Trehalulose
Trehalulose is a microbial metabolite and a beneficial structural isomer of Sucrose (HY-B1779). Trehalulose attenuates blood glucose and insulin response. Trehalulose exhibits antioxidant activity to support oxidative stability. Trehalulose can be used for food and beverage applications, and can be used for the research of dental caries, diabetes, obesity.
For research use only. We do not sell to patients.
- CAS No.: 51411-23-5
- Formula: C12H22O11
- Molecular Weight:342.30
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All Endogenous Metabolite Isoforms
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Biological Activity
Description
IC50 & Target
[1]|
Microbial Metabolite |
In Vitro
Trehalulose (1.25-5 %) activates human epidermal fibroblast cells and reduces UV-induced oxidative stress[1].
Trehalulose (1%) minimally inhibits the activity of α-glucosyltransferase from Pseudomonas mesoacidophila MX-45, reducing relative activity to 98% of the control[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Rats[1]
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Dosage:1.47 g/kg bw
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Administration:p.o.; daily; 26 weeks
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Result:Was hydrolyzed into glucose and fructose by the sucrase-isomaltase complex in the rat intestinal system.
Showed efficient digestibility.
Caused no significant side effects such as diarrhea even after prolonged intake for 26 weeks.
Chemical Information
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CAS No. 51411-23-5
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Molecular Weight 342.30
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Formula C12H22O11
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SMILES
O(CC([C@H]([C@@H]([C@@H](CO)O)O)O)=O)[C@H]1O[C@H](CO)[C@@H](O)[C@H](O)[C@H]1O
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Structure Classification
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Initial Source
Pseudomonas mesoacidophila MX-45
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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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 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
Purity & Documentation
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Data Sheet (271 KB)
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SDS (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Handling Instructions (2659 KB)
References
[1]. Seevanathan Y, et al. Trehalulose: Exploring its benefits, biosynthesis, and enhanced production techniques. Carbohydr Res. 2024;545:109293. [Content Brief]
[2]. Nagai Y, et al. Characterization of alpha-glucosyltransferase from Pseudomonas mesoacidophila MX-45. Biosci Biotechnol Biochem. 1994;58(10):1789-1793. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Keywords
- Trehalulose
- 51411-23-5
- Endogenous Metabolite
- α-glucosidase
- Pseudomonas mesoacidophila MX-45
- recombinant trehalose synthase (TreM)
- human epidermal fibroblast cells
- Metschnikowia reukaufii
- amylosucrase-type enzyme (DdAS)
- Deinococcus deserti
- Blastobotrys adeninivorans
- oral streptococci glucosyltransferases
- Maltase (BaAG2)
- Inhibitor
- inhibitor
- inhibit