptosis across the nervous, reproductive, immune, and metabolic systems. This review synthesizes evidence on its integrated signaling and physiological functions to address the lack of a comprehensive multisystem pathophysiology overview. METHODS: A systematic literature search was conducted on PubMed and Web of Science, using keywords such as "GPR3", "GPCR", "neurodegeneration", "metabolism", "immune", "reproduction", "agonist", "inhibitor", and "therapeutic target". This search identified GPR3's roles in neurodegenerative diseases, immune inflammation, reproduction, and energy metabolism. The analysis focused on signaling pathways, ligand regulation, and therapeutic potential. RESULTS: The research indicates that GPR3 is involved in neuronal survival, synaptic plasticity, and microglial activity via the cAMP/PKA, PI3K/Akt, and β - arrestin pathways. It promotes amyloid - β formation in Alzheimer's disease (AD), yet provides neuroprotection in Parkinson's disease (PD) models. It may contribute to anxiety/depression - like states, maintain oocyte meiotic arrest in the ovary, and activate thermogenic genes in adipose tissue. GPR3 modulates immune responses. Using oleic acid (OA) and diphenyleneiodonium (DPI) as activators, and AF64394 and cannabidiol (CBD) as antagonists, it shows potential in disease models. CONCLUSION: GPR3 acts as a central molecular hub integrating neural, metabolic, immune, and reproductive signaling, highlighting its potential as a therapeutic target for chronic multisystem disorders. However, its dual roles in certain pathologies and translation challenges necessitate further research.

BACKGROUND: Systemic lupus erythematosus (SLE) still lacks highly specific biomarkers; high-throughput metabolomics offers a route to elucidate disease-defining metabolic perturbations. OBJECTIVE: This systematic review aims to identify common metabolite changes related to SLE. METHODS: PubMed, Web of Science, Scopus, and the Cochrane Library were searched through November 2024 for human observational studies comparing the metabolomic profiles of adult SLE patients with those of healthy controls. Random-effects meta-analyses used the ratio of means (RoM); heterogeneity was assessed using the I² statistic. RESULTS: Forty-six studies comprising 2,238 SLE patients and 1,761 healthy controls (total n = 3,999) were included. Ten metabolites, each reported in ≥2 of the five eligible studies, were quantitatively synthesized. Compared with controls, isoleucine (RoM = 0.73, 95 % CI = 0.72-0.74, I² = 0 %), leucine (RoM = 0.81, 95 % CI = 0.80-0.81, I² = 0 %), and tryptophan (RoM = 0.73, 95 % CI = 0.64-0.84, I² = 75 %) were significantly lower in SLE, whereas methionine was significantly higher (RoM = 1.54, 95 % CI = 1.26-1.88, I² = 88 %). Lipid remodeling included elevated oleic acid (RoM = 1.42, 95 % CI = 1.19-1.69, I² = 0 %) and reduced capric acid (RoM = 0.80, 95 % CI = 0.67-0.95, I² = 31 %). Qualitative synthesis revealed consistent reduction of tricarboxylic acid intermediates, accumulation of acylcarnitines, and an oxidized-lipid signature (e.g., 9-hydroxyoctadecadienoic acid, leukotriene B4), implying mitochondrial stress and redox imbalance. CONCLUSIONS: Metabolomic profiling identifies a reproducible SLE signature: relative to controls, branched-chain (isoleucine, leucine) and aromatic (tryptophan) amino acids are lower, methionine is higher, and lipid profiles show higher oleic and lower capric acids, patterns consistent with impaired mitochondrial energetics and altered one-carbon flux.

Tiger nut (Cyperus esculentus L.) is rapidly emerging as a model crop for sustainable food systems for its exceptional nutritional profile as well as the underexplored potential for whole-plant valorization. Previous reviews have cataloged the general composition and application of tiger nut, this review would like to provide a novel and systematic synthesis focusing on three groundbreaking fronts: firstly, the unique molecular regulatory network governing high oleic acid accumulation in tubers. Secondly, the advanced green extraction technologies surpass conventional methods in efficiency and sustainability for obtaining high-quality oil, starch, and protein, while mitigating nutrient degradation. Thirdly, a "zero-waste" utilization framework, detailing how by-products (press cake) could be transformed into high-value products was scarcely integrated into existing literature. This review integrates cutting-edge insights on starch nano-modification, protein functionalization, and the synergistic health effects of bioactive compounds. It not only summarizes existing knowledge, but also charts a strategic roadmap for future research on tiger nuts, emphasizing molecular breeding, circular bioeconomy, and evidence-based health claim validation to unlock the full industrial potential of tiger nuts. © 2025 Institute of Food Technologists.

OBJECTIVES: Neuroinflammation contributes to the pathogenesis of multiple neurological and neurodegenerative diseases but is also involved in non-degenerative conditions such as aging, sleep disorders, depression, and metabolic dysfunctions. Among dietary factors with potential neuroprotective activity, olive oil and its phenolic compounds have attracted interest for their anti-inflammatory properties. This systematic review aimed to assess the effects of olive oil and its main phenolic compounds on neuroinflammation in preclinical in vivo studies. METHODS: A systematic search was conducted using PubMed, Scopus, and Web of Science to identify controlled in vivo studies evaluating the impact of olive oil or its phenolic compounds on neuroinflammatory markers. Thirty-two studies met the inclusion criteria and were critically analyzed for experimental model, type of intervention, and neuroinflammation-related outcomes. RESULTS: Olive oil, particularly extra-virgin olive oil (EVOO) rich in phenolic compounds, showed anti-inflammatory effects in several models, although results were inconsistent. In contrast, phenolic compounds such as hydroxytyrosol, oleuropein, oleacein, and oleocanthal more consistently reduced glial activation and pro-inflammatory cytokines across diverse experimental paradigms. Hydroxytyrosol emerged as the most frequently studied and effective compound. DISCUSSION: The preclinical evidence supports the anti-neuroinflammatory potential of olive oil and its phenolic compounds, though the variability in experimental design, compound characterization, and outcome measures limits translational interpretation. While isolated compounds demonstrated more robust effects than whole oil, high doses and lack of pharmacokinetic data raise questions about clinical relevance. Future research should address these limitations and evaluate the neuroimmune effects of olive oil-derived compounds in human studies.

