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D-3-Hydroxybutyric Acid (β-Hydroxybutyrate) Assay Kit

Product code: K-HDBA
€161.00

60 assays (manual) / 600 assays (microplate) / 740 assays (auto-analyser)

Prices exclude VAT

Available for shipping

Content: 60 assays (manual) / 600 assays (microplate) / 740 assays (auto-analyser)
Shipping Temperature: Ambient
Storage Temperature: Short term stability: 2-8oC,
Long term stability: See individual component labels
Stability: > 2 years under recommended storage conditions
Analyte: D-3-Hydroxybutyric Acid
Assay Format: Spectrophotometer, Microplate, Auto-analyser
Detection Method: Absorbance
Wavelength (nm): 492
Signal Response: Increase
Linear Range: 0.4 to 12 µg of D-3-hydroxybutyric acid per assay
Limit of Detection: 0.074 mg/L
Reaction Time (min): ~ 6 min
Application examples: Egg, egg products (e.g. egg powder) and other materials (e.g. biological cultures, samples, etc.).
Method recognition: Methods based on this principle have been accepted by EEC

The D-3-Hydroxybutyric Acid (β-Hydroxybutyrate) Assay Kit is suitable for the specific measurement and analysis of D-hydroxybutyric acid in eggs and egg products and other foods and beverages.

Note for Content: The number of manual tests per kit can be doubled if all volumes are halved.  This can be readily accommodated using the MegaQuantTM  Wave Spectrophotometer (D-MQWAVE).

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Scheme-K-HDBA HDBA Megazyme

Advantages
  • Very competitive price (cost per test) 
  • All reagents stable for > 2 years after preparation 
  • Very rapid reaction (~ 3 min) 
  • No wasted diaphorase solution (stable suspension supplied)  
  • Mega-Calc™ software tool is available from our website for hassle-free raw data processing 
  • Standard included 
  • Suitable for manual, microplate and auto-analyser formats
Documents
Certificate of Analysis
Safety Data Sheet
FAQs Assay Protocol Data Calculator Product Performance
Publications
Publication

NIK links inflammation to hepatic steatosis by suppressing PPARα in alcoholic liver disease.

Li, Y., Chen, M., Zhou, Y., Tang, C., Zhang, W., Zhong, Y., Chen, Y., Zhou, H. & Sheng, L. (2020). Theranostics, 10(8), 3579.

Background: Inflammation and steatosis are the main pathological features of alcoholic liver disease (ALD), in which, inflammation is one of the critical drivers for the initiation and development of alcoholic steatosis. NIK, an inflammatory pathway component activated by inflammatory cytokines, was suspected to link inflammation to hepatic steatosis during ALD. However, the underlying pathogenesis is not well-elucidated. Methods: Alcoholic steatosis was induced in mice by chronic-plus-binge ethanol feeding. Both the loss- and gain-of-function experiments by the hepatocyte-specific deletion, pharmacological inhibition and adenoviral transfection of NIK were utilized to elucidate the role of NIK in alcoholic steatosis. Rate of fatty acid oxidation was assessed in vivo and in vitro. PPARα agonists or antagonists of MEK1/2 and ERK1/2 were used to identify the NIK-induced regulation of PPARα, MEK1/2, and ERK1/2. The potential interactions between NIK, MEK1/2, ERK1/2 and PPARα and the phosphorylation of PPARα were clarified by immunoprecipitation, immunoblotting and far-western blotting analysis. Results: Hepatocyte-specific deletion of NIK protected mice from alcoholic steatosis by sustaining hepatic fatty acid oxidation. Moreover, overexpression of NIK contributed to hepatic lipid accumulation with disrupted fatty acid oxidation. The pathological effect of NIK in ALD may be attributed to the suppression of PPARα, the main controller of fatty acid oxidation in the liver, because PPARα agonists reversed NIK-mediated hepatic steatosis and malfunction of fatty acid oxidation. Mechanistically, NIK recruited MEK1/2 and ERK1/2 to form a complex that catalyzed the inhibitory phosphorylation of PPARα. Importantly, pharmacological intervention against NIK significantly attenuated alcoholic steatosis in ethanol-fed mice. Conclusions: NIK targeting PPARα via MEK1/2 and ERK1/2 disrupts hepatic fatty acid oxidation and exhibits high value in ALD therapy.

