Search Results (181)

Background/Objectives: Paeonia delavayi, a high-altitude-adapted medicinal and oil-producing plant, exhibits broad elevational distribution. Understanding how environmental factors regulate its growth across altitudes is critical for optimizing cultivation and exploiting its economic potential. Methods: In this study, we conducted a comprehensive Iso-Seq and RNA-seq analysis to elucidate the transcriptional profile across diverse altitudes and three seed developmental stages. Results: Using Pacbio full-length cDNA sequencing, we identified 39,267 full-length transcripts, with 80.03% (31,426) achieving successful annotation. RNA-seq analysis uncovered 11,423 and 9565 differentially expressed genes (DEGs) in response to different altitude and developmental stages, respectively. KEGG analysis indicated that pathways linked to fatty acid metabolism were notably enriched during developmental stages. In contrast, pathways associated with amino acid and protein metabolism were significantly enriched under different altitudes. Furthermore, we identified 34 DEGs related to fatty acid biosynthesis, including genes encoding pivotal enzymes like biotin carboxylase, carboxyl transferase subunit alpha, malonyl-CoA-acyl carrier protein transacylase, 3-oxoacyl-ACP reductase, 3-hydroxyacyl-ACP dehydratase, and stearoyl-ACP desaturase enoyl-ACP reductase. Additionally, ten DEGs were pinpointed as potentially involved in high-altitude stress response. Conclusions: These findings provide insights into the molecular mechanisms of fatty acid biosynthesis and adaptation to high-altitude stress in peony seeds, providing a theoretical foundation for future breeding programs aimed at enhancing seed quality. Full article

Fat deposition plays a key role in determining porcine meat quality traits, with lipid droplets serving as critical organelles for lipid storage in adipose tissue. Inhibiting lipid droplet biogenesis disrupts the lipid storage capacity of adipocytes. The Stearoyl-CoA Desaturase (SCD) family is crucial in regulating polyunsaturated fatty acid/monounsaturated fatty acid (PUFA/MUFA) composition, while its role in lipid droplet formation remains unclear. This study employed CRISPR/Cas9 to create SCD1-deficient porcine renal epithelial cells (PK15), enabling an investigation into SCD1’s role in fatty acid composition and lipid droplet regulation. RNA-seq analysis was conducted to elucidate the mechanisms underlying SCD1’s impact on lipid droplet numbers. Results showed that SCD1 deletion significantly decreased triacylglycerols (TAG) content, altered fatty acid composition, and decreased lipid droplet numbers. Conversely, SCD1 overexpression increased lipid droplet numbers, confirming SCD1’s role in regulating lipid droplet abundance. RNA-seq analysis revealed that SCD1 regulates lipid metabolism via Calsyntenin 3β (CLSTN3B). Experimental validation confirmed the SCD1-CLSTN3B regulation of lipid droplet numbers. In summary, we discovered the role of SCD1 in regulating the number of lipid droplets, highlighting its potential impact on lipid metabolism and adipocyte function in pigs. Full article

Genetic polymorphisms have a great impact on enhancing quantitative traits in cattle. In this study, Fatty acid synthase (FASN) g. 16024 (A>G), Stearoyl-CoA desaturase (SCD) g. 10329 (C>T), and pleomorphic adenoma gene (PLAG1) g. 25003338 (C>G) genotypic and allelic polymorphisms were evaluated, along with their associations with fatty acid composition, adipogenic gene expression, and carcass characteristics (carcass weight, yield grade, backfat thickness, and marbling score) in Hanwoo steers. A total of 128 Hanwoo steers were selected for this study and the Polymerase chain reaction–restriction fragment length polymorphism (PCR-RFLP) method was used to identify polymorphism of these genes. The AG genotype and G allele in FASN g. 16024 (A>G), CT genotype and T allele in SCD g. 10329 (C>T), and GG genotype and G allele in PLAG1 g. 25003338 (C>G) showed higher frequency and positively correlated with carcass traits, yield, and quality grades. Fatty acid composition results indicate that C18:3n-6, C20:1, and C20:2n-6 were significantly higher in the AA genotype of FASN gene, C14:1 and C18:3n-6 in the CC genotype, and C16:1 in the TT genotype of SCD gene. C12:0, C14:0, C16:1, C18:0, and C20:0 were higher in the CC genotype of PLAG1 gene. Furthermore, RT-qPCR analysis of adipogenesis-related genes (AMP-activated protein kinase-α (AMPKα), Carnitine palmitoyl transferase-1β (CPT1), G-coupled protein receptor-43 (GPR43), and SCD) across different SNP genotypes suggests a systemic interaction between genetic factors and adipogenesis in beef cattle. This study emphasizes the significance of FASN g. 16024 (A>G), SCD g. 10329 (C>T), and PLAG1 g. 25003338 (C>G) SNPs for genetic selection to enhance beef quality and elucidate lipid metabolic pathways in Hanwoo cattle. Full article