Extra virgin olive oil (EVOO) has recognized antioxidant and anti-inflammatory properties, mainly because its composition, great levels of oleic acid, and phenolic compounds (PC). Thus, the aim of this systematic review was to synthesize the results of randomized controlled clinical trials (RCTs) of regular consumption of EVOO in biomarkers of inflammation and oxidative stress. Twenty-three RCTs met the inclusion criteria, involving 1138 participants, showed some type of risk of bias and the certainty of the evidence ranged from moderate to very low. Biomarkersas such ox-LDL, TNF-alpha, CRP, IL-6, IL-10, and IL-18 were associated with changes in inflammatory and oxidative states after EVOO consumption. EVOO consumption reduced ox-LDL when compared with medium and low PC olive oils together: -4.59 U/l [(95%CI: -8.1 to -1.08), I2: 45.4%; p = 0.103] and with low PC olive oil only: -7.73 U/l [(95%CI: -14.63 to -0.82 U/l], I2: 42%; p = 0.16)]. CRP was also reduced compared to low PC olive oils: -0.99 mg/l [(95%CI: -1.66 to -0.31); I2: 68.8%; p = 0.00)], but showed considerable heterogeneity. In conclusion, PC levels demonstrate an association with anti-inflammatory and antioxidant effects. The consumption of EVOO tends to reduce the risk of chronic non-communicable diseases, especially individuals adhering to the Mediterranean diet.

The recovery and reuse of agro-industrial by-products (AIBP) in livestock feeding fully align with the goals set by the European Union, aimed at achieving climate neutrality by 2050. The literature contains many studies related to the inclusion of these products in ruminant diets, with particular interest in those rich in bioactive substances, such as polyphenols, which can provide various benefits to both animals and productions. However, the reported results, particularly regarding milk production and quality, are highly variable, depending on numerous factors such as species, inclusion level, polyphenol dose, other diet ingredients etc. The objective of this study was to evaluate the effects of dietary supplementation with AIBP rich in polyphenols on milk production and composition, and fatty acid profile in dairy sheep and goat. The systematic search was conducted using Scopus, Web of Science, and PubMed databases. Only studies with sheep and goat were included. The data analysed were extracted from 41 scientific papers and the considered AIBP came from grape, olive, tomato, citrus, cocoa and coffee processing. The effects of AIBP were analysed using random-effects statistical models to examine the standardised mean difference between AIBP and control treatment. The heterogeneity was then explored by a meta-regression. A meta-regression was also used to test the effect of the dosage of polyphenols in the diet (g of polyphenols/kg of diet). A test for subgroup differences was carried out through a meta-analysis considering the by-product type. Supplementation with AIBP did not affect the milk yield either in sheep and goat. Supplementation with AIBP in sheep diet led to an increase in monounsaturated fatty acids (MUFA), oleic acid (OA, C18:1cis-9), vaccenic acid (VA, C18:1trans-11), and to a decrease in saturated fatty acids (SFA). Polyunsaturated fatty acids (PUFA), PUFA n-3, VA, and linolenic acid (C18:3 n3) increased in response to the dosage of polyphenols in sheep diet. In goat, the inclusion of by-products in the diet led to a decrease in SFA and an increase in MUFA, VA, LNA, and rumenic acid (RA, C18:2cis-9,trans-11), while the dosage was never signifi

BACKGROUND: The gut is responsible for the digestion and absorption of nutrients, immune regulation, and barrier function. However, factors like poor diet, stress, and infection, can disrupt the balance of the gut microbiota and lead to intestinal inflammation and dysfunction. PURPOSE: This systematic review aims to evaluate the effects of dietary plants-derived essential oil components on gut health and intestinal functions in animal models. METHODS: The literature was gathered from the Scopus, Web of Science, PubMed, and Embase databases by using related search terms, such as "dietary plants", "dietary sources", "essential oils", "gut health", "intestine", "anti-inflammatory", "antioxidant", and "gut microbiota". RESULTS: The results indicate that plant-derived dietary essential oil components, such as butyrolactone-I, carvacrol, cinnamaldehyde, citral, D-limonene, eugenol, farnesol, geraniol, indole, nerolidol, oleic acid, thymol, trans-anethole, vanillin, α-bisabolol, α-linolenic acid, α-pinene, α-terpineol, β-carotene, β-caryophyllene, and β-myrcene have been found to regulate gut health by influencing vital signalling pathways associated with inflammation. Dietary essential oil components modulate the expression of tumor necrosis factor alpha, interleukin 1 beta (IL-1β), interleukin (IL)-6, IL-10, inducible nitric oxide synthase, cyclooxygenase-2, toll-like receptor-4, matrix metalloproteinase, and interferon gamma in mitigating gut inflammation. The primary signalling molecules controlled by these molecules were AMP-activated protein kinase (AMPK), protein kinase B, extracellular signal-regulated kinase, c-Jun N-terminal kinase, mitogen-activated protein kinase, myeloid differentiation primary response 88, nuclear factor erythroid-2-related factor-2, and phosphoinositide 3-kinase (PI3K). Moreover, these phytochemicals have been shown to improve glucose homeostasis by regulating glucose transporter 4, glucagon-like peptide-1, peroxisome proliferator-activated receptor gamma, nuclear factor kappa B, AMPK, PI3K, and uncoupling protein-1. They can also reduce thiobarbituric acid reactive substance, malondialdehyde, and oxidative stress and enhance superoxide

BACKGROUND AND AIM: Clinical evidence for early identification and diagnosis of liver cirrhosis (LC) caused by different types of liver disease is limited. We investigated this topic through a meta-analysis of quantitative metabolomics. METHODS: Four databases were searched until October 31, 2022 for studies comparing metabolite levels between patients with different types of liver disease and control individuals. A random-effects model was applied for the meta-analysis. RESULTS: This study included 55 studies with 8266 clinical participants, covering 348 metabolites. In LC related to drug-induced liver injury (DILI), hepatitis B virus (HBV) infection, and non-alcoholic fatty liver disease (NAFLD), the primary bile acid biosynthesis (taurocholic acid: SMD, 1.08[0.81, 1.35]; P < 0.00001; glycocholic acid: SMD, 1.35[1.07, 1.62]; P < 0.00001; taurochenodeoxycholic acid: SMD, 1.36[0.94, 1.78]; P < 0.00001; glycochenodeoxycholic acid: SMD, 1.49[0.93, 2.06]; P < 0.00001), proline and arginine (l-proline: SMD, 1.06[0.53, 1.58]; P < 0.0001; hydroxyproline: SMD, 0.81[0.30, 1.33]; P = 0.002), and fatty acid biosynthesis (palmitic acid: SMD, 0.44[0.21, 0.67]; P = 0.0002; oleic acid: SMD, 0.46[0.19, 0.73]; P = 0.0008; stearic acid: SMD, 0.37[0.07, 0.68]; P = 0.02) metabolic pathways were significantly altered. CONCLUSION: We identified key biomarkers and metabolic characteristics for distinguishing and identifying LC related to different types of liver disease, providing a new perspective for early diagnosis, disease monitoring, and precise treatment.

