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Bilirubin Diglucuronide

The Experts below are selected from a list of 126 Experts worldwide ranked by ideXlab platform

Toshio Yamamoto – 1st expert on this subject based on the ideXlab platform

  • Type II Crigler-Najjar syndrome with intrahepatic cholestasis
    Journal of Gastroenterology, 1994
    Co-Authors: Atsushi Kagita, Akira Kambe, Yukihiko Adachi, Toshinori Kamisako, Toshio Yamamoto

    Abstract:

    A 58-year-old Japanese man was admitted to our hospital with appendicitis and marked unconjugated hyperBilirubinemia (11.6 mg/dl). The jaundice worsened following appendectomy, and the directreacting Bilirubin increased, probably due to the ceftizoxime administered postoperatively. Bilirubin Diglucuronide was the main component of the serum direct-reacting Bilirubin (51%) in serum measured by liquid chromatography. Because the discontinuation of ceftizoxime did not markedly improve the jauncice, epomediol, 200 mg tid, was administered orally. There was a marked decrease of serum Bilirubin with an increase in the δ Bilirubin/(conjugated Bilirubin + δ Bilirubin) ratio. After improvement of jaundice to below the pre-surgical level (4.4 mg/dl), we analyzed the duodenal bile for Bilirubin fractions; those showed a marked reduction in Bilirubin Diglucuronide and a marked increase in Bilirubin monoglucuronide, which was consistent with type II Crigler-Najjar syndrom. A marked increase of Bilirubin Diglucuronide in serum of this patient during cholestasis suggests that Bilirubin conjugation proceeds in this syndrome when excretion of conjugated Bilirubin decreases.

  • functional integrity of hepatocyte canalicular membrane transport of taurocholate and Bilirubin Diglucuronide in eisai hyperBilirubinuria rats
    Life Sciences, 1993
    Co-Authors: Yukihiko Adachi, Hiroaki Kobayashi, Mika Shouji, Motokazu Kitano, Yoshifumi Okuyama, Toshio Yamamoto

    Abstract:

    Abstract Eisai hyperBilirubinuria rats (EHBR) are characterized by conjugated hyperBilirubinemia, and impaired or defective excretion of Bilirubin, reduced glutathione and other organic anions from hepatocytes. Hepatocyte canalicular membrane vesicles (CMV) from EHBR and normal SD rats were studied with regard to taurocholate (TC) transport driven by ATP or a membrane potential and bicarbonate-stimulated Bilirubin Diglucuronide (BDG) transport. ATP-dependent uptake or association of BDG with CMV was also studied in both strains of rats. No significant differences in the uptake of TC and BDG by CMV were observed. This indicates the functional integrity of the canalicular transporters for both organic anions in EHBR. Biliary excretion of taurolithocholic acid sulfate (TLCS) is defective in EHBR. However, TLCS inhibited ATP-dependent TC uptake by SD rat CMV competitively, which may be against the hypothesis that a common organic anion carrier is defective in canalicular membranes of jaundiced rats.

  • Bilirubin Diglucuronide transport by rat liver canalicular membrane vesicles stimulation by bicarbonate ion
    Hepatology, 1991
    Co-Authors: M Yukihiko D Adachi, Hiroaki Kobayashi, Yoshiaki Kurumi, Mika Shouji, Motokazu Kitano, Toshio Yamamoto

    Abstract:

    The purpose of this study was to provide further insight into the mechanism of Bilirubin Diglucuronide excretion through the hepatocyte canalicular membrane by investigating the uptake of (3H)Bilirubin Diglucuronide by purified canalicular membrane vesicles of rat liver. The uptake was analyzed by a rapid filtration technique. The difference between vesicle-associated (3H)Bilirubin Diglucuronide at 37° C and at 0° C during the initial 1 min was regarded as uptake. Twenty second uptake was saturated by increasing the (3H)Bilirubin Diglucuronide concentration at a vesicle-inside-directed 100 mmol/L KCl gradient (Km = 75 μmol/L, Vmax = 320 pmol/mg protein 20 sec at 37° C). No sodium dependency was observed. When canalicular membrane vesicles were preincubated with nonlabeled Bilirubin Diglucuronide, the uptake increased 1.3-fold (transstimulation). Vesicle-inside-positive potential induced by valinomycin and potassium caused a 1.4-fold increase in the uptake. When Cl− was replaced by equivalent ion concentrations of SO, HCO, NO and SCN−, the uptake was 78%, 244%, 68% and 50%, respectively, and specific stimulation by HCO was observed (Km = 75 μmol/L, Vmax = 700 pmol/mg protein 20 sec at a vesicle-inside-directed 100 mmol/L KHCO3 gradient at 37° C). The uptake was inhibited in a dose-dependent manner by the addition of 4,4′-diisothiocyanatostilbene-2,2′-disulfonic acid. The uptake was ATP independent. From these results, it was concluded that Bilirubin Diglucuronide transport through the canalicular membrane is carrier mediated, electrogenic and stimulated by HCO. (HEPATOLOGY 1991;14:1251–1258.)

