Lipids最新文献

Dyslipidemia is a key comorbidity in prediabetes and type 2 diabetes (T2D). Curcumin, from turmeric, may improve lipid levels, but evidence is inconsistent. This meta-analysis evaluates its efficacy on lipid profiles in this population. We searched PubMed, Web of Science, and Scopus until August 2025 for RCTs on curcumin/turmeric in adults with prediabetes/T2DM. Data on lipids (triglycerides, total cholesterol, LDL-C, HDL-C) were pooled using a random-effects model, expressed as weighted mean differences (WMD) with 95% confidence intervals (CIs). Twenty-seven RCTs (31 arms) were included. Curcumin/turmeric supplementation significantly reduced triglycerides (WMD: -13.73 mg/dL; 95% CI: -19.49, -7.96), total cholesterol (WMD: -5.24 mg/dL; 95% CI: -9.42, -1.07), and LDL-C (WMD: -5.72 mg/dL; 95% CI: -8.62, -2.82) and increased HDL-C (WMD: 2.14 mg/dL; 95% CI: 1.08, 3.20). Effects on apolipoproteins were non-significant. Significant heterogeneity was observed (I² > 80%). Subgroup analyses indicated greater benefits in diabetic patients, those with higher baseline lipids, and with specific formulations. The certainty of evidence (GRADE) was low for all outcomes. Curcumin/turmeric supplementation yields modest improvements in the lipid profile of individuals with prediabetes and diabetes. However, significant heterogeneity and low certainty of evidence limit the robustness and clinical applicability of these findings. Therefore, the results should be interpreted with caution. Future trials should prioritize enhanced formulations and longer durations.

miR-4458 is linked to cancer, and PRTG, an AS-related RA pathway gene, is a predicted target. This study clarifies miR-4458's role in AS and whether it modulates VSMC behaviors via PRTG and the RA pathway. Vascular smooth muscle cells (VSMCs) were treated with oxidized low-density lipoprotein (ox-LDL) to establish AS models, and RT-qPCR was applied to detect expression levels of miR-4458, PRTG, α-SMA, SM22α, vimentin, osteopontin, CRABP2, and RARRES1. Cell viability and migration ability were assessed via Cell Counting Kit-8 (CCK-8) and Transwell assay. Targeting between miR-4458 and PRTG was verified via dual-luciferase reporter gene assay (DLR assay).ox-LDL treatment upregulated miR-4458, downregulated PRTG, and enhanced cell viability and migration. miR-4458 overexpression promoted ox-LDL-mediated cell viability and migration, and facilitated VSMC phenotypic transformation. In contrast, miR-4458 knockdown counteracted the aforementioned ox-LDL effects. PRTG was confirmed as a target of miR-4458 via DLR assay, and its knockdown significantly enhanced the stimulatory effect of miR-4458 knockdown on cell viability and migration. miR-4458 is highly expressed in AS, which can promote the transformation of smooth muscle cells (SMCs) to smooth muscle cells (SEMs), as well as the proliferation and migration of SMCs, thereby accelerating the progression of AS. Interaction between the miR-4458/PRTG axis and retinoic acid (RA) signaling pathway could be harnessed therapeutically to modulate VSMC phenotype in ox-LDL-induced AS.

This study aimed to explore the differences of peripheral blood (PB) and bone marrow serum lipidomic profiles in severe aplastic anemia (SAA) patients and their significance in predicting earlier immunosuppressive therapy (IST) response. A cohort of 11 newly diagnosed SAA patients and 15 healthy controls were enrolled between June 2020 and November 2022, and six of the SAA patients received ATG-based IST. PB and BM serum were collected for further LC-MS/MS analysis. Compared to donors, SAA patients exhibited more pronounced abnormalities in lipid metabolism profiles within BM serum relative to PB serum. Specifically, elevated levels of free fatty acids (FA), fatty acid esters of hydroxyl fatty acids (FAHFA), and phosphatidylserine (PS) were noted in the BM serum of SAA patients. Following treatment, there was a noted increase in acylcarnitine (ACar), hexosylceramide non-hydroxy fatty acid-sphingosine (HexCer-NS), and sulfur hexosyl ceramide hydroxy fatty acid (SHexCer), while levels of lysophosphatidylcholine (LPC) and oxidized phosphatidylcholine (OxPC) diminished, particularly in complete or partial response (CR/PR) patients. Acknowledging the changes of BM lipidomics may contribute to earlier prediction of ATG-based IST response in SAA patients.