Lipids are a large group of natural compounds, together with proteins and carbohydrates, and are essential for various processes in the body. After death, the organism's tissues undergo a series of reactions that generate changes in some molecules, including lipids. This means that determining the lipid change profile can be beneficial in estimating the postmortem interval (PMI). These changes can also help determine burial sites and advance the localization of graves. The aim was to explore and analyze the decomposition process of corpses, focusing on the transformation of lipids, especially triglycerides (TGs) and fatty acids (FAs), and the possible application of these compounds as markers to estimate PMI and detect burial sites. A systematic review of 24 scientific articles from the last 23 years (2000-2023) was conducted. The results show that membrane glycerophospholipids (such as phosphatidylcholine and phosphatidylglycerol, among others) are the most studied, and the most promising results are obtained, with decreasing patterns as PMI varies. Fatty acids (FAs) are also identified as potential biomarkers owing to the variations in their postmortem concentration. An increase in saturated fatty acids (SFAs), such as stearic acid and palmitic acid, and a decrease in unsaturated fatty acids (UFAs), such as oleic acid and linoleic acid, were observed. The importance of intrinsic and extrinsic factors in decomposition is also observed. Finally, as for the burial sites, the presence of fatty acids and some sterols in burial areas of animal and human remains can be verified. In conclusion, glycerophospholipids and fatty acids are good markers for estimating PMI. It has been observed that there are still no equations for estimating the PMI that can be applied to forensic practice, as intrinsic and extrinsic factors are seen to play a vital role in the decomposition process. As for determining burial sites, the importance of soil and textile samples has been demonstrated, showing a direct relationship between saturated fatty acids, hydroxy fatty acids, and some sterols with decomposing remains.

CONTEXT: In 2020, 13.6 million children under 5 years suffered from severe acute malnutrition (SAM)/wasting. Standard ready-to-use therapeutic foods (RUTFs) improve polyunsaturated fatty acid (PUFA) status but contain suboptimal amounts of omega-3 (n-3) PUFAs with unbalanced n-6-to-n-3 PUFA ratios. OBJECTIVES: The aim was to compare the effects of RUTFs with different essential fatty acid contents on PUFA status, neurodevelopmental, and clinical outcomes (mortality, comorbidities, and recovery) of children with severe wasting. DATA SOURCES: Twelve databases, trial repositories, and article references with no publication limitations. DATA EXTRACTION: Ten studies from randomized, quasi, and cluster-randomized controlled trials providing RUTFs as home treatment to children 6-59 months with SAM/wasting were included. DATA ANALYSIS: Plasma phospholipid eicosapentaenoic acid content was higher in children receiving RUTF with altered essential fatty acid contents compared with standard RUTF (0.20 [0.15-0.25], P < 0.00001). Docosahexaenoic acid (DHA) status only improved in children receiving RUTF with added fish oil (0.33 [0.15-0.50], P = 0.0003). The Malawi Developmental Assessment tool (MDAT) global development and problem-solving assessment scores were higher in global assessment and gross motor domains in children receiving added fish oil compared with standard formulation (0.19 [0.0-0.38] and 0.29 [0.03-0.55], respectively). Children receiving high-oleic-acid RUTF (lowering the n-6:n-3 PUFA ratio of the RUTF) with or without fish oil had significantly higher scores in social domains compared with those receiving the standard formulation (0.16 [0.00-0.31] and 0.24 [0.09-0.40]). Significantly higher mortality risk was found in children receiving a standard formulation compared with RUTF with a lower n-6:n-3 PUFA ratio (0.79 [0.67-0.94], P = 0.008). CONCLUSION: Although lowering n-6:n-3 PUFA ratios did not increase plasma DHA, it improved specific neurodevelopmental scores and mortality due to lower linoleic acid (high-oleic-acid peanuts), higher alpha-linolenic acid (altered oil), or both. Additional preformed n-3 long-chain PUFAs (fish oil) with RUTF improved the c

Background: Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) refers to fatty liver disease associated with metabolic syndrome. MASLD causes alterations in lipid metabolism, which can be regulated with a diet rich in polyphenols. The present study aims to evaluate the effects of daily consumption of 400 g of "Navelina" oranges for 4 weeks on serum lipid profiles in a group of 60 patients with MASLD, to identify specific lipid species associated with improvements in hepatic steatosis. Methods: Blood samples were collected from all participants, and biochemical measurements and a serum lipidomic profile were performed. Finally, a Spearman correlation analysis was used to assess the relationships between serum lipidomic fatty acids and biochemical lipid markers. Results: In the experimental treatment arm, serum lipidomic analysis showed a slight decrease in Arachidonic acid (AA) and the Arachidonic acid/Eicosapentaenoic acid ratio (AA/EPA ratio) but no significant interaction between time and treatment was detected. In the same group, Oleic acid, MUFAs and the AA/EPA ratio were significantly and negatively correlated with HDL (r = -0.368, p = 0.046), (r = -0.384, p = 0.036), and (r = -0.522, p = 0.003), respectively. Conversely, EPA and n-3 PUFAs were positively and significantly correlated with HDL (r = 0.447, p = 0.013) and (r = 0.403, p = 0.027) respectively. Conclusions: Furthermore, this study represents one of the first clinical trials to shed a light on the potential association of "Navelina" orange polyphenols on serum fatty acid profiles in patients with MASLD, supporting studies on the nutraceutical effect of oranges on lipid metabolism.