Yukihiko Adachi – 2nd expert on this subject based on the ideXlab platform

  • Type II Crigler-Najjar syndrome with intrahepatic cholestasis
    Journal of Gastroenterology, 1994
    Co-Authors: Atsushi Kagita, Akira Kambe, Yukihiko Adachi, Toshinori Kamisako, Toshio Yamamoto

    Abstract:

    A 58-year-old Japanese man was admitted to our hospital with appendicitis and marked unconjugated hyperBilirubinemia (11.6 mg/dl). The jaundice worsened following appendectomy, and the directreacting Bilirubin increased, probably due to the ceftizoxime administered postoperatively. Bilirubin Diglucuronide was the main component of the serum direct-reacting Bilirubin (51%) in serum measured by liquid chromatography. Because the discontinuation of ceftizoxime did not markedly improve the jauncice, epomediol, 200 mg tid, was administered orally. There was a marked decrease of serum Bilirubin with an increase in the δ Bilirubin/(conjugated Bilirubin + δ Bilirubin) ratio. After improvement of jaundice to below the pre-surgical level (4.4 mg/dl), we analyzed the duodenal bile for Bilirubin fractions; those showed a marked reduction in Bilirubin Diglucuronide and a marked increase in Bilirubin monoglucuronide, which was consistent with type II Crigler-Najjar syndrom. A marked increase of Bilirubin Diglucuronide in serum of this patient during cholestasis suggests that Bilirubin conjugation proceeds in this syndrome when excretion of conjugated Bilirubin decreases.

  • functional integrity of hepatocyte canalicular membrane transport of taurocholate and Bilirubin Diglucuronide in eisai hyperBilirubinuria rats
    Life Sciences, 1993
    Co-Authors: Yukihiko Adachi, Hiroaki Kobayashi, Mika Shouji, Motokazu Kitano, Yoshifumi Okuyama, Toshio Yamamoto

    Abstract:

    Abstract Eisai hyperBilirubinuria rats (EHBR) are characterized by conjugated hyperBilirubinemia, and impaired or defective excretion of Bilirubin, reduced glutathione and other organic anions from hepatocytes. Hepatocyte canalicular membrane vesicles (CMV) from EHBR and normal SD rats were studied with regard to taurocholate (TC) transport driven by ATP or a membrane potential and bicarbonate-stimulated Bilirubin Diglucuronide (BDG) transport. ATP-dependent uptake or association of BDG with CMV was also studied in both strains of rats. No significant differences in the uptake of TC and BDG by CMV were observed. This indicates the functional integrity of the canalicular transporters for both organic anions in EHBR. Biliary excretion of taurolithocholic acid sulfate (TLCS) is defective in EHBR. However, TLCS inhibited ATP-dependent TC uptake by SD rat CMV competitively, which may be against the hypothesis that a common organic anion carrier is defective in canalicular membranes of jaundiced rats.

  • The effects of temporary occlusion of the superior mesenteric vein or splenic vein on biliary Bilirubin and bile acid excretion in rats
    Journal of Laboratory and Clinical Medicine, 1991
    Co-Authors: Yukihiko Adachi, Toshinori Kamisako, Toshio Yamamoto

    Abstract:

    Abstract To elucidate the possible implication of hepatic blood supply to the occurrence of hepatolithiasis, the rat superior mesenteric vein, which drains blood from the intestine, or the splenic vein, which drains from the spleen, was occluded for 30 minutes. Changes in the hepatic oxygen saturation index, intrahepatic uridine diphosphate-glucuronic acid concentration, bile flow, and the excretion of Bilirubin as well as its fraction, along with bile acid in bile before and after the procedure, were observed. In association with superior mesenteric vein occlusion, oxygen saturation index, hepatic uridine diphosphate-glucuronic acid concentration, bile flow, bile acid concentration in bile, and percentage of biliary Bilirubin Diglucuronide were all decreased. incubation of bile under sterile conditions from rats with occluded superior mesenteric veins resulted in precipitation of mainly calcium salt of fatty acid. in contrast, splenic vein occlusion caused no changes except for a decrease in biliary Bilirubin concentration. incubation of bile from rats with occluded splenic veins did not induce precipitation. From these findings it can be concluded that blood flow in the superior mesenteric vein is the primary source of oxygen supply to the rat liver and that this vein plays an important role in maintaining bile flow, bile acid excretion, and Bilirubin conjugation and in preventing the precipitation of bile (possibly preventing hepatolithlasis).

