Latest research on TUDCA

Tauroursodeoxycholic acid is the more hydrophilic form of ursodeoxycholic acid, which is the more abundant naturally produced bile acid in humans. Tauroursodeoxycholic acid, on the other hand, is produced abundantly in bears and has been used for centuries as a natural remedy in some Asian countries. It is approved in Italy and Turkey for the treatment of cholesterol gallstones and is an investigational drug in China, Unites States, and Italy. Tauroursodeoxycholic acid is being investigated for use in several conditions such as Primary Biliary Cirrhosis (PBC), insulin resistance, amyloidosis, Cystic Fibrosis, Cholestasis, and Amyotrophic Lateral Sclerosis. The only completed clinical trial thus far is a phase III clinical trial comparing tauroursodeoxycholic acid and ursofalk in PBC adult patients, but as of June 2013 no results of this trial have been published.

TUDCA dosage

Interestingly, TUDCA antagonizes FXR activation by synthetic agonist GW4064, and TUDCA is rapidly hydrolyzed by gut bacterial BSH (C.X. and A.D.P., unpublished observations), suggesting that high doses of TUDCA might inhibit FXR signalling, resulting in improved insulin resistance. [source, 2015]
Adult (12–16 weeks) rats received a daily intraperitoneal dose of TUDCA (500 mg/kg) or vehicle (phosphate-buffered saline) for 6 days. [source, 2015]
To test the neuroprotective effect of TUDCA on retinal function, full-field ERG recording was performed in parallel on a group of rats that received a daily intraperitoneal dose of TUDCA three days prior to NDMA administration, and until their sacrifice (Fig 1A). [source, 2015]
We demonstrate that TUDCA can restore ERK activation in the presence of super-low dose LPS, as well as the NET formation in neutrophils. [source, 2015]
Importantly, we observed that a unique dose of TUDCA was still capable of protecting the liver against LPS-induced steatohepatitis foci formation and necrosis (Supplementary Figure S2A), liver injury (Supplementary Figure S2B) and apoptosis (Supplementary Figure S2C) independently of the grade of steatosis (Supplementary Figure S2A). [source, 2015]
However, higher doses of TUDCA with side effects were employed in the rd1 model, leaving this conclusion regarding rd1 uncertain [53]. [source, 2014]
Significant proliferation of CASMC by treatment with 20–80 ng/ml PDGF-BB for 48 h (Figure S1) and absence of toxicity of treatment with 4-PBA (Figure S2A) or TUDCA (Figure S2B) at the dose of up to 0.5 mM for 48 h in CASMC were confirmed in an MTS assay. [source, 2014]
The TUDCA dose and time of administration were previously reported in this rat model (Yao et al. 2013) and in insulin‐resistant humans (Kars et al. 2010). [source, 2014]
A dose of sodium 4‐phenylbutyric acid (4‐PBA, 250 mg/kg) or tauroursodeoxycholic acid (TUDCA, 250 mg/kg) was injected intraperitoneally once daily for 8 weeks. [source, 2013]
To further verify whether the effect of ox-LDL on adipocytes is associated with ER stress activation, the adipocytes were pretreated for 12 hours with various doses of TUDCA(580549, Calbiochem, Gibbstown, NJ)) ( 0- 400µM) ,a chemical chaperone known to ameliorate ER stress [15], and then stimulated with 50 μg/ml of ox-LDL plus ACAT inhibitor 58035 for 48 hours. [source, 2013]