OBJECTIVES: Pregnant patients with cardiovascular and metabolic risk factors are at increased risk of hypertension in pregnancy. Adherence to Mediterranean-based diets high in extra virgin olive oil (EVOO) is associated with decreased risk. We performed a randomized, double-blind placebo-controlled trial of EVOO supplementation in reproductive-aged women to investigate its effects on cardiovascular function and markers of metabolic dysfunction and inflammation. STUDY DESIGN: Healthy nulliparous women were randomized to 40 g/day of EVOO high in oleic acid and phenols or an identical dose of sunflower seed oil for 8 weeks. Cardiovascular assessment, lipid profiles, insulin sensitivity and serum cytokines were assessed at baseline and post intervention. MAIN OUTCOME MEASURES: Blood pressure, vessel distensibility, metabolic assessment, serum cytokine levels. RESULTS: Twelve women in the EVOO group and 15 in the control group completed the trial. Compliance was >97 % in both groups. EVOO supplementation reduced fasting insulin (-0.31 ± 0.52 U/mL, p = 0.03), but increased LDL cholesterol (+5.1 ± 4.0 mg/dL, p = 0.047). No differences in blood pressure were observed, though EVOO was associated with a lower blood pressure response to volume challenge and a trend toward lower hemoglobin A1c (p = 0.06). IL-10 decreased in EVOO but increased in controls, -0.05 ± 0.03 vs +0.07 ± 0.03, p = 0.01). Unique to the EVOO group, a reduction in the chemokine MCP-1 positively correlated with a reduction in systolic blood pressure (r = 0.59, p = 0.042) and MAP (r = 0.59, p = 0.042). CONCLUSIONS: EVOO supplementation in women of reproductive age may have beneficial metabolic and anti-inflammatory effects.

BACKGROUND: Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) may improve inflammatory conditions. We previously demonstrated that supplementation with EPA+DHA in adults elevates anti-inflammatory oxylipins in human plasma and adipose tissue. However, the localization of EPA/DHA in plasma lipid pools [phosphatidylcholines (PC), triglycerides (TAG), cholesteryl esters (CE), and nonesterified fatty acids (NEFA)] and how this relates to the downstream oxylipin levels remains unknown. OBJECTIVES: This study aimed to identify the incorporation of supplemental EPA+DHA into plasma PC, TAG, CE, NEFA, and the impact on downstream oxylipins. METHODS: We conducted an exploratory analysis with available samples (n = 21, 20 female, 1 male, age 35-49 y) from a previous double-blind, placebo-controlled trial of participants randomly assigned to consume either 3 g of EPA+DHA concentrate (1.1 g EPA + 0.8 g DHA) or corn oil (CO) [1.65 g linoleic acid (LA) + 0.81 g oleic acid] daily for 12 wk. Plasma was analyzed using gas chromatography and mass spectrometry to quantify fatty acids and oxylipins, respectively. RESULTS: EPA+DHA supplementation increased EPA levels across PC, CE, NEFA, and TAG pools, and increased DHA levels in PC, CE, and TAG pools. Conversely, supplementation decreased LA levels in PC, CE, and NEFA pools, and decreased arachidonic acid (AA) levels in PC and NEFA pools. EPA+DHA supplementation also led to significant shifts in oxylipin concentrations compared with baseline, with predominant increases in anti-inflammatory and decreases in proinflammatory oxylipins. CO supplementation decreased TAG AA levels and modified concentrations of several AA-derived oxylipins. Levels of EPA+DHA and derived oxylipins were significantly higher across lipid pools following supplementation with EPA+DHA compared with CO. CONCLUSIONS: These findings offer insights into supplemental EPA+DHA localization to different circulating lipid pools, which have implications for understanding how to mitigate systemic inflammation. Furthermore, studies are needed to evaluate relationships between the changes in polyunsaturated fatty acids, oxylipins, and markers of inflammation. The s

Whole milk powder (WMP) produced from pasture-fed dairy herds has been shown to have increased concentrations of unsaturated fatty acids (FA), including, but not limited to, ALA (C18:3 n-3) and oleic acid (C18:1 cis-9), compared to WMP derived from indoor herds consuming total mixed ration (TMR). Dairy products have been shown to have neutral or beneficial effects on cardiometabolic health, however, evidence on WMP in this area is lacking. Given the global market for WMP as a food ingredient, an investigation into the effect of TMR-fed vs pasture-fed WMP on human health is warranted. Therefore, the aim of this study was to test the effect of WMP derived from TMR-fed and pasture-fed herds on circulating FA concentrations and other markers of cardiometabolic health in adults. Healthy subjects were randomized to receive up to 200 g WMP/day as part of a 6-week crossover trial, with a 4-week washout period. WMP was produced from milks of TMR-fed and pasture-fed cows. WMPs were isocaloric and macro-nutrient matched. The primary outcome was difference in circulating FA between weeks 0 and 6. Changes in cholesterol concentrations, glycemic control, blood pressure and anthropometry were secondary outcomes. Dietary intake was also analyzed. A total of n 29 participants, 58.6% male, with a mean±SE age of 39.8±2.3 years and BMI of 26.12±1.39 kg/m2 completed the study protocol. No time × treatment interactions were observed for cholesterol concentrations, markers of glycemic control, blood pressure or anthropometry. There was no time × treatment interaction for classes of FA, however, the very long-chain saturated FA, lignoceric acid (C24:0), decreased in response to pasture-fed WMP consumption (-0.05±0.04 %TFA) with no change observed in response to the TMR WMP consumption (0.00±0.04 %TFA, P=.041), although this was not significant after Bonferroni correction for Type 2 error. Chronic, high-dose consumption of TMR and pasture-fed WMP had no effect on cardiometabolic health in healthy adults, despite different fatty acid composition. Comparison of foods with a proven dairy matrix effect, e.g., cheese made from TMR-fed and pasture-fed milks, may have more promising effects on

BACKGROUND AND AIMS: Nuts are recognized for their potential health benefits, yet little is known about their postprandial impact on metabolic responses and oxidative stress. This study aimed to evaluate the acute effect of a shake containing a mixture of 30g cashew nuts (Anacardium occidentale L.) and 15g Brazil nuts (Bertholletia excelsa H.B.K.) on glucose levels, lipid profiles, and oxidative stress markers in individuals with overweight or obesity. METHODS AND RESULTS: This was a clinical, randomized, controlled, single-blind, crossover study. On two test days, fifteen subjects consumed either a control (without nuts) or a test shake. Metabolic biomarkers were analyzed at fasting and 60, 120, and 240 min after shake intake. Compared to the control, the shake with nuts promoted specific changes in oxidative stress and metabolic markers. Differences were observed at 120 min after beverage consumption regarding superoxide dismutase (SOD) (control: 117.7 ± 14.6 vs. test: 82.1 ± 10.0 U/mL; p < 0.05) and at 240 min regarding malondialdehyde (MDA) concentrations (control: 5.0 ± 0.2 vs. test: 4.4 ± 0.3 μM/mg; p < 0.05). Also, at 240 min postprandial, complement C3 and stearic acid concentrations were higher in the test group than in the control, and a positive correlation was observed between them (p < 0.05). However, no differences were observed when considering time x intervention. CONCLUSION: Our findings suggest that cashew and Brazil nuts did not promote acute metabolic changes. We highlight that the mixed nuts decreased lipid peroxidation but did not improve antioxidant status in individuals with overweight or obesity.