Hiroaki Kobayashi – 3rd expert on this subject based on the ideXlab platform

  • functional integrity of hepatocyte canalicular membrane transport of taurocholate and Bilirubin Diglucuronide in eisai hyperBilirubinuria rats
    Life Sciences, 1993
    Co-Authors: Yukihiko Adachi, Hiroaki Kobayashi, Mika Shouji, Motokazu Kitano, Yoshifumi Okuyama, Toshio Yamamoto

    Abstract:

    Abstract Eisai hyperBilirubinuria rats (EHBR) are characterized by conjugated hyperBilirubinemia, and impaired or defective excretion of Bilirubin, reduced glutathione and other organic anions from hepatocytes. Hepatocyte canalicular membrane vesicles (CMV) from EHBR and normal SD rats were studied with regard to taurocholate (TC) transport driven by ATP or a membrane potential and bicarbonate-stimulated Bilirubin Diglucuronide (BDG) transport. ATP-dependent uptake or association of BDG with CMV was also studied in both strains of rats. No significant differences in the uptake of TC and BDG by CMV were observed. This indicates the functional integrity of the canalicular transporters for both organic anions in EHBR. Biliary excretion of taurolithocholic acid sulfate (TLCS) is defective in EHBR. However, TLCS inhibited ATP-dependent TC uptake by SD rat CMV competitively, which may be against the hypothesis that a common organic anion carrier is defective in canalicular membranes of jaundiced rats.

  • Bilirubin Diglucuronide transport by rat liver canalicular membrane vesicles stimulation by bicarbonate ion
    Hepatology, 1991
    Co-Authors: M Yukihiko D Adachi, Hiroaki Kobayashi, Yoshiaki Kurumi, Mika Shouji, Motokazu Kitano, Toshio Yamamoto

    Abstract:

    The purpose of this study was to provide further insight into the mechanism of Bilirubin Diglucuronide excretion through the hepatocyte canalicular membrane by investigating the uptake of (3H)Bilirubin Diglucuronide by purified canalicular membrane vesicles of rat liver. The uptake was analyzed by a rapid filtration technique. The difference between vesicle-associated (3H)Bilirubin Diglucuronide at 37° C and at 0° C during the initial 1 min was regarded as uptake. Twenty second uptake was saturated by increasing the (3H)Bilirubin Diglucuronide concentration at a vesicle-inside-directed 100 mmol/L KCl gradient (Km = 75 μmol/L, Vmax = 320 pmol/mg protein 20 sec at 37° C). No sodium dependency was observed. When canalicular membrane vesicles were preincubated with nonlabeled Bilirubin Diglucuronide, the uptake increased 1.3-fold (transstimulation). Vesicle-inside-positive potential induced by valinomycin and potassium caused a 1.4-fold increase in the uptake. When Cl− was replaced by equivalent ion concentrations of SO, HCO, NO and SCN−, the uptake was 78%, 244%, 68% and 50%, respectively, and specific stimulation by HCO was observed (Km = 75 μmol/L, Vmax = 700 pmol/mg protein 20 sec at a vesicle-inside-directed 100 mmol/L KHCO3 gradient at 37° C). The uptake was inhibited in a dose-dependent manner by the addition of 4,4′-diisothiocyanatostilbene-2,2′-disulfonic acid. The uptake was ATP independent. From these results, it was concluded that Bilirubin Diglucuronide transport through the canalicular membrane is carrier mediated, electrogenic and stimulated by HCO. (HEPATOLOGY 1991;14:1251–1258.)

  • hepatic uptake of Bilirubin Diglucuronide analysis by using sinusoidal plasma membrane vesicles
    Journal of Biochemistry, 1990
    Co-Authors: Yukihiko Adachi, Hiroaki Kobayashi, Jayanta Roychowdhury, Namita Roychowdhury, Rolf K H Kinne, Thao Tran, Irwin M Arias

    Abstract:

    : In order to characterize the mechanism for Bilirubin transport in the liver, the uptake of Bilirubin Diglucuronide (BDG) into purified sinusoidal plasma membrane vesicles was investigated. BDG uptake was saturable, and was inhibited by sulfobromophthalein and unconjugated Bilirubin, but was not affected by sodium taurocholate. BDG uptake was sodium-independent and was stimulated by intravesicular Bilirubin or BDG (trans-stimulation). BDG transport showed strong potential sensitivity; vesicle inside-negative membrane potential created by different anion gradients inhibited BDG uptake whereas vesicle inside-positive membrane potential generated by potassium gradients and valinomycin markedly stimulated BDG transport. These data suggest that BDG, sulfobromophthalein, and probably unconjugated Bilirubin share a common transporter in liver cells which is sodium independent, membrane-potential-dependent and capable of exchange. The direction of transport in vivo may be governed by the intracellular concentration of BDG and of other yet unidentified organic anions sharing this transporter.