ACACa ELISA kit
- Known as:
- ACACa Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-ACACa-Hu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- ACACa ELISA kit
Related genes to: ACACa ELISA kit
- Gene:
- ACACA NIH gene
- Name:
- acetyl-CoA carboxylase alpha
- Previous symbol:
- ACAC, ACC
- Synonyms:
- ACC1
- Chromosome:
- 17q12
- Locus Type:
- gene with protein product
- Date approved:
- 1989-09-11
- Date modifiied:
- 2018-05-03
Related products to: ACACa ELISA kit
Human ELC ELISA KIT 96 TEST
OxiSelect In Vitro ROS/RNS Assay Kit (Green Fluorescence), Trial Size
OxiSelect Methylglyoxal (MG) Competitive ELISA Kit
OxiSelect Methylglyoxal (MG) Competitive ELISA Kit
OxiSelect TBARS Assay Kit (MDA Quantitation), Trial Size
OxiSelect Total Antioxidant Capacity (TAC) Assay Kit, Trial Size
OxiSelect™ In Vitro ROS RNS Assay Kit (Green Fluorescence), Trial Size(1-3)-beta-D-glucan Sandwich ELISA, Double Antibody(1-Kit )11,12-EET DHET Immunoassay Kit(1-Kit )11,12-EET_DHET Immunoassay Kit(1-Kit) 11,12-DHET Immunoassay Kit(1-Kit) 14,15-DHET Human Urine ELISA Kit(1-Kit) 14,15-DHET Hypertension ELISA Kit(1-Kit) 14,15-DHET sEH activity ELISA Kit(1-Kit) 14,15-EET DHET Hypertension ELISA Kit Related articles to: ACACa ELISA kit
- Dysregulation of brain cholesterol homeostasis is increasingly recognized as a critical driver of Alzheimer's disease (AD) pathogenesis. G protein-coupled receptor 146 (GPR146) has emerged as a pivotal regulator of systemic cholesterol metabolism; however, its role in the central nervous system and AD remains elusive. Here, we report that GPR146 deficiency in mice modulates ERK/PKA signaling without affecting baseline physiology or general behavior. Following intracerebroventricular (i.c.v.) injection of amyloid-β (Aβ)42 oligomers, GPR146 was associated with altered Aβ42-evoked ERK/PKA/Akt signaling both in vivo and in vitro. Mechanistically, Gpr146 ablation potentiated microglial Aβ phagocytosis, which correlated with the transcriptional upregulation of phagocytic receptors, including TREM2, GPR34, P2Y6, and CR3, alongside increased expression of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6). Moreover, GPR146 deficiency was linked to elevated levels of blood-brain barrier (BBB)-associated markers Cldn-5 and Glut-1 protein levels, while attenuating Aβ‑induced inflammatory responses in brain endothelial cells. At the metabolic level, GPR146 knockout modulated the expression of key enzymes governing glucose (GLUT1, GLUT3, G6PD, PFK, HK) and lipid (HMGCS1, ACACA, FASN, SCD1) metabolism and markedly reduced Aβ‑elicited lipid droplet accumulation in the cortex and hippocampus. Collectively, our findings establish GPR146 as a novel neurometabolic regulator whose deficiency correlates with enhanced Aβ phagocytosis, maintenance of BBB-associated proteins, and altered cerebral metabolism, thereby presenting a potential therapeutic axis for early AD intervention. - Source: PubMed
Publication date: 2026/08/05
Yang ShaobinLi YanhongGuo YanlingLi YumengLi MeiqiLi HongxiaZhang Yimeng - This study aimed to investigate the effects of stevia extract (SE) on growth performance and meat quality of broilers and reveal possibly mechanisms. Four hundred Arbor Acres male broilers (1 d old, 40 ± 1 g) were randomly assigned to 5 treatments with 8 replicates of 10 broilers per replicate. Broilers in the control (CON) group were fed the basal diet, while broilers in the other 4 treatment groups were fed the basal diet supplemented with 50, 100, 150, and 200 mg/kg SE, respectively. Dietary supplementation with SE effectively improved breast meat quality and tended to increase