BACKGROUND AND AIMS: The prevalence of metabolic syndrome has been increasing in young adults, concomitant with the occurrence of increased abdominal adiposity. We previously reported that consuming tree nuts, as replacement for typical high-carbohydrate snacks, reduces visceral fat and waist circumference in young adults who have one or more metabolic syndrome risk factors. We aimed to investigate the effects of tree nuts snack consumption on plasma and adipose tissue fatty acid profiles along with changes in the expression of adipose tissue genes involved in thermogenesis, glycemia, adipocyte signaling, lipolysis, and immunity. METHODS: A randomized parallel-arm 16-week intervention trial was conducted in 84 adults aged 22-36 years. Participants in both groups were provided with caloric goals for weight maintenance, daily menus, and pre-portioned snacks at every other week visits with study registered dietitians. Changes in dietary fatty acid intakes, plasma and abdominal subcutaneous adipose tissue (SAT) triglycerides fatty acid profiles using gas-liquid chromatography, and the expression of 241 genes in abdominal SAT were evaluated. RESULTS: Consuming tree nuts snacks increased mono- and polyunsaturated fatty acid intakes yielding a 9-fold greater dietary unsaturated to saturated fat ratio. The tree nuts snack group also had significantly greater improvements in plasma 16:1/16:0 ratio; plasma phospholipids oleic and gamma linolenic acid content; plasma diglycerides, triglycerides, and cholesterol esters oleic acid content; and total plasma monounsaturated fatty acids. While abdominal SAT only showed trends for increased oleic acid content and unsaturated to saturated fat ratio, the tree nuts snacks participants had altered expression of 13 genes in abdominal SAT that have roles in nutrient sensing, energy homeostasis, and vulnerability to obesity. CONCLUSIONS: Replacing typical high-carbohydrate snacks with tree nuts results in more favorable dietary, plasma, and adipose tissue fatty acid profiles that could aid in preventing the development of excess adiposity and cardiometabolic disease states including metabolic syndrome. CLINICAL TRIAL REGISTRY: This tri

There is limited evidence on the effects of different dietary sources of fats on detailed blood fatty acids (FAs). We aimed to evaluate the effects of coconut oil, olive oil and butter on circulating FA concentrations, and examine the associations between changes in plasma FAs and changes in metabolic markers. We conducted secondary analyses in the COB (coconut oil, olive oil and butter) Trial that evaluated 96 healthy adults in a 4-week parallel randomized clinical trial of three dietary interventions: 50 g/d of extra-virgin coconut oil (n = 30), extra-virgin olive oil (n = 33), or unsalted butter (n = 33). We measured plasma phospholipid FA concentrations (mol% of total) using gas chromatography. Using linear regression, we estimated the effects of the interventions on changes in FAs and the associations of changes in selected FAs with changes in metabolic markers. Coconut oil doubled lauric acid (C12:0) and myristic acid (C14:0), butter increased those to a lesser extent, and olive oil reduced those. β (95% confidence interval) for changes in C12:0 comparing coconut oil to butter and olive oil were +0.04 (0.03-0.05) and +0.05 (0.04-0.06) mol%, respectively; for C14:0, +0.24 (0.17-0.32) and +0.37 (0.29-0.45), respectively. Olive oil increased oleic acid (OA) approximately by 1 mol%, while coconut oil and butter had little effect on OA. Butter increased odd-chain SFAs and trans-FAs while olive oil and coconut oil decreased them. Changes in FAs mostly showed no significant associations with changes in metabolic markers. The interventions of equal amounts of different food FA sources altered circulating FA concentrations differently.

The rate of cardiovascular disease (CVD) death is higher in men than women before age 50 y, but the gap between sexes significantly narrows after menopause. Lipid mediators derived from EPA, DHA and AA play a role in inflammation and CVD. The aim of our study was to assess whether plasma concentrations of these lipid mediators differ between postmenopausal women and men. Twelve postmenopausal women and 9 men with low-grade chronic inflammation completed a randomized, double-blind, crossover study consisting of a 4-week lead-in placebo phase (3 g/d high-oleic acid sunflower oil) followed by randomization to either 3 g/d DHA or 3 g/d EPA for 10 weeks and crossover for additional 10 weeks, separated by a washout phase. Plasma phospholipid content of EPA, DHA and AA and plasma concentrations of their derived lipid mediators were measured at the end of the placebo lead-in phase (baseline) and the DHA and EPA supplementation phases. There were no sex differences in plasma phospholipid EPA, DHA and AA at baseline and after DHA and EPA supplementation. However, plasma concentrations of lipid mediators derived from EPA, DHA and AA via 15-lipoxygenase were lower in postmenopausal women than men, especially after supplementation. Sex differences in EPA- and DHA-derived lipid mediators with anti-inflammatory and pro-resolving actions may partly explain the faster rise in CVD in postmenopausal women than age-matched men.

BACKGROUND: The tumoricidal complex alpha1-oleate targets bladder cancer cells, triggering rapid, apoptosis-like tumor cell death. Clinical effects of alpha1-oleate were recently observed in patients with non-muscle invasive bladder cancer (NMIBC), using a randomized, placebo-controlled study protocol. AIMS: To investigate if there are dose-dependent effects of alpha1-oleate. MATERIALS AND METHODS: Here, patients with NMIBC were treated by intravesical instillation of increasing concentrations of alpha1-oleate (1.7, 8.5, or 17 mM) and the treatment response was defined relative to a placebo group. RESULTS: Strong, dose-dependent anti-tumor effects were detected in alpha1-oleate treated patients for a combination of molecular and clinical indicators; a complete or partial response was detected in 88% of tumors treated with 8.5 mM compared to 47% of tumors treated with 1.7 mM of alpha1-oleate. Uptake of alpha1-oleate by the tumor triggered rapid shedding of tumor cells into the urine and cell death by an apoptosis-like mechanism. RNA sequencing of tissue biopsies confirmed the activation of apoptotic cell death and strong inhibition of cancer gene networks, including bladder cancer related genes. Drug-related side effects were not recorded, except for local irritation at the site of instillation. DISCUSSION AND CONCLUSIONS: These dose-dependent anti-tumor effects of alpha1-oleate are promising and support the potential of alpha1-oleate treatment in patients with NMIBC. © 2024 The Author(s). Cancer Medicine published by John Wiley & Sons Ltd.

