Sodium Taurocholate: Roles in Medical uses

Sodium taurocholate is a bile salt that is contained in the simulated intestinal fluid for testing formulation performance. In previous studies, it has been reported to effectively inhibit the nucleation and crystal growth of drugs from supersaturated solutions generated by amorphous solid dispersions. Scientists observed the extended nucleation induction time of 11 structurally diverse drugs from supersaturated solutions containing Sodium taurocholate. Sodium taurocholate hydrate was used as an emulsifier in in situ preparation of digestive enzymes. Taurocholic acid is the main end product of cholesterol catabolism. During enterohepatic circulation, bile taurocholic acid is converted by the microorganisms to taurodeoxycholic acid and deoxycholic acid. These are reabsorbed by the liver via a carrier-mediated process and converted by liver enzymes to taurocholic acid.

Sodium Taurocholate Cotransporting Polypeptide (NTCP) Deficiency in Early Infancy

Sodium taurocholate cotransporting polypeptide (NTCP) is a carrier protein in the basolateral membrane of the hepatocyte to uptake bile acids from plasma, playing a crucial role in the enterohepatic circulation of bile acids. Although the causative gene SLC10A1 was cloned as early as in 1994 and NTCP function has been studied extensively. Citrin, a bipartite protein in the mitochondrial inner membrane, has been well-known as the aspartate-glutamate carrier isoform 2 (AGC2), playing a significant role in the malate shuttle, urea cycle as well as gluconeogenesis from lactate. To the best of our knowledge, although the clinical and molecular characteristics of NICCD has been studied for years, patients with Sodium taurocholate deficiency complicated by NICCD have never been reported thus far. Very recently, our team diagnosed three pediatric patients suffering from citrin deficiency and Sodium taurocholate deficiency as well, and their molecular and clinical findings were reported herein. The prominent evidence suggestive of NTCP deficiency in the three patients was persistent hypercholanemia after age 1 year. As the major carrier protein in the enterohepatic circulation of bile salts, NTCP uptakes conjugated bile salts from the plasma compartment into the hepatocyte in a sodium-dependent way. [1]

It was noteworthy that, although hypercholanemia was the unique clinical presentation for Sodium taurocholate cotransporting polypeptide deficiency, this biochemical change itself was just a nonpathognomonic marker suggestive cholestatic liver disease, making NTCP deficiency be covered up by NICCD at early infancy, as in the three pediatric patients reported in this study. As a reasonable explanation, their HBV carrier status might be responsible for their mild hypercholanemia. Actually, besides functioning as a carrier protein to uptake bile acids from plasma, NTCP had proven to be a functional receptor for HBV to cross the basolateral membrane, entering into the hepatocyte. It was reported that the Sodium taurocholate cotransporting polypeptide residues between 157 to 165 were important for pre-S1 lipopeptide binding of the HBV large envelope protein, and contributed to HBV infections on HepG2 cells. In conclusion, this paper reported three pediatric patients with NTCP deficiency complicated by citrin deficiency. The findings indicated that NTCP deficiency could be covered up by citrin deficiency during early infancy; however, in citrin-deficient patients with intractable hypercholanemia following resolved cholestatic jaundice, NTCP deficiency should be taken into consideration.

Sodium Taurocholate Micelles in Fluorometrix Analysis

Sodium taurocholate (3α,7α, 12α-trihydroxy-5β-cholanoyl taurine, sodium salt), NaTC, is a micelleforming bile salt. The three hydroxy groups on the cholic acid part of the molecule play an important role in the micellar characteristics of Sodium taurocholate, and, along with the taurine group, serve to solubilize NaTC in aqueous solutions. The micellar properties of NaTC are relatively insensitive to experimental conditions. The aggregation number and critical micelle concentration (CMC) show very little dependence on pH in the range of 1.6–10, on counterion concentration, and on temperature in the range of 10–60 °C. A CMC of 3 mM was found from the shift in the absorption wavelength maximum of Rhodamine 6G.[2]

The effects of metal cations include Eu3+, Tb3+ and Al3+, on the fluorescence intensities of polycyclic aromatic hydrocarbon (PAH) compounds in NaTC micelles. Enhancements as large as 18-fold were observed, and the extent of enhancement tends to increase with decreasing aqueous solubility of the PAH. The fluorescence of relatively soluble PAHs such as phenanthrene and carbazole was quenched by the metal ions in Sodium taurocholate solutions, suggesting that the more soluble PAHs may not even be bound to the NaTC micelles. Calibration curves were found for several PAHs in Sodium taurocholate solutions, and were used in the calculation of detection limits for the PAHs which were compared to detection limits obtained in SDS micellar solutions.

References

[1]Lin H, Qiu JW, Rauf YM, Lin GZ, Liu R, Deng LJ, Deng M, Song YZ. Sodium Taurocholate Cotransporting Polypeptide (NTCP) Deficiency Hidden Behind Citrin Deficiency in Early Infancy: A Report of Three Cases. Front Genet. 2019 Nov 7;10:1108. doi: 10.3389/fgene.2019.01108. PMID: 31788003; PMCID: PMC6856633.

[2]McGown LB, Nithipatikom K. Sodium Taurocholate Micelles in Fluorometrix Analysis. J Res Natl Bur Stand (1977). 1988 May-Jun;93(3):443–4. doi: 10.6028/jres.093.112. Epub 1988 Jun 1. PMCID: PMC5181955.

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