Arabinoxylan (Medium viscosity)
Based on 1 Customer Validation
Arabinoxylan Medium viscosity is an orally active Dectin-1 splice variant modulator, glucose absorption inhibitor, and chyme viscosity enhancer. Arabinoxylan Medium viscosity inhibits particulate β-glucan-induced Dectin-1A activation and mildly suppresses Dectin-1B activation. In human dendritic cells stimulated with particulate β-glucan, Arabinoxylan Medium viscosity reduces the production of IL-10 and TNF-α, and increases the production of IL-4 and IL-23. Arabinoxylan Medium viscosity also supports antifungal immune responses without activating TLR2, TLR4 or TLR5, and does not induce cytokine production when used to stimulate human dendritic cells alone. Arabinoxylan Medium viscosity increases small intestinal chyme viscosity, gets degraded in the large intestine to produce short-chain fatty acids, reduces glucose absorption and insulin response, and improves glucose homeostasis. Arabinoxylan Medium viscosity supports microbial fermentation and the growth of beneficial microbiota in the gastrointestinal tract, prevents bile acid reabsorption, and delays starch digestion. Arabinoxylan Medium viscosity can be used in research related to type 2 diabetes, impaired glucose tolerance, and metabolic syndrome.
Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.
- Reinheit : 95%
- CAS. Nr.: 9040-27-1
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Speicherung:
Store at room temperature 3 years.
In solvent -80°C, 2 years , -20°C, 1 year
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Biologische Aktivität
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Chemical Information
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Lösungsmittel & Löslichkeit
- Protokoll
- Reinheit & Dokumentation
- Verweise
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Help & FAQs
Biologische Aktivität
Beschreibung
IC50 & Target
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Dectin-1 |
IL-10 |
IL-4 |
IL-23 |
In Vitro
The viscosity of Arabinoxylan solution increases significantly with rising concentration, exhibiting shear-thinning behavior; viscous behavior dominates at low viscosity, while molecular chains undergo hyperentanglement at high viscosity, leading to a transition from viscoelasticity to elasticity. Additionally, the solution follows the Cox-Merz rule and has no complex long-range structure[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
Arabinoxylan Medium viscosity (accounting for 7.1% of dry matter; administered orally; daily dosing; for 7 consecutive weeks) improves glucose homeostasis, as evidenced by reduced levels of fasting blood glucose, OGTT response, insulin, and HbA1c, while also delaying the onset of diabetes in Zucker diabetic fatty rats[3].
Arabinoxylan Medium viscosity (accounting for 10% of dry matter; p.o.; daily; for 3 consecutive weeks) does not alter glucose homeostasis or incretin hormone levels in normoglycemic pigs[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:portal vein-catheterized[3]
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Dosage:7.8% of dry matter
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Administration:p.o.; single dose
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Result:Reduced net portal glucose absorption at 60 minutes postprandially.
Lowered insulin secretion at 30 minutes postprandially.
Reduced incremental area under the curve (iAUC) for glucose to 74% of control value.
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Animal Model:Zucker Diabetic Fatty (ZDF)[3]
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Dosage:7.1% of dry matter
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Administration:p.o.; daily; 7 weeks
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Result:Reduced fasting blood glucose, glucose responses to oral glucose tolerance test (OGTT), insulin concentrations, and glycated hemoglobin A1c (HbA1c) levels compared to control.
Improved insulin sensitivity, increased insulin responses, and delayed the onset of diabetes relative to control.
Chemical Information
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CAS. Nr. 9040-27-1
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Appearance Solid
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Color White to off-white
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SMILES
[Arabinoxylan (Medium viscosity)]
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Structure Classification
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Initial Source
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Store at room temperature 3 years
In solvent -80°C 2 years -20°C 1 year
Lösungsmittel & Löslichkeit
In Vitro:
H2O : 20 mg/mL (Need ultrasonic)
Protokoll
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Research Protocol for Endocrine Diseases
Endocrine diseases often arise from disrupted hormone production, hormone signaling, or target-tissue responsiveness; for diabetes-focused endocrine disease models, insulin signaling regulates glucose uptake, hepatic glucose output, lipid metabolism, and β-cell compensation. Type 2 diabetes develops through interacting defects in insulin resistance, β-cell dysfunction, adipose inflammation, hepatic glucose overproduction, altered incretin signaling, and ectopic lipid metabolism. A major unresolved question is whether endocrine dysfunction is driven primarily by target-tissue insulin resistance, intrinsic β-cell failure, immune/inflammatory stress, or combined multi-organ failure that differs by disease stage.