BACKGROUND: Constipation is prevalent after bariatric surgery and glucagon-like-peptide 1 (GLP-1) analogues. Increasing fat content in the distal small intestine and colon can enhance colonic peristalsis, potentially alleviating symptoms of constipation. AIM: We investigated whether oleic acid can ameliorate constipation in patients undergoing bariatric surgery or receiving GLP-1 analogues. METHODOLOGY: Fourteen adults with chronic constipation according to Rome IV criteria following bariatric surgery or GLP-1 analogues were on stable treatment for constipation for more than 4 weeks. This randomized double-blind crossover trial compared microcapsules containing 21.25 g of oleic acid delivered in the distal small intestine or the stomach. The primary outcome was changed in the number of bowel motions over 24 h. Exploratory endpoints included alterations in straining, diarrhoea, faecal leakage over 24 h and hunger, fullness, nausea and calorie intake for the 3 h after ingesting the microcapsules. FINDINGS: Receiving oleic acid into the distal small intestine increased number of bowel movements per day (2.5 vs 1.1, p = 0.009) and caused softer stool consistency (p = 0.03). 9/14 of the control group passed motions and 13/14 of the intervention group passed motions in 24 h (p = 0.059). No significant differences were observed in straining (p = 0.65), rapid bowel movements (p = 0.08), accidental leakage (p = 0.32), hunger, fullness, nausea or food intake between the groups (all p > 0.05). There were no disparities in safety profile between groups. CONCLUSION: Microcapsules containing oleic acid delivered to the distal small intestine appear to be a safe and effective relief from chronic constipation in patients undergoing bariatric surgery and/or receiving GLP-1 analogues. © 2024. The Author(s).

Lipid recovery efficiency from microalgal biomass is a critical factor in the commercial viability of biodiesel. Scenedesmus sp. presents a robust cell wall that necessitates the evaluation of specialised disruption techniques to enhance intracellular lipid release and subsequent fuel quality. This study investigated the efficacy of five cell disruption methods-microwaves, ultrasonication, lyophilisation, autoclaving, and electroporation-integrated with three distinct extraction procedures: cold extraction, Soxhlet extraction system, and microwave-assisted extraction. The qualitative and quantitative impacts of these treatments were assessed by analysing the fatty acid methyl ester (FAME) profiles via gas chromatography (GC) following transesterification. The highest total lipid yield (88.97%) was achieved through a combination of microwave disruption and Soxhlet extraction. However, the maximal proportion of methyl esters was obtained when ultrasonication was paired with microwave-assisted extraction (97.64%). Surface analysis using scanning electron microscopy (SEM) of samples subjected to different disruption procedures could support the conclusions. Similarly, when the microalgal biomass was lyophilised beforehand, microwave extraction increased the oleic acid content. These results indicate that the choice of disruption and extraction protocols significantly influences both lipid recovery rate and the proportion of fatty acids in the chemical composition of microalgae. Tailoring these processes is essential for optimising the fatty acid profile for high-quality biodiesel production.

Background: Excessive abdominal fat deposition is a major challenge in the chicken farming industry, making it essential to elucidate the molecular mechanisms underlying chicken adipogenesis. Nuclear Respiratory Factor 1 (NRF1) has been reported to suppress chicken adipogenesis by downregulating peroxisome proliferator-activated receptor gamma (PPARγ) expression. Protein Phosphatase 1 Catalytic Subunit Gamma (PPP1CC) is a multifunctional phosphatase involved in various biological processes; however, its role in chicken adipogenesis remains unclear. Objective: This study aimed to investigate the functional role and underlying mechanism of PPP1CC in chicken preadipocyte differentiation. Methods: Co-immunoprecipitation (Co-IP) and immunofluorescence assays were performed to determine the interaction between PPP1CC and NRF1 in DF1 cells. Bioinformatic analysis predicted potential NRF1 dephosphorylation sites targeted by PPP1CC, based on which NRF1 mutants mimicking dephosphorylation were constructed. Phos-tag SDS-PAGE combined with Western blot analysis were used to verify PPP1CC-mediated dephosphorylation of wild-type NRF1. Dual-luciferase reporter assays were used to evaluate the effect of PPP1CC-mediated dephosphorylation on NRF1-regulated PPARγ P1 promoter transcriptional activity. ChIP-qPCR was employed to assess the occupancy of NRF1 to the PPARγ P1 promoter upon PPP1CC overexpression. The effect of PPP1CC overexpression was assessed on preadipocyte differentiation using Oil Red O staining and marker gene expression analysis. Results: PPP1CC interacted with NRF1 in both the cytoplasm and nucleus of DF1 cells. Overexpression of PPP1CC significantly promoted NRF1 dephosphorylation during oleic acid-induced preadipocyte differentiation and increased endogenous NRF1 expression. Moreover, dual-luciferase assays showed that while PPP1CC strengthened the inhibitory effect of wild-type NRF1 on PPARγ P1 promoter transcriptional activity, it exerted no additional suppression on the already low activity mediated by the dephosphorylation-mimicking NRF1 mutants. Consistently, ChIP-qPCR results demonstrated that PPP1CC overexpression enhanced the occupancy of NRF1 to the PP

Homeobox protein MEIS2 has been strongly implicated in colorectal cancer (CRC) progression and metastatic potential, making its targeted inhibition a promising therapeutic strategy. However, recently developed MEIS inhibitors are limited by poor aqueous solubility, instability under physiological conditions, and insufficient intracellular accumulation, which restrict their clinical applicability. To overcome these challenges, a multifunctional hybrid nanoemulsome system was developed by integrating boron-silane-doped carbon dots (CDs) with chitosan via glutaraldehyde crosslinking, followed by emulsification with oleic acid and non-ionic surfactants (Span 80 and Tween 20/80) in the presence of a MEIS inhibitor (MEISi-2). The resulting composite exhibited high structural stability, excellent biocompatibility, and a drug encapsulation efficiency of 96.2%. Fourier-transform infrared spectroscopy (FTIR) and dynamic light scattering (DLS) analyses confirmed successful hybridization and the formation of nanoemulsions with an average particle size of approximately 320 nm following drug loading. The system demonstrated controlled drug release under physiological conditions. In vitro studies using HCT116 CRC and HaCaT healthy keratinocytes revealed effective cellular uptake and selective cytotoxicity. The intrinsic fluorescence properties of CDs enabled real-time monitoring of intracellular drug delivery via DAPI-channel imaging. Overall, this hybrid nanoemulsome platform provides a stable and efficient delivery system for MEIS inhibitors and represents a promising strategy for the treatment of CRC. Furthermore, this approach may be extended to other poorly soluble amphiphilic therapeutic agents.