Serine β-lactamase-like protein (LACTB), a mitochondrial protease, has incompletely characterized roles in metabolic pathways. We employed Mendelian randomization to investigate LACTB's causal relationships with lipid metabolism, metabolic syndrome (MetS), and chronic kidney disease (CKD). We performed a comprehensive Mendelian randomization (MR) analysis using genome-wide association study summary statistics. Cis-expression quantitative trait loci from the eQTLGen consortium identified genetic instruments for LACTB. Two-sample MR approaches, including inverse variance weighted, MR-Egger, and weighted median methods, were applied. The cisMR-conditional maximum likelihood (cisMR-cML) method validated LACTB-related causal associations. GTEx Portal data independently replicated the LACTB-CKD relationship. LACTB exhibited significant negative causal effects on metabolic syndrome (95% CI: 0.91-0.99, p = 0.02) and chronic kidney disease (95% CI: 0.83-0.97, p = 0.009). cisMR-cML validation confirmed significant causal associations between LACTB and lipid profiles after Bonferroni correction. Metabolic syndrome demonstrated a robust positive causal effect on CKD (95% CI: 1.15-1.42, p = 8.45 × 10^-6), with high-density lipoprotein showing a significant negative causal relationship with CKD (95% CI: 0.89-0.97, p = 0.0009). Mediation analysis revealed metabolic syndrome mediated 11.8% of the total effect between LACTB and CKD (mediation effect: -0.01, 95% CI: -0.024 to -0.0003). Our study elucidates LACTB's critical role in metabolic regulation, identifying a potential therapeutic target for preventing chronic kidney disease progression. By delineating complex interactions between LACTB, lipid metabolism, metabolic syndrome, and kidney function, we provide novel insights for precision medicine in metabolic and renal health.

Celiac disease (CD), an autoimmune disorder triggered by gliadin, is treated with a strict gluten-free diet. While omega-3 intake is known to reduce inflammation in other autoimmune diseases, its role in CD remains unclear due to limited data on fatty acid intake in this population. To assess the dietary intake of polyunsaturated fatty acids (PUFAs) in patients with CD compared with healthy controls. In this cross-sectional study, patients with CD and age- and sex-matched healthy controls were evaluated. Sociodemographic data and dietary intake were assessed using a validated food frequency questionnaire administered by a trained dietitian. Intakes of total fat, saturated, monounsaturated, polyunsaturated (omega-6 and omega-3) fatty acids, and micronutrients were analyzed along with the food sources of these fats. Compared with controls, CD patients had significantly higher intakes of total fat, saturated fat, total PUFA, omega-6, omega-3 (all p < 0.041), and calcium (p = 0.013), but lower iron intake (p < 0.020). The omega-6/omega-3 ratio did not differ between groups. Relative to FAO/WHO recommendations, CD patients consumed more energy, protein, cholesterol, zinc, vitamin B12, and fiber, but less trans fats, iron (p < 0.001), and vitamin D (p < 0.006). In both groups, omega-3 intake came mainly from fatty fish and lipid-rich foods, while omega-6 intake was primarily from oils. Both groups showed inadequate omega-3 intake, potentially predisposing them to low-grade inflammation. The findings suggest that optimizing fatty acid intake, particularly in gluten-free diets, may benefit CD patients and warrant further research.

Ischemic stroke is frequently associated with symptomatic intracranial atherosclerotic stenosis (sICAS), is a leading cause of global disability and mortality. Current guidelines recommend dual antiplatelet and intensive statin therapies. Proprotein convertase subtilisin 9/kexin type 9 (PCSK9) inhibitors have emerged as a potent lipid-lowering therapy, potentially influenced by genetic variations, particularly in the CYP2C19 gene. This study at Xuzhou Central Hospital from January 2021 to December 2023 included 151 patients divided into a statin group (n = 73) and a PCSK9 inhibitor (PCSK9i) group (n = 78). It evaluated lipid profiles, inflammatory markers, neurological function, and clinical outcomes over a 180-day follow-up period, with additional analysis stratified by CYP2C19 genotype. The PCSK9i group demonstrated significant improvements in lipid parameters compared to the statin group, including greater reductions in low-density lipoprotein cholesterol (LDL-C) (p = 0.008), total cholesterol (TC) (p < 0.001), and triacylglycerols (TAG) (p = 0.041), along with apolipoprotein A1 (ApoA1) and apolipoprotein B (ApoB) (both p < 0.001). Inflammatory markers, particularly interleukin-6 (IL-6), significantly reduced in the PCSK9i group (p < 0.001). In the PCSK9i group, CYP2C19 rapid metabolizers achieved greater reductions in LDL-C (p = 0.021), ApoB (p = 0.003), and IL-6 levels (p = 0.041) compared to slow metabolizers. Post-treatment modified Rankin Scale (mRS) scores were significantly lower in rapid metabolizers compared to slow metabolizers (p = 0.018), though clinical events occurred infrequently in both subgroups. This study demonstrates that PCSK9 inhibitor therapy combined with statins provides enhanced lipid-lowering and anti-inflammatory effects compared to statin monotherapy in sICAS patients. While the CYP2C19 genotype may influence specific treatment responses, particularly lipid parameters, its impact on clinical outcomes requires further investigation.