Background: Glycolipid metabolism is essential for maintaining metabolic homeostasis. As a new postbiotic, pasteurized Akkermansia muciniphila (P-AKK) is important for the regulation of immunity and metabolism. Objectives: This study aimed to evaluate the effects of P-AKK on glycolipid metabolism in Caenorhabditis elegans fed a high glucose diet. Results: We discovered that feeding nematodes P-AKK improved their healthy lifespan when fed a high-glucose diet. Furthermore, P-AKK contributes to reducing the accumulation of glucose, advanced glycation end products, and lipids and maintains a better physiological state. In addition, P-AKK improved the composition of free fatty acids and decreased the total free fatty acid content of C. elegans. Transcriptome sequencing analysis revealed that P-AKK induced significant enrichment of carbohydrate, oxidative phosphorylation, and fatty acid metabolism pathways. These significantly enriched biological processes were closely related to glucose and lipid metabolism. Among them, P-AKK activated the β-oxidation of fatty acids while inhibiting the de novo synthesis of fatty acids to regulate fatty acid metabolism. Conclusions: The administration of P-AKK positively affected the body phenotypes of C. elegans under high glucose conditions. P-AKK mitigated the fat accumulation induced by a high-glucose diet by regulating key metabolic enzymes, including acyl-CoA synthetase and stearoyl-CoA desaturase. Full article

Inflammatory bowel disease is a risk factor for brain dysfunction; however, the underlying mechanisms remain largely unknown. In this study, we aimed to explore the potential molecular mechanisms through which intestinal inflammation affects brain function and to verify these mechanisms. Mice were treated with multiple cycles of 1% w/v dextran sulfate sodium (DSS) in drinking water to establish a chronic colitis model. Behavioral tests were conducted using the open field test (OFT), tail suspension test (TST), forced swimming test (FST), and Morris water maze test (MWM). Brain metabolomics, transcriptomics, and proteomics analyses were performed, and key target proteins were verified using qPCR and immunofluorescence. Four cycles of DSS administration induced colitis, anxiety, depression, and spatial memory impairment. The integrated multi-omics characterization of colitis revealed decreased brain chenodeoxycholic acid (CDCA) levels as well as reduced stearoyl-CoA desaturase (Scd1) gene and protein expression. Transplantation of the colitis microbiome resulted in anxiety, depression, impaired spatial memory, reduced CDCA content, decreased Scd1 gene and protein expression, and lower concentrations of monounsaturated fatty acids (MUFAs), palmitoleate (C16:1), and oleate (C18:1) in the brain. In addition, CDCA supplementation improved DSS-induced colitis, alleviated depression and spatial memory impairment, and increased Scd1 gene and protein expression as well as MUFA levels in the brain. The gut microbiome induced by colitis contributes to neurological dysfunction, possibly through the CDCA–Scd1 signaling axis. CDCA supplementation alleviates colitis and depressive behavior, likely by increasing Scd1 expression in the brain. Full article