Hepatocellular steatosis, an early stage within the non-alcoholic fatty liver disease (NAFLD) spectrum, is characterized by excessive lipid accumulation and oxidative stress in hepatocytes. This study examined the protective role of Lysine-Proline-Valine (KPV), an endogenous tripeptide derived from α-melanocyte-stimulating hormone, against oleic acid (OA)-induced oxidative damage and lipid accumulation in hepatic epithelial HepG2 cells. OA treatment markedly enhanced hepatic lipid deposition by upregulation of fatty acid synthase (FAS) expression. Treatment with KPV (100 µg/mL) significantly attenuated OA-induced lipid accumulation and suppressed FAS expression without inducing cytotoxicity. Mechanistic analysis revealed that KPV reduced reactive oxygen species generation, thereby preventing activation of extracellular signal-regulated kinase. KPV also downregulated AKT phosphorylation, leading to inhibition of mTORC1 phosphorylation under hepatic steatosis conditions. Furthermore, KPV regulated the phosphorylation of peroxisome proliferator-activated receptor gamma, a key transcription factor in de novo lipogenesis, thereby normalizing FAS expression. These findings suggest that KPV acts as an effective antioxidant regulator of lipogenic signaling and may hold potential as a therapeutic candidate for attenuating hepatocellular steatosis. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s10616-026-00967-z. © The Author(s), under exclusive licence to Springer Nature B.V. 2026. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.

Blue swimming crabs (Portunus pelagicus) consistently command higher prices in domestic and global markets due to elevated demand. Due to the rising issue of low crab larvae survival, farmers have begun using artificial hormones to increase survival rates and ensure hatchery production aligns with market demands. However, the outcomes of using artificial hormones are concerning, as these compounds pose serious risks to aquatic organisms, humans, and the environment. To address the harmful effects of artificial hormones, efforts are now focused on identifying affordable and eco-friendly plant-based alternatives, such as spinach (Spinacia oleracea), which contains bioactive compounds that could promote crab larval growth and survival. This study aimed to investigate the efficacy of spinach in improving the growth performance of P.pelagicus larvae. This was accomplished by enriching Artemia with spinach, allowingit to serve as a nutrient-enhanced live feed. Compounds in the spinach leaf wereextracted with methanol and analysed through GC-MS to identify potential growth-related compounds. LC50 analysis (1,000 ppm-2,000 ppm) was conducted on Artemia todetermine the optimal enrichment concentration (1,600 ppm) before use in larval feeding.Results indicated spinach contains compounds such as steroids (5.9%), palmitic acid(5.2%), oleic acid (2.5%) and flavonoids (3.6%) that can potentially improve larval growth.Toxicity analysis showed that the 1,600 ppm treatment was the LC50, meaning it is theoptimal concentration for Artemia enrichment, delivering the highest amount of bioactivecompounds without affecting Artemia survival. Larvae were fed spinach-enriched Artemia(1,600 ppm) and compared with unenriched Artemia (control). The 1,600 ppm treatmentresulted in significantly higher survival at various larval stages (Z1-Z2: 82.6%, Z2-Z3:91.9%, M-C1: 38.1%), shorter intermoult periods for Z2-Z3 (2.9 days), Z3-Z4 (3.1 days),and M-C1 (3.8 days) and higher SGR (M: 22.5% day-1, C1: 24.5% day-1). Larval steroidanalysis supported these findings, with treatment 1,600 ppm yielding higher steroid levels across all stages (511.63-3953 pg/mL), suggesting that spinach-derived steroids m

BACKGROUND: Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder. Emerging evidence indicates that fatty acid oxidation is impaired in both patients with AD and AD animal models. In the brain, fatty acid metabolism occurs predominantly in astrocytes. Diets enriched in monounsaturated fatty acids (MUFAs) are often recommended for individuals with AD. Oleic acid (OA), a common dietary MUFA, has been shown to reduce amyloid plaque accumulation in transgenic mouse models of AD. Moreover, OA decreases the expression of acetyl-CoA carboxylase beta (ACACB/ACC2), a key regulator of fatty acid β-oxidation. However, the precise mechanism by which OA may alleviate amyloid plaque deposition through modulation of brain fatty acid metabolism remains unclear. OBJECTIVE: To determine whether dietary OA supplementation partially restores astrocytic fatty acid metabolism by suppressing ACACB and enhancing fatty acid β-oxidation, thereby attenuating AD-related pathology. METHODS: Using NHANES 2011-2014 data, we applied survey-weighted multivariable logistic regression to examine the association between energy-adjusted MUFA intake and low cognitive function, with adjustment for multiple testing. We then screened GEO datasets to identify AD-associated genes involved in fatty acid metabolic dysregulation, identifying ACACB as a candidate target. The expression of ACACB and its downstream effector carnitine palmitoyltransferase 1A (CPT1A) were validated in mouse and cell models. APP/PS1 mice received dietary OA supplementation, followed by behavioral testing and brain histopathological analyses. In parallel, an Aβ1-42-induced astrocyte injury model was used to assess lipid droplet accumulation, mitochondrial function, and cellular energy metabolism. ACACB knockdown/overexpression and CPT1A overexpression were used to test pathway-specific effects of OA. RESULTS: Higher MUFA intake was associated with better cognitive function. ACACB as a key fatty acid metabolism-related gene in AD. In APP/PS1 mice, OA improved cognitive performance and reduced Aβ plaque deposition, accompanied by decreased ACACB and increased CPT1A expression in brain tissue. In vitro, OA modulat

