L-FABP ELISA
- Known as:
- L-FABP Enzyme-linked immunosorbent assay test
- Catalog number:
- kt-563
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Kamiya biomedical company
- Gene target:
- L-FABP ELISA
Related products to: L-FABP ELISA
Related articles to: L-FABP ELISA
- Fatty acids undergo re-esterification to form triglycerides or are directly oxidized for energy production following absorption. Fatty acid binding protein 1 (FABP1), a key transporter highly expressed in both hepatic and intestinal tissues, directs the metabolic fate of absorbed fatty acids. Although its role in facilitating fatty acid transport and lipogenesis in the liver is well established, the functional mechanisms of intestinal FABP1 remain poorly understood due to the complexity of the intestinal microenvironment. In this study, using animal models with intestinal-specific FABP1 knockout and gut microbiota depletion, we demonstrate that intestinal FABP1 directly facilitates the absorption of dietary fatty acids, and that gut microbiota regulate FABP1-mediated dietary fatty acid absorption through metabolites. Notably, the abundance of exhibits an inverse correlation with FABP1-dependent obesity progression in an arachidonic acid-induced model. Supplementation with markedly alleviates this obese phenotype. Through FABP1 protein-based metabolite enrichment coupled with untargeted metabolomics, we identified L-norleucine as a competitive FABP1 inhibitor despite its smaller molecular size relative to long-chain fatty acids. L-norleucine possesses a hydrophobic alkyl chain structurally analogous to fatty acids and a hydrophilic amino acid moiety, which may explain its binding to FABP1. Critically, L-norleucine constitutes a major metabolite in the gut, which may play an underappreciated role in regulating lipid homeostasis. Collectively, this study uncovers a previously unrecognized gut microbiota-FABP1 axis governing lipid homeostasis, offering therapeutic insights for metabolic disorders. - Source: PubMed
Publication date: 2026/05/28
Li JuanMa ZhengcaiZhang JinyinSun ChunyongWu HuiminLi XiaoduoLi ZhengWang HuiqingYang YubinShang LianchunYang ZhipengZhu JianyuLiu JifeiManzoor RakiaTang LiLi XuegangYe XiaoliMa Hang - Chaihu Guizhi Ganjiang Decoction (CGGD) is a clinically proven prescription effective against metabolic dysfunction-associated steatohepatitis (MASH). However, its chemical constituents with the lipid-lowering and anti-inflammatory bioactivities and underlying mechanisms remain unclear. This study aimed to characterize the chemical profile of CGGD while elucidating their lipolytic and anti-inflammatory activities and mechanisms. Using UHPLC-Q-TOF-MS/MS, 209 compounds were identified in CGGD, categorized into 52 saponins, 103 flavonoids, 17 gingerols, 21 organic acids, and 16 others, with 13 putative unvalidated new compounds. Nineteen prototype components were detected in hepatic tissues, with saikosaponin A, baicalin, wogonoside, skullcapflavone II, and glycyrrhizin exhibiting strong binding affinities toward PPARα and TLR4 proteins. These components significantly reduced triglyceride (TG) accumulation in FFA-induced HepG2 steatosis cells, confirmed by oil red O staining and TG quantification. Mechanistically, saikosaponin A and baicalin upregulated PPARα and its downstream genes (CPT1A, FABP1, ACOX1) to promote fatty acid transport and oxidation. Meanwhile, saikosaponin A, baicalin, and wogonoside significantly suppressed mRNA expression of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) in LPS-stimulated RAW264.7 macrophages, and saikosaponin A and wogonoside further inhibited the expression of TLR4, MyD88, and phosphorylated NFκB, thereby attenuating inflammation. In conclusion, this study established a comprehensive methodology for profiling the chemical constituents of CGGD and identified saikosaponin A, baicalin, wogonoside, skullcapflavone II, and glycyrrhizin as its key anti-MASH components. Their lipid-lowering and anti-inflammatory activities were mediated through the PPARα-regulated fatty acid metabolism pathway and the TLR4/MyD88/NFκB signaling pathway, respectively, offering a scientific basis for the clinical application of CGGD in MASH. - Source: PubMed
Publication date: 2026/05/18