This experiment was arranged to explore the impacts of dietary MHA on liver lipid metabolism in largemouth bass. A total of 480 fish (14.49 ± 0.13 g) were randomly allocated into four groups, each with three replicates. They were then given four different diets containing graded levels of MHA (0.0, 3.0, 6.0, and 9.0 g/kg) for 84 days. The results showed that dietary MHA increased hepatic lipid vacuoles and lipid content (p < 0.05). Dietary supplementation with MHA 9.0 g/kg diets increased the activities of acetyl-coA carboxylase (ACC), fatty acid synthase (FAS), and stearoyl-coA desaturase 1 (SCD-1). Dietary MHA up-regulated the mRNA expressions of liver lipid synthesis (ACC, FAS, SCD-1 and SREBP-1c) (p < 0.05). Furthermore, compared with the 0.0 g/kg diet group, the group supplemented with 9.0 g/kg MHA in the diet exhibited a significant decrease in the activities of liver lipid-oxidation-related enzymes (acetyl-CoA carboxylase (ACC), fatty acid synthase (FAS), and stearoyl-CoA desaturase 1 (SCD-1), as well as HSL and CPT1) and the gene expressions of ATGL, HSLa, HSLb, CPT1a, and PPARα (p < 0.05). Additionally, the mRNA expressions and protein levels of SIRT1 and AMPK in the 9.0 g/kg MHA-supplemented group were significantly lower than those in the 0.0 g/kg diet group (p < 0.05). Overall, the present results suggested that dietary MHA could increase lipid accumulation through regulating SIRT1/AMPK signaling pathways in the livers of largemouth bass. Full article

Metabolic dysfunction associated with steatotic liver disease (MASLD) is the result of disturbed lipid metabolism. In MASLD, the accumulation of free fatty acids (FFAs) in hepatocytes causes lipotoxicity mediated by oxidative stress. Coffee compounds are known for their beneficial effects in MASLD; however, the mechanisms still need to be further explored. The aim of this study was to elucidate the protective mechanisms of coffee compounds against palmitate-induced lipotoxicity in primary hepatocytes. Methods: Primary hepatocytes were isolated from male Wistar rats and treated with palmitate (1 mmol/L) in combination with caffeine (CF: 1 mmol/L) or chlorogenic acid (CGA: 5 µmol/L). Mitochondrial ROS production, palmitate-induced necrosis, antioxidant response, ER stress markers and lipid droplet (LD) formation were assessed. Monoacylglycerols 2-SG (2-Stearolylglycerol), 2-OG (2-Oleoylglycerol) and SCD-1 (Stearoyl-CoA Desaturase 1) inhibitors were used to modulate LD formation. LD formation in steatotic Zucker rat hepatocytes was also investigated. Results: CF and CGA prevented palmitate-induced cell death and reduced ROS production. CF and CGA induced the antioxidant response, especially HO-1 expression, but had no significant effect on ER stress markers. CF and CGA increased LD formation in palmitate-treated cells. This effect was significantly reduced by 2-SG and SCD-1 inhibitors but enhanced by 2-OG. Lipid droplets were associated with lower palmitate toxicity and reduced ROS production. Conclusions: CF and CGA protect hepatocytes from lipotoxicity via modulation of the antioxidant response and enhance lipid droplet formation via an SCD-1-dependent mechanism. Oxidative stress-related toxicity in hepatocytes can be prevented by enhancing LD formation. Full article

Dietary interventions with food-derived natural products have emerged as a promising strategy to alleviate obesity. This study aims to investigate the anti-obesity effect of Hericium erinaceus protein (HEP) and its underlying mechanism. Our results demonstrated that HEP exhibited excellent radical scavenging activity in vitro. In vivo, HEP intervention reduced pancreatic lipase activity in the intestine and enhanced fat excretion, thereby inhibiting the absorption of dietary fats. Meanwhile, HEP ameliorated the body weight and organ indexes, dyslipidemia, insulin resistance, hepatic steatosis, and liver oxidative stress injuries in obese mice. The results of real-time PCR (qRT-PCR) and Western blot analyses indicated that HEP upregulated the expression of peroxisome proliferator-activated receptor α (PPARα), subsequently upregulated the expression of liver fatty acid oxidation-related genes (lipoprotein lipase (LPL), carnitine palmitoyltransferase 1a (CPT-1a), and acyl-CoA oxidase 1 (ACOX1)) and downregulated the expression of lipogenesis-related genes (sterol regulatory element-binding protein-1c (SREBP-1c), stearoyl-coenzyme A desaturase 1 (SCD-1), and fatty acid synthase (FASN)), thereby ameliorating lipid metabolism disorders. Therefore, these findings demonstrated that HEP exerted protective effects on lipid metabolism disorders by activating the PPARα pathway, indicating its potential as a dietary supplement for the prevention and amelioration of obesity. Full article