As a cholesterol metabolite, cholesterol sulfate (CS) is widely distributed in the human body, and its role as a regulatory factor has been continuously explored from the 1980s to the present day. However, changes in CS in metabolic disorders have not been systematically investigated. Here, rodent models of insulin resistance, fatty liver, and atherosclerosis were established. The CS content, CS to cholesterol ratio, and CS to total bile acids (TBA) ratio in the serum and liver of these model mice were compared with those of normal mice. Results showed the CS content was increased in fatty liver and atherosclerosis models of mice; meanwhile, it might be influenced by genotype, such as CD36 deficiency. The changes in the CS to cholesterol ratio were related to the amount and distribution of cholesterol. Besides, there was competition between the catabolism of cholesterol to bile acids or CS, as evidenced by the opposite trend between the TBA to cholesterol ratio and the CS to TBA ratio. Moreover, for the first time, it has been discovered that CS is enriched in lipid droplets, which further substantiates the close association between CS and lipid metabolism. Building on studies that demonstrated the beneficial effects of CS supplementation in alleviating lipid metabolic disorders, we first proposed the hypothesis that an increase in CS content may be protective against lipid metabolic disorders. This study provided a new perspective on the role of CS as a regulatory factor in metabolic disorders.

This in silico network-pharmacology investigation delineates the molecular interplay linking statin-induced Coenzyme Q10 (CoQ10) deficiency to statin-associated muscle symptoms (SAMS). GeneCards-derived targets related to SAMS, CoQ10 deficiency, and statins were integrated, and the intersecting gene set was analyzed through STRING-based protein-protein interaction mapping, followed by hub-gene prioritization using CytoHubba. Functional enrichment via ShinyGO revealed that the 145 common genes converge predominantly on inflammatory, metabolic, and mitochondrial pathways. Tumor necrosis factor (TNF) emerged as a principal regulatory node, exerting influence through Mitogen-Activated Protein Kinase (MAPK)-mediated apoptotic and stress-response cascades that plausibly contribute to mitochondrial dysfunction, oxidative stress, impaired energy metabolism, and myocellular injury in the context of CoQ10 depletion. The constructed pathway-based interaction network illustrates how suppression of the mevalonate pathway by statins disrupts CoQ10 biosynthesis, sensitizing muscle tissue to cytokine-driven inflammatory signaling and amplifying apoptotic susceptibility. Collectively, the findings highlight the TNF-MAPK axis as a mechanistic core of SAMS pathophysiology and underscore the interconnected roles of immune activation, lipid metabolic imbalance, and mitochondrial impairment. These insights provide a molecular rationale for therapeutic strategies targeting mitochondrial preservation or inflammatory modulation, including CoQ10 supplementation, and reinforce the need for experimental and clinical validation to substantiate computationally derived predictions.

Primary dysmenorrhea (PD) has always been a significant clinical challenge affecting women's health. Traditional Chinese medicine (TCM) has attracted considerable research interest owing to its advantages of multiple target and multiple pathway. This study employed urinary lipidomics technology combined with ultra-performance liquid chromatography-quadrupole time-of-flight mass spectrometry (UPLC-O-TOF-MS) to systematically elucidate the preventive mechanisms and therapeutic targets of Danggui Shaoyao San (DSS) in a PD rat model. A total of 34 lipid biomarkers representing the dysregulated lipid metabolism in PD were preliminarily identified. Except for 3alpha-hydroxy-5beta-chola-7,9(11)-dien-24-oic acid and 16-oxoandrostenediol, all 32 lipids had high diagnostic significance. And then, the metabolic alterations related to DSS intervention through the regulation of lipid biomarkers and related pathways were discovered. Among the differentially expressed lipids, 29 lipid biomarkers were significantly restored by DSS administration. Through the pathway enrichment analysis, two key perturbation pathways related to DSS therapy were found, including arachidonic acid metabolism, and primary bile acid biosynthesis, which had the potential to become new therapeutic targets for treating PD. These investigations demonstrated that DSS may have a significant efficacy on the progression of PD by multi-target regulation of lipid biomarkers and lipidomics-guided biochemical pathways, providing a scientific foundation for its clinical application.

Dysregulated lipid metabolism fuels cancer progression through enhanced lipogenesis, cholesterol synthesis, and fatty acid oxidation. Herbal bioactives provide multi-targeted molecular interventions capable of restoring lipid homeostasis while minimizing toxicity. Guggulsterone (GS), a plant-derived steroidal compound from Commiphora mukul, exemplifies this paradigm by modulating key regulators such as ATP citrate lyase (ACLY), acetyl-CoA carboxylase (ACC), farnesoid X receptor (FXR), and AMP-activated protein kinase (AMPK). Through these actions, it suppresses oncogenic lipid signaling, reprograms the tumor microenvironment, and enhances apoptotic sensitivity. This article outlines the molecular underpinnings of GS's lipid-lowering and antitumor effects, emphasizing its potential as a pharmacological scaffold for metabolic reprogramming in cancer.