average daily gain (ADG) in broilers. Compared with the CON group, 150 mg/kg SE reduced 48 h drip loss and peak shear force of breast muscle (P < 0.05). Both 150 and 200 mg/kg SE decreased total cholesterol (TC) and triglyceride (TG) contents, while 100 and 150 mg/kg SE reduced malondialdehyde (MDA) concentration in breast muscle (P < 0.05). SE altered fatty acid (FA) composition: 150 mg/kg SE decreased the proportion of C24:0, and 200 mg/kg SE decreased C22:6n3 (P < 0.05). Linear regression analysis identified 150 mg/kg as the optimal SE level for meat quality improvement, which also downregulated FASN and ACACA mRNA expression (P < 0.05). Untargeted metabolomics revealed that 150 mg/kg SE modulated glycerophospholipid metabolism. Further validation confirmed that 150 mg/kg SE increased phospholipid (PL) content in breast muscle and improved endoplasmic reticulum (ER) and mitochondrial (MT) homeostasis. These changes were accompanied by reduced mRNA and protein expression of ER stress biomarkers (GRP78, PERK, IRE1, XBP1) and the MT chaperone HSP60 (P < 0.05). In conclusion, SE improves broiler breast meat quality via regulating the glycerophospholipid metabolism and enhancing endoplasmic reticulum and mitochondrial homeostasis. Regression analysis in this study indicates that the optimal SE supplementation amount for broilers is 150 mg/kg. - Source: PubMed
Publication date: 2026/07/08
Meng JiagengLv JirongChen XianxinYang LinxuJiang YilongJia GangChen XiaolingFeng BinChe LianqiangZhao Hua - This experiment was conducted to investigate the effects of mulberry leaf powder (MLP) on alleviating fatty liver hemorrhagic syndrome (FLHS) in laying hens. A total of 180 healthy 33-week-old Hy-Line Gray laying hens were randomly assigned to 3 groups, with 6 replicates per group and 10 chickens per replicate, and fed a basal diet (CON), high-energy-low-protein (HELP) diet (FLHS), and HELP + 5% MLP diet (MLP), respectively. The experiment lasted 56 days. Results showed that the HELP diet successfully induced FLHS, characterized by an increased liver index, hepatic steatosis, and oxidative stress (P < 0.05). MLP significantly alleviated FLHS-induced hepatic steatosis, and enhanced antioxidant capacity (superoxide dismutase, catalase, glutathione peroxidase, total antioxidant capacity, and glutathione) in serum and liver (P < 0.05). Transcriptomic analysis identified 102 differentially expressed genes, whose expression was increased by FLHS but reversed by MLP, including SREBF1, SLC27A4, PLIN2, ACOT13, APOA4, GLRX, and MSRB1, which mainly participate in lipid droplet dynamics and redox homeostasis. qRT-PCR confirmed that upregulated expression of lipogenic genes (such as FASN, ACACA, SCD, and ELOVL6) and the downregulated expression of oxidative stress-responsive genes (SOD1 and GPX1) in the FLHS group were normalized by MLP (P < 0.05), accompanied by increased expression of PPARα, CPT1A, and CD36 (P<0.05). 16S rRNA sequencing revealed that MLP reduced the abundance of Desulfovibrio, Rikenellaceae_RC9_gut_group, Intestinimonas, and Shuttleworthia, and enriched Faecalibacterium and Bifidobacterium in the cecum of FLHS laying hens (P < 0.05). Furthermore, MLP increased acetate, propionate, and butyrate levels, and decreased isobutyrate and isovalerate levels (P < 0.05). Correlation analysis showed that cecal acetate, propionate, butyrate, Faecalibacterium and Bifidobacterium were positively correlated with hepatic antioxidant enzyme activities (P < 0.05), and negatively correlated with hepatic lipogenic gene expression, hepatic lipid deposition and oxidative stress markers (P < 0.05). These findings indicated that MLP alleviated hepatic lipid metabolism disorders and oxidative stress in FLHS laying hens, which might be achieved by modulating gut microbiota structure and short-chain fatty acid production. - Source: PubMed