Colorectal cancer (CRC) is recognized as the third most lethal cancer worldwide. While existing treatment options demonstrate considerable efficacy, they are often constrained by non-selectivity and substantial side effects. Recent studies indicate that lipid metabolism significantly influences carcinogenesis, highlighting it as a promising avenue for developing targeted anticancer therapies. The purpose of the study was to see if acyl-coenzyme A: cholesterol acyltransferase 1 (ACAT1), 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR), and stearoyl-CoA 9-desaturase (SCD1) are good metabolic targets and whether the use of inhibitors of these enzymes together with 5-fluorouracil (5-FU) would have a synergistic effect on CRC cell viability. To confirm that the correct lipid targets were chosen, the expression levels of ACAT1, HMGCR, and SCD1 were examined in CRC patients and cell models. At first, each compound (Avasimibe, Lovastatin, MF-438, and 5-FU was tested separately, and then each inhibitor was paired with 5-FU to assess the synergistic effect on cell viability. Gene expression of selected enzymes significantly increased in tissue samples obtained from CRC patients and cancer cell lines (HT-29). Inhibition of any of the selected enzymes reduced CRC cell growth in a dose-dependent manner. More importantly, the combination of 5-FU + Avasimibe (an ACAT1 inhibitor) and 5-FU + MF-438 (an SCD1 inhibitor) produced a stronger antiproliferative effect than the inhibitors alone. 5-FU combined either with Avasimibe or MF-438 showed a synergistic effect with an HSA score of 47.00 at a dose of 0.3 + 30 µM, respectively (2.66% viability rate vs. 46%; p < 0.001), and 39.34 at a dose of 0.3 + 0.06 µM (46% vs. 10.33%; p < 0.001), respectively. The association of 5-FU with Lovastatin (HMGCR inhibitor) did not significantly impact CRC cell viability in a synergistic manner. Inhibition of lipid metabolism combined with standard chemotherapy is a promising strategy that reduces CRC cell viability and allows for the use of a lower drug dose. The combination of 5-FU and Avasimibe has the greatest therapeutic potential among studied compounds. Full article

In this work, we studied the relationships between the most representative fatty acids (FAs) and their ratios in red blood cell (RBC) membranes and dietary fatty acids alongside several cardiometabolic risk factors. Twenty-six individuals were enrolled with a mean age of 50.4 ± 12.7 years (16 males and 10 females). By bivariate analysis, dietary oleic acid (OA) correlated negatively with C20:4n-6 (AA) (p = 0.031) in RBCs. With multivariate regression analysis, dietary OA (p < 0.001) is an independent predictor and negatively associated with AA levels in RBCs, while the elongation of very-long-chain fatty acids 6 (ELOVL6) and stearoyl-CoA desaturase 16 (SCD16) activities (p < 0.05) was positively associated with AA levels in RBCs. The multivariate regression models also showed that dietary OA was an independent predictor and positively associated with C22:5n-3 (DPA) in RBCs. Furthermore, BMI positively correlated with SCD16, and both SCD16 and SCD18 were positively associated with triacylglycerols levels. In addition, SCD16 positively and significantly correlated with LDL-c and the LDL-c/HDL-c ratio and negatively correlated with the ApoA1/ApoB ratio, and SCD16 and ELOVL6 were significantly associated with HDL molecular subfractions. Therefore, our data underline that OA, SCD16 and ELOVL6 can interfere with n-3 and n-6 partition in biomembranes such as RBCs, suggesting an important molecular (patho)physiological regulatory mechanism role in controlling bioactive molecules’ availability such as those involved in the immune-inflammatory response. Full article