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Publication
The effect of enhanced acetate influx on Synechocystis sp. PCC 6803 metabolism.

Thiel, K., Vuorio, E., Aro, E. M. & Kallio, P. T. (2017). Microbial Cell Factories, 16(1), 21.

Background: Acetate is a common microbial fermentative end-product, which can potentially be used as a supplementary carbon source to enhance the output of biotechnological production systems. This study focuses on the acetate metabolism of the photosynthetic cyanobacterium Synechocystis sp. PCC 6803 which is unable to grow on acetate as a sole carbon source but still can assimilate it via acetyl-CoA—derived metabolic intermediates. In order to gain insight into the acetate uptake, associated limitations and metabolic effects, a heterologous acetate transporter ActP from Escherichia coli was introduced into Synechocystis to facilitate the transport of supplemented acetate from the medium into the cell. Results: The results show that enhanced acetate intake can efficiently promote the growth of the cyanobacterial host. The effect is apparent specifically under low-light conditions when the photosynthetic activity is low, and expected to result from increased availability of acetyl-CoA precursors, accompanied by changes induced in cellular glycogen metabolism which may include allocation of resources towards enhanced growth instead of glycogen accumulation. Despite the stimulated growth of the mutant, acetate is shown to suppress the activity of the photosynthetic apparatus, further emphasizing the contribution of glycolytic metabolism in the acetate-induced effect. Conclusions: The use of acetate by the cyanobacterium Synechocystis sp. PCC 6803 is at least partially restricted by the import into the cell. This can be improved by the introduction of a heterologous acetate transporter into the system, thereby providing a potential advantage by expanding the scope of acetate utilization for various biosynthetic processes.

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Publication
Physiological assessment of the effects of changing water levels associated with reservoir management on fattening rates of neotropical migrants at a stopover site.

Wagner, D. N., Green, D. J., Pavlik, M., Cooper, J. & Williams, T. D. (2014). Conservation Physiology, 2(1), cou017.

Riparian habitat makes up a small fraction of the landscape but provides important stopover habitat for migratory birds. Hydroelectric dam operations cause fluctuations in water levels that can change the amount or quality of riparian habitat, which in turn might affect potential fattening rates of migrant birds. Here we used plasma metabolite analysis to estimate variation in fattening rate in relationship to variable water levels associated with reservoir management in four species of neotropical migratory songbirds using riparian habitat at a dam-impacted stopover site in Revelstoke, British Columbia, Canada. Residual plasma triglyceride, our measure of estimated fattening rate, varied systematically with time of day and Julian date and varied consistently among species, but did not vary with age or sex. Controlling for potentially confounding variables, we found no inter-annual variation in estimated fattening rate, even though there were marked differences in water levels among years. Likewise, there was no relationship between daily variation in water levels and estimated fattening rate. Data on feather isotopes (δD), indicative of migratory origin, did not add explanatory power to our models. There was inter-annual variation in plasma glycerol and β-hydroxybutyrate levels and significant, though weak, relationships between these metabolites and water level (higher metabolite levels when drier) that might indicate effects on ‘body condition’ independent of fattening rate. Our study suggests that, at present, although hydroelectric dam operations influence water levels in the Arrows Lake Reservoir and adjacent riparian habitats, this does not significantly impact fattening rates of migratory passerines using these habitats.

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Safety Information
Symbol : GHS07
Signal Word : Warning
Hazard Statements : H319, H412
Precautionary Statements : P264, P273, P280, P305+P351+P338, P337+P313, P501
Safety Data Sheet
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