Publication date: 2026/07/16
Xuan LingLiu HongliZhang HengGao QingtaoShang YanLiu XuelanYan PeipeiShi TianhongFu Chunyan - Lactation performance is a pivotal economic trait in sheep production, yet its underlying epigenetic regulatory mechanisms remain poorly understood. In the present study, we integrated ATAC-seq and RNA-seq to compare chromatin accessibility landscapes and transcriptomic in mammary gland tissues from Sewa sheep (SWS) and East Friesian sheep (EFS). Histological characterization revealed that SWS exhibited significantly smaller mammary acini area, smaller lipid droplet area, and reduced lipid droplet diameter compared to EFS. ATAC-seq analysis identified 15,902 differentially accessible regions (DARs) between the two breeds, with motif enrichment analysis uncovering key transcription factors potentially governing lactation traits. RNA-seq analysis revealed 1,163 differentially expressed genes (DEGs), which were involved in lactation regulation. Integrated analysis identified 441 overlapping genes, and enriched in glycolysis/gluconeogenesis (e.g., PGAM1, ENO1) and pyruvate metabolism (e.g., ACACA, ACSS1, ACYP1). Collectively, our study provides new insights into the epigenetic regulatory mechanisms underlying lactation performance differences in sheep. - Source: PubMed
Publication date: 2026/07/29
Li WentaoXu JiaminSheng JiashunLi PengboZhang ZuokeLuo XinSong TianzengFu TongGao TengyunZhang TianliuSun Yu - Type 2 diabetes mellitus (T2DM) is a metabolic disorder characterized by glycolipid dysregulation and hepatic steatosis. Centella asiatica (CA) and its triterpenoid constituents exert metabolic benefits. In addition, previous metabolomics study found that asiatic acid regulated pyrimidine metabolism in obese mice, while the key target and pathway were undefined. This study investigated the regulatory effects of CA and its active constituents on T2DM-related glycolipid disorders, focusing on the pyrimidine metabolism pathway. T2DM mice were established using a high-fat diet combined with streptozotocin (STZ) and treated with Centella asiatica ethanolic extract or asiatic acid (AA), with glibenclamide as a positive control. Then, glycolipid metabolism, hepatic function, pyrimidine metabolites, and related mechanisms were assessed using biochemical assays, LC-MS/MS, cellular experiments, molecular analyses, and molecular docking. CAE and AA significantly reduced FBG (decreased by 51.01% and 53.01%), improved glucose intolerance, corrected dyslipidemia, alleviated hepatic steatosis, and attenuated insulin resistance in T2DM mice. They elevated hepatic uridine, cytidine, and UDP-glucose (UDPG) levels, promoted glycogen synthesis, inhibited uridine phosphorylase 1 (UPP1) activity, upregulated UDPG synthesis genes (PGM1, UGP2), and downregulated lipogenic genes (ACACA, Fasn, SREBP1/2). Molecular docking indicated specific binding of AA and asiaticoside to UPP1. This work distinguishes from our prior research by identifying UPP1 as a functional target and elucidating the detailed molecular mechanism. CA improves T2DM-associated glycolipid disorders and hepatic injury by modulating the pyrimidine metabolism-UDPG-glycogen synthesis pathway and targeting UPP1, highlighting its therapeutic potential for metabolic diseases. - Source: PubMed
Publication date: 2026/06/27
Shen YunjiaoYao YuanyuanLiu ZhihuiLi YiCao ShijieFeng Xinchi