The present study investigates the water-induced formation of liquid crystalline (LC) structures from a premix. The latter consisted of oleic acid (oil phase), d-α-tocopheryl polyethylene glycol 1000 succinate (TPGS; surfactant), and Transcutol P (cosurfactant). Pseudoternary phase diagrams were constructed at three ratios of the surfactant-cosurfactant mixture (Smix) and investigated for phase transition. The compositions with 3:1 Smix ratio were comprehensively characterized along a water dilution line. Polarized light microscopy revealed the onset of birefringence with increasing water content, indicative of the evolution of LC structures. This was further verified by the shifts in scattering peaks and the emergence of higher-order Bragg peaks in SAXS experiments. The observed structures were denoted as nonlamellar liquid crystals. Amplitude and frequency sweep tests showed that the as-formed phases were viscoelastic and exhibited structural resilience under shear. Ex vivo bioadhesion experiments showed a prolonged residence of the LC formulation in the chicken ileum. The formulation was loaded with budesonide (BDS), and its efficacy was studied in a male C57BL/6 mouse model of ulcerative colitis (UC). Subsequent to rectal administration, therapeutic outcomes were compared in terms of biochemical and histopathological data. Western blotting was performed to evaluate the expression of colonic epithelial tight junction proteins (occludin and ZO-1). We found that the rectally administered formulation can alleviate the symptoms and pathological signatures of UC. The formulation exerted its effects by suppressing the oxidative stress-inflammation axis and restoring the integrity of the colonic barrier.

Licochalcone E is a chalcone isolated from Glycyrrhiza uralensis and G. inflata Batal. This study explored the effect of licochalcone E on improving hepatic steatosis in obese mice and evaluated the role of licochalcone E in regulating lipid accumulation in hepatocytes. In vitro, oleic acid-induced hepatocytes were treated with licochalcone E to investigate its effect on lipid metabolic pathways. In animal experiments, male C57BL/6 mice were fed with a high-fat diet (HFD) and treated with licochalcone E by intraperitoneal injection for 12 weeks to assess its effects on biochemical indexes and hepatic steatosis. Furthermore, mice were fed a methionine/choline-deficient (MCD) diet and administered licochalcone E, followed by evaluation of liver fibrosis. Licochalcone E effectively reduced body weight, epididymal and inguinal fat weight, and adipocyte size in HFD-induced obese mice. Licochalcone E treatment of obese mice also reduced hepatic lipid accumulation and improved hepatocyte steatosis. Licochalcone E regulated the expression of lipogenesis- and lipolysis-related genes in the livers of obese mice and increased AMPK phosphorylation and Sirt1 expression in the liver. Licochalcone E also attenuated hepatic inflammation and oxidative stress in obese mice. Furthermore, treatment of MCD-induced mice with licochalcone E reduced the number of lipid vacuoles and the extent of fibrosis and inhibited liver inflammation. In FL83B hepatocytes, licochalcone E could regulate lipogenesis and lipolysis, and increase the phosphorylation of AMPK and ACC. These findings provide new insights into the role of licochalcone E in regulating lipid metabolism and preventing hepatic steatosis.

Metabolic dysfunction-associated steatotic liver disease (MASLD) has emerged as a global health issue due to its increasing prevalence associated with lifestyle changes and its strong correlation with metabolic syndrome. Farnesoid X receptor (FXR) is a nuclear receptor that plays a pivotal role in regulating bile acid, lipid, and glucose metabolism, making it an attractive therapeutic target for liver and metabolic diseases. In this study, we investigated the effects of MHY5456, a synthetic agonist of FXR, on hepatic metabolism and fibrosis. MHY5456 enhanced the transcriptional activity of FXR in a concentration-dependent manner. Treatment of AC2F rat liver-derived cells with MHY5456 resulted in the downregulation of genes involved in lipid accumulation and an upregulation of mitochondrial-related gene expression. Additionally, MHY5456 significantly reduced oleic acid (OA)-induced lipid accumulation. To assess its anti-fibrotic potential, we tested its effects on transforming growth factor-beta (TGF-β)-induced fibrosis in LX2 human hepatic stellate cells (HSCs). MHY5456 significantly suppressed the expression of fibrosis-related genes and proteins. In vivo, administration of MHY5456 to mice fed a methionine-choline-deficient (MCD) diet alleviated hepatic fibrosis, inflammation, and lipid accumulation. These results show that FXR activation by MHY5456 modulates lipid metabolism and fibrotic pathways, suggesting its potential as a pharmacological candidate for liver and metabolic disorders, including MASLD. Further pharmacological and toxicological studies are needed to confirm its therapeutic relevance.

The mechanisms underlying diabetes-associated cognitive dysfunction (DACD) are not fully understood, and microglial metabolic dysfunction is emerging as a key contributor. This study investigates whether stearoyl-CoA desaturase 2 (SCD2) alleviates cognitive impairment by modulating microglial lipid metabolism and function. Bioinformatics analysis of a single-cell RNA-seq dataset (GSE201644) identified SCD2 downregulation in diabetic (db/db) microglia. A T2D mouse model underwent hippocampal overexpression of SCD2 via AAV injection. In vitro, high glucose (HG)-treated BV2 microglia-like cells were subjected to SCD2 overexpression or oleic acid (OA) supplementation. Mitochondrial function (OCR, ATP, ETC complexes), lipid droplet accumulation (BODIPY, PLIN2), and inflammation (TNF-α, IL-6) were assessed. Cognitive behaviour (MWM, NOR) and neurophysiology (synaptic markers, neuronal survival) were evaluated. Diabetic microglia exhibited reduced SCD2 expression, impaired oxidative phosphorylation and lipid droplet accumulation (LDAM). SCD2 overexpression or OA rescued mitochondrial function, mitigated lipid droplet accumulation and attenuated inflammation. In vivo, hippocampal SCD2 overexpression attenuated neuroinflammation, preserved synaptic integrity and improved cognition in diabetic mice. SCD2 is essential for maintaining microglial lipid and mitochondrial homeostasis in diabetes. Restoring SCD2 function alleviates neuroinflammation and synaptic deficits, thereby rescuing cognitive impairment, highlighting its therapeutic potential for DACD. © 2026 The Author(s). Cell Proliferation published by Beijing Institute for Stem Cell and Regenerative Medicine and John Wiley & Sons Ltd.