Background/Objectives: Obesity is a key factor in metabolic syndrome (MetS) development. Consumption of a high-fat diet (HFD) accelerates the onset of obesity and associated metabolic complications. Protaetia brevitarsis (PB) has been traditionally utilized in Korean medicine for its antioxidant, anti-diabetic, anticancer, and hepatoprotective effects. However, specific effects of PB hydrolysate on skeletal muscles have not been fully elucidated. Therefore, this study sought to assess the influence of PB on HFD-induced MetS, focusing on the lipid metabolism and inflammatory responses mediated by AMP-activated protein kinase activation. Methods: To induce obesity, 6-week-old C57BL/6J mice were maintained on an HFD for 8 weeks, after which PB hydrolysate was orally administered for 16 weeks while the HFD regimen was sustained. A glucose tolerance test was conducted orally to evaluate glucose regulation, and forelimb grip strength was assessed upon completion of the experimental period. Histological assessments, serum biochemical analysis, lipid extraction, Western blot analysis, and quantitative reverse-transcription polymerase chain reaction (qRT-PCR) were performed following euthanasia. Results: PB significantly reduced ectopic lipid deposition in skeletal muscles, enhanced muscle strength, and improved insulin sensitivity by increasing fatty acid oxidation via AMP-activated protein kinase/carnitine palmitoyltransferase 1 activation and inhibiting lipogenesis via stearoyl-CoA desaturase 1 gene downregulation. Furthermore, PB alleviated HFD-induced low-grade chronic inflammation by decreasing systemic monocyte chemoattractant protein 1 levels, thereby reducing ectopic fat deposition. Conclusions: This study highlights the potential of PB as a nutraceutical to mitigate MetS in HFD-fed mice. Full article

Multiply adverse effects including declines in production performance and excessive fat deposition were noticed with the extension of the laying cycle in hens, which are pertinent to animal welfare and human food safety. This study aimed to investigate the effect of dietary supplementation of bile acids (BAs) on production performance and lipid metabolism in late-phase laying hens. A total of 144 70-week-old hens were distributed into three treatments with eight replicates per treatment, including the basal diet with 0 (Ctrl), 95.01 (Low-BA), and 189.99 mg/kg (High-BA) of porcine BAs, respectively. The test period was from 70 to 75 weeks. The supplementation of BAs did not significantly alter laying performance during the trial, whereas it increased (p < 0.05) the total follicles compared to the Ctrl diet. The eggs from the hens fed the BA diet exhibited increased (p > 0.05) relative weight of eggshell and yolk color than those that consumed the Ctrl diet. There were no significant changes following BA treatment regarding the serum lipid profile. Dietary BA treatment reduced the total triglyceride in livers to different extents, resulting in the decreased diameter and area of vacuoles in liver tissues. The low-dose BA treatment decreased the mRNA levels of fatty acid synthase (FASN) and stearoyl-CoA desaturase (SCD), while promoting the expression of lipoprotein lipase (LPL) compared to the Ctrl group (both p < 0.05). Of note, the expressions of farnesoid X receptor (FXR), apical sodium-dependent bile acid transporter (ASBT), and ileum bile acid-binding protein (IBABP) were notably downregulated (p < 0.05) by the low-dose BA treatment. Dietary BA treatment had no apparent effects on laying performance, whereas it increased the follicle frequency, eggshell weight, and yolk color. Moreover, a diet containing 95.01 mg/kg of BAs depressed ileal BA resorption and hepatic fatty deposition by reducing lipogenesis and promoting lipolysis, which may have a beneficial effect on the liver in late-phase layers. Full article