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Research Protocol for Microbiome Analysis
Microbiome analysis characterizes microbial communities in biological or environmental samples by measuring community composition, diversity, taxonomic structure, functional potential, and associations with host or environmental phenotypes. 16S rRNA gene amplicon sequencing is commonly used for bacterial and archaeal taxonomic profiling, while shotgun metagenomics provides higher taxonomic resolution and direct functional information, including microbial genes, pathways, viruses, fungi, and antimicrobial-resistance genes when sequencing depth and host-DNA contamination are adequately controlled. Microbiome results are strongly affected by sample collection, storage, DNA extraction, contamination, sequencing method, reference database, and bioinformatic pipeline; therefore, standardized protocols, negative controls, mock communities, and transparent analysis workflows are required. Unresolved issues include low-biomass contamination, compositional-data bias, inconsistent species-level c
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
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Monocyte-derived dendritic cell differentiation
Human monocyte-derived dendritic cells are generated by isolating PBMC-derived monocytes and culturing them with GM-CSF plus IL-4, which produces cells with dendritic-cell antigen-presenting properties, reduced monocyte phenotype, and increased dendritic-cell functional readouts such as antigen uptake, allogeneic T-cell stimulation, and expression of markers including HLA-DR, CD80, CD86, CD83, CD1a, or CD209 depending on protocol and maturation state. The main readout is phenotypic and functional differentiation: immature MoDCs are commonly evaluated by loss or reduction of CD14 with acquisition of dendritic-cell markers and antigen uptake capacity, whereas mature MoDCs are evaluated by increased CD83, CD80, CD86, HLA-DR, and T-cell stimulatory function after exposure to maturation stimuli such as TNF-α or a cytokine/PGE2 cocktail.
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Research Protocol for Metabolic Diseases
AMP-activated protein kinase, AMPK, is a conserved cellular energy sensor that responds to reduced cellular energy status and coordinates metabolism by increasing ATP-generating catabolic pathways while suppressing ATP-consuming anabolic processes. In metabolic disease research, the AMPK pathway is experimentally relevant because it regulates hepatic lipid synthesis, fatty acid oxidation, glucose production, skeletal-muscle glucose disposal, mTORC1-linked biosynthesis, autophagy, mitochondrial homeostasis, and whole-body energy balance. The central pathway logic is that energy stress, metformin, exercise-like stimulation, or direct AMPK activators increase AMPKα Thr172 phosphorylation and downstream substrate phosphorylation, including ACC and RAPTOR. Phosphorylation of ACC suppresses lipogenesis and supports fatty acid oxidation, whereas phosphorylation of RAPTOR suppresses mTORC1 signaling and links cellular energy status to growth and protein synthesis control. The pathway is linked
Reinheit & Dokumentation
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Data Sheet (271 KB)
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SDS (251 KB)
- English - EN (251 KB)
- Français - FR (251 KB)
- Deutsch - DE (251 KB)
- Norwegian - NO (251 KB)
- Español - ES (251 KB)
- Swedish - SV (251 KB)
- Italian - IT (251 KB)
- Korean - KR (251 KB)
- Portuguese - PT (251 KB)
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Handling Instructions (2659 KB)
Verweise
[1]. Sahasrabudhe NM, et al. Arabinoxylan activates Dectin-1 and modulates particulate β-glucan-induced Dectin-1 activation. Mol Nutr Food Res. 2016;60(2):458-467. [Content Brief]
[3]. Knudsen KEB, et al. Arabinoxylan Concentrate from Wheat as a Functional Food Ingredient to Improve Glucose Homeostasis. Nutrients. 2025;17(9):1561. Published 2025 Apr 30. [Content Brief]
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
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