Wu HaoWang TengtengCai ShengnanQiao YunLiu JieLi YuetingXiao Hongbin - The modification of cardiometabolic risk factors is a major strategy to prevent metabolic dysfunction-associated fatty liver disease (MAFLD), given the current lack of approved pharmacological treatments. This study investigated whether oleacein (OLEA), a key polyphenol in olive oil, can prevent dyslipidemia and hepatic steatosis in apolipoprotein E knockout (ApoE-KO) mice, a model of atherosclerosis and metabolic disturbance. C57BL/6J wild-type (WT, = 16) and ApoE-KO ( = 16) mice were assigned to four groups ( = 8) and fed for 10 weeks: WT mice received either a standard diet (WT + STD) or an atherogenic diet (WT + ATD), while ApoE-KO mice received the atherogenic diet without (ApoE-KO + ATD) or with OLEA supplementation (50 mg kg day, oral; ApoE-KO + ATD + OLEA). Metabolic parameters, serum lipid profile, and hepatic triglyceride (TG) content were determined, alongside markers of liver injury, oxidative status (SOD expression and activity), and lipid metabolism (including SCD1 expression). OLEA supplementation significantly improved the serum lipid profile and reduced hepatic TG accumulation ( < 0.05), effects associated with marked downregulation of hepatic SCD1, indicating inhibition of lipogenesis, FABP1 and CPT1. In addition, OLEA restored hepatic SOD1 and SOD2 expression and enhanced serum SOD activity, suggesting reinforcement of antioxidant defenses. Overall, OLEA exerted strong anti-dyslipidemic and hepatoprotective effects in ApoE-KO mice, likely through the combined modulation of lipid synthesis and redox homeostasis. These findings highlight the potential of OLEA as a promising natural compound for preventing diet-induced metabolic and hepatic disorders associated with MAFLD. - Source: PubMed
Publication date: 2026/05/15
Ormonde BeatrizCosta VâniaVieira PedroAlves AndréViana SofiaReis FlávioPaiva-Martins Fátima - Human exposure to micro- and nanoplastics is increasingly recognized as a global concern, yet their long-term effects on human health remain poorly understood. Defining the cellular consequences of chronic exposure is essential for reliable risk assessment and informed environmental and public health strategies. Here, we investigated the impact of prolonged culture in presence of nanoplastics, using an in vitro hepatocyte model (HepG2) exposed to environmentally relevant concentrations (10⁴ and 10⁶ particles/mL). After 28 days, no significant changes in morphology or cell viability were observed. Despite this apparent tolerance, prolonged exposure produced marked metabolic alterations. Cellular lipid content increased in a dose-dependent manner after 120 h, peaked at day 14 (120% ± 16 and 133% ± 12), remained stable until day 21, and declined thereafter. This response was accompanied by altered expression of key lipid metabolism regulators, including SREBP-1C, FABP1, PPAR-α, and PPAR-γ. Lipidomic analysis further revealed a shift in lipid composition from day 14 onward, with increased saturated fatty acids and reduced unsaturated lipids. Although total lipid accumulation partially resolved by day 28, suggesting adaptive responses, the lipidome continued to remodel toward a potentially pathological profile. This metabolic shift was paralleled by an inflammatory signal, as indicated by increased TNF-α expression after 7 days. Together, these findings show that prolonged exposure to low nanoplastic concentrations elicits substantial lipid remodeling, potentially predisposing hepatocytes to lipotoxic and inflammatory states. - Source: PubMed
Publication date: 2026/05/12
Mognetti BarbaraMannino GiuseppeBrossa AlessiaMolino VeraFranco FrancescoBerta Giovanni NicolaoBovolin Patrizia - Ginsenoside Rg1 (G-Rg1) can effectively ameliorate lipopolysaccharide-induced renal injury. The impact and mechanism of G-Rg1 in renal ischemia-reperfusion (I/R) injury are not yet understood. This study aimed to examine the role and mechanism of G-Rg1 in kidney I/R injury. The renal I/R injury mice and mouse kidney cells were applied as renal I/R injury models. Researchers analyzed the functions and mechanisms of G-Rg1 using techniques like cell proliferation, apoptosis, clone formation assay, ELISA, HE staining, immunohistochemical staining, Immunofluorescence staining, qRT-PCR, and Western blot analysis. Our findings indicate that G-Rg1 pretreatment protects against renal I/R injury by lowering serum creatinine and urea nitrogen levels, mitigating histological damage and apoptosis, and reducing inflammation and oxidative stress. These beneficial effects were accompanied by the suppression of fatty acid binding protein 1 (FABP1) and heme oxygenase-1 (HO-1) expression and the promotion of nuclear factor erythroid 2-related factor 2 (Nrf2) nuclear translocation. However, the therapeutic effect of G-Rg1 was inhibited by FABP1 overexpression. The mechanism by which G-Rg1 ameliorates renal I/R injury may be related to the inhibition of FABP1 expression and thus regulation of the Nrf2/HO-1 pathway. - Source: PubMed
Publication date: 2026/05/03
Chang XiaodongZhang LuZheng GuangyiZhang HongyuXue HenFeng Wanyan