This study aimed to explore the effects of sodium butyrate on liver metabolism in goats subjected to a high-concentrate diet. We randomly assigned twelve Saanen-lactating goats into two groups, one of which received a high-concentrate diet (concentrate: forage = 60:40, control group), while the other received the same basal diet supplemented with sodium butyrate (SB) (10 g/kg basal diet, SB group). Compared with the control diet, the SB diet considerably increased the milk fat percentage and content (p < 0.05), with an increase of 0.67% in the milk fat content of the SB group. By employing a global metabolomics approach based on ultra-performance liquid chromatography–tandem mass spectrometry (UPLC–MS/MS), we identified 6748 ions in ESI+ mode and 3573 ions in ESI− mode after liver isolation from both groups. A total of twenty-three metabolites, including phospholipids, fatty acids, and ribose phosphate, were found to be dysregulated according to a search against the human metabolome database (HMDB). Pathway analysis revealed activation of the pentose phosphate pathway, glycerophospholipid metabolism, and unsaturated fatty acid synthesis. The SB diet also modulated the expression of key lipogenic enzymes, such as acetyl-CoA carboxylase (ACC) and stearoyl-CoA desaturase (SCD-1), which are downstream targets of the transcription factor sterol regulatory element-binding proteins-1c (SREBP-1c), inducing a significant upregulation (p < 0.05). Furthermore, 6-phosphogluconate dehydrogenase (6PGDH) levels in the liver were elevated after the lactating goats were fed the SB diet (p < 0.05). Our study reveals that the SB diet may offer substantial benefits in enhancing the milk quality of subacute ruminal acidosis (SARA) goats. This is accomplished by augmenting the activity of the liver pentose phosphate pathway and the process of de novo fatty acid synthesis in lactating goats. Full article

In this study, we investigated the anti-fatigue effects of black ginseng ginsenosides using exercise performance tests, serum analyses, and gene expression profiling. No significant differences in dietary intake or body weight were observed between groups. The low-dose black ginseng (LBG) group showed no significant improvements in swimming and rotating rod tests. In contrast, the medium (MBG)- and high-dose (HBG) groups showed notable increases in swimming time and significant improvements in the rotating rod test. All treatment groups exhibited longer running times, particularly the HBG group. Serum analysis revealed increased muscle and hepatic glycogen, catalase, and lactate dehydrogenase levels in the MBG and HBG groups, whereas lactate, lipid peroxide, and superoxide dismutase levels were decreased. Additionally, gene expression analysis showed significant upregulation of key antioxidant and mitochondrial function genes, including those encoding cationic amino acid transporter 2, stearoyl-CoA desaturase-2, nuclear respiratory factor 1, nuclear factor erythroid 2-related factor 2, mitochondrial transcription factor A, cytochrome c oxidase II, and NADH–ubiquinone oxidoreductase core subunit 1, particularly in the HBG group, indicating enhanced antioxidant capacity and improved mitochondrial function. These findings suggested that black ginseng ginsenosides effectively mitigated fatigue. Full article

The SCD is a rate-limiting enzyme that catalyzes the synthesis of monounsaturated fatty acids (MUFAs) in dairy cows; however, its role in the mammary gland of buffalo is not well understood. In this study, we isolated and characterized the complete coding sequence (CDS) of the buffalo SCD gene from mammary gland tissue and investigated its effects on milk fat synthesis using bioinformatics analyses, tissue differential expression detection, and cellular functional experiments. The cloned SCD gene has a CDS length of 1080 bp, encoding a protein of 359 amino acids. This protein is hydrophilic, lacks a signal peptide, and contains four transmembrane domains, including 10 conserved motifs and a Delta9-FADS domain, characteristic of the fatty acid desaturase family involved in unsaturated fatty acid biosynthesis within the endoplasmic reticulum. Molecular characterization revealed that the physicochemical properties, conserved domains, structures, and functions of buffalo SCD are highly similar to those in other Bovidae species. Among the tissues analyzed, SCD expression was highest in the mammary gland during lactation and in the cerebellum during dry-off period. Notably, SCD expression in the mammary gland was significantly higher during lactation compared to the dry-off period. Subcellular localization experiments confirmed that SCD functions in the endoplasmic reticulum of buffalo mammary epithelial cells (BuMECs). Functional overexpression and interference experiments in BuMECs demonstrated that SCD promotes milk fat synthesis by affecting the expression of lipid synthesis-related genes such as ACACA, FASN, and DGAT1, as well as milk fat regulatory genes like SREBFs and PPARG, thereby influencing intracellular triglyceride (TAG) content. Additionally, 18 single-nucleotide polymorphisms (SNPs) were identified in the buffalo SCD gene, with a specific SNP at c.-605, showing potential as molecular markers for improving milk production traits. These findings highlight that the SCD gene is a key gene in buffalo milk fat synthesis, involved in the de novo synthesis of milk fatty acids. Full article