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.

Polycystic ovary syndrome (PCOS) is a heterogeneous reproductive endocrine condition in women, with implications in fertility and long-term metabolic health. PCOS with hyperandrogen (HA-PCOS; hyperandrogenic PCOS) has been recently identified as one of the four subtypes of PCOS. Dyslipidemia is known to be associated with clinical hyperandrogenism in PCOS. Indeed, patients with HA-PCOS were found to have the highest incidence of dyslipidemia among patients with the other three subtypes of PCOS. In the present study, we identified genes involved in lipid-associated processes (namely, lipid biosynthetic process, lipid catabolic process, hyperlipidemia, hypolipidemia and lipid homeostasis) whose expression are changed in granulosa cells from HA-PCOS patients compared to those from non-PCOS women, in order to identify molecular factors contributing to the highest risk of dyslipidemia incidence observed in patients with hyperandrogenic PCOS. We found 27 lipid biology-associated genes (ACSM1, ACSM3, AGPAT4, AJUBA, ALDH1A2, CCDC3, LPL, P2RX1, PITPNM1, PRLR, PTGIS, SLC44A5, SPTSSB, ST8SIA5, IDH1, ITPKA, PPM1L, SPTLC2, ADRA2A, ASPG, IRS1, PLB1, IDH1, LCT, NUDT8, SMPDL3A and SYNE2) whose transcript levels are significantly downregulated or upregulated in granulosa cells of women with HA-PCOS compared to those in control women. The majority of these genes have not been previously studied in the context of PCOS, and are possible candidates for further research to better understand the contribution of high androgen levels to dyslipidemia in PCOS. Targeting of high androgen-induced dyslipidemia might be of high clinical importance in the treatment of women with HA-PCOS.

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.

Energy metabolism manipulation strategy, enhancing fat metabolism while reducing the dependence on glucose, is beneficial to improve exercise performance. The multi-ingredient supplements (MIS) mixed with valine, isoleucine, leucine, β-alanine, creatine, L-carnitine, quercetin, and betaine were found to be able to improve the endurance performance of mice, which was associated with a shift of energy substrates from glucose to fatty acids. Thus, we hypothesized that the MIS regulating lipid metabolism contributes to enhancing exercise endurance in mice. The present study aimed to explore the alterations in the biochemical composition of mice treated with the MIS using a metabolomics strategy after they were subjected to endurance exercise. The serum metabolite profile was investigated using ultrahigh performance liquid chromatography tandem mass spectrometry. Results showed that significant changes in lipid metabolism were observed in the MIS-treated mice during endurance exercise compared with the vehicle control. Specifically, the MIS treatment reduced glycerophospholipids, glycerolipids, long-chain fatty acids, and inflammatory signaling arachidonic acid derivatives, and increased medium-long-chain acylcarnitine levels relative to the exercised group. Furthermore, the levels of dimethylglycine (DMG), citrate (CA), glycerol, creatine, and corticosterone were also increased after the MIS supplementation, which was associated with the changes in the pathways of serotoninergic synapses, CA cycles, and amino acid metabolisms. In conclusion, the MIS tested in this study effectively alters serum metabolomics profiles, which provides further evidence to support a shift in energy substrate utilization contributing to the ability of the MIS to improve exercise performance.

High plasma levels of saturated fatty acids (SFAs) are associated with lifestyle diseases such as atherosclerosis and diabetes, whereas the accumulation of very long-chain fatty acids (VLCFAs) is believed to be responsible for neuropathy in certain types of peroxisomal disorders. Despite their clinical relevance, the toxicity mechanisms of fatty acids (FAs) remain poorly understood, largely because of the challenges in solubilizing them for invitro experiments. We recently developed a method to form stable complexes of FAs with bovine serum albumin (BSA) using isopropanol as the solvent. Here, we demonstrate the stability and concentration range of FA/BSA and lysophosphatidylcholine (LysoPtdCho)/BSA complexes prepared using this method. These complexes exhibit enhanced solubility, retain their biological activity in cellular uptake assays, and remain stable for up to 12 months. We believe that our method will contribute to a better understanding of the toxicity and metabolism of SFAs and SFA-LysoPtdChos, and offer new insights into their roles in metabolic diseases and peroxisomal disorders.

Dietary polyunsaturated fatty acids (PUFA), including conjugated linolenic acids, are increasingly investigated for their potential health benefits. Zebrafish have emerged as a promising invivo model for studying the metabolism and effects of such bioactive compounds. The present study tested whether zebrafish tissues could be enriched with specific PUFA through dietary modulation. To do so, six-month-old female zebrafish were divided into four groups and fed purified diets over an eight-week period, each diet containing a distinct lipid source: sunflower oil (rich in linoleic acid), linseed oil (rich in alpha-linolenic acid), fish oil (rich in eicosapentaenoic acid and docosahexaenoic acid), and pomegranate seed oil (rich in punicic acid, a conjugated linolenic acid). Body mass, length, and whole-body fatty acid profile were then assessed. An efficient incorporation of linoleic acid, alpha-linolenic acid, eicosapentaenoic acid, docosahexaenoic acid, or punicic acid into zebrafish tissues was observed, depending on the dietary source. Linoleic acid and alpha-linolenic acid underwent partial bioconversion into longer and more unsaturated fatty acids. Fish fed with pomegranate seed oil were enriched in conjugated linoleic acids (rumenic acid and 18:2 (trans-9, trans-11)), suggesting the presence of a Δ13 reductase activity in zebrafish. These findings highlight the suitability of zebrafish as an invivo model for investigating the impacts of specific dietary and metabolically derived PUFA in the context of health and disease.

We investigated molecular characteristics and tissue distribution of elongation of very long chain fatty acids (ELOVL) genes in the chicken (Gallus gallus) genome. The research specifically examines the expression levels of these genes in chickens fed diets enriched with varying concentrations of curcumin. The aim is to uncover the potential roles and functions of ELOVL genes in the metabolism of fatty acids (FAs) in this species. In the experimental design, Hy-Line Brown commercial laying hens were selected for a feeding trial lasting 10 weeks. During this period, the hens were fed diets supplemented with curcumin at 100, 200, 300, and 400 mg/kg. The results revealed several critical insights: (1) It was confirmed that the ELOVL genes in Gallus gallus are orthologues of those found in vertebrates, indicating a shared evolutionary lineage; (2) There were noteworthy differences in how ELOVL genes, except ELOVL1 and ELOVL7, were distributed across various tissues and how they responded to dietary curcumin, prompting the need for comprehensive promoter analyses to better understand their functions in chickens; (3) The addition of curcumin to the diet did not increase omega-3 FAs in egg yolk; and (4) Dietary curcumin modulated ELOVL mRNA transcription in Gallus gallus. However, the intricate and multifaceted nature of FA metabolism presents challenges to fully grasping the implications of these results, highlighting the necessity for further in-depth investigations in this area.