Comparative quantification of two hepatic udp-glucuronosyltransferase bilirubin isoforms mrnas in various thyroid states in rat

Bilirubin and bile acids may modulate their own metabolism via regulating uridine diphosphate‐glucuronosyltransferase expression in the rat

“…It has been hypothesized that other isoforms of the UGT1 family, which are also responsible for the conjugation of bilirubin, may play a compensatory role when the function of UGT1A1 is not sufficient. 22 However, the results of this study do not support this notion as the higher concentration of bilirubin (60 μmol/L), which did not further induce the expression of UGT1A1, also did not further induce the expression of UGT1A5.…”

Influence of vitamin A status on the regulation of uridine (5′-)diphosphate-glucuronosyltransferase (UGT) 1A1 and UGT1A6 expression by L-triiodothyronine

“…As previously reported, pharmacological doses of L-T3 significantly decreased the glucuronidation of bilirubin, whereas that of 1-naphthol was increased in the liver of rats receiving a vitamin A-balanced diet (Masmoudi et al 1996(Masmoudi et al , 1997b. The unique dose of L-T3 given to the different rats to elicit the responses corresponds to a dose which is able to saturate the thyroid hormone nuclear receptors, and thus to induce a maximal pharmacological effect, without any thyrotoxicity (Oppenheimer et al 1977).…”

“…The standard sequence controls for variables such as amount and amplifiability' of DNA, and for tube-to-tube variation in amplification efficiency. b-Actin mRNA was simultaneously co-amplified in the same test-tube, and semiquantitative analysis was performed as previously described (Masmoudi et al 1996(Masmoudi et al , 1997b. Extraction of total RNA was performed using RNAXEL kit (Eurobio, Les Ulis, France) according to the protocol suggested by the supplier.…”

“…Thyroid hormones regulate the gene expression of UGT1A1 and UGT1A6 at the transcriptional level without affecting the half-lives of their mRNA. This regulation requires a de novo protein biosynthesis (Masmoudi et al 1997b). The mechanism whereby L-T3 exerts an opposite effect on the gene encoding UGT1A1 and UGT1A6 is still unknown, but previous studies revealed that, upon ligand binding, intracellular receptors for hormones act as dimeric transcriptional factors to activate or repress the expression of nuclear target genes by binding to specific DNA sequences (Bendik & Pfahl, 1994).…”

Weight Loss and Severe Jaundice in a Patient with Hyperthyroidism

“…In line with this, several authors have described centrilobular hepatocyte apoptosis in a rat model [15] and in humans [16]; his was also observed in our patient. In the isolated perfused rat liver, hyperthyroidism decreased bilirubin UDP-glucuronosyltransferase activity in the liver [17] with lowered mRNA levels of distinct UDP-glucuronosyltransferase isoforms [18,19] resulting in a decreased ratio of conjugated to total bilirubin [17]. Expression and hormone-dependent inhibition of UDP-glucuronosyltransferase isoforms differ between individuals [20].…”