The bile acids filtered through the glomeruli nearly completely escape urinary excretion due to an efficient tubular reabsorption process. Reabsorption is mediated by the sodium-dependent bile acid transporter ASBT, which is localized in the brush border membranes of proximal tubular cells. The purpose of the present study was to assess whether tubular taurocholate transport is regulated by sex hormones. Clearance studies and studies on proximal tubular cells freshly isolated from rat kidneys were performed. The studies with the isolated proximal tubular cells revealed a cell to bath 3H-taurocholate accumulation ratio of 5.63+/-0.28 in male and of 3.67+/-0.43 in female rats (p<0.01). This difference in cellular taurocholate uptake was corroborated by the clearance studies, which showed a 3H-taurocholate clearance of 133.9+/-28.1 in male rats and of 262.0+/-45.4 microl/min x 100 g b.w. in female rats (p<0.05). Testosterone treatment of female rats did not significantly alter the cell to bath 3H-taurocholate accumulation ratio. However, the cellular taurocholate accumulation significantly decreased, by 61.6+/-10.1%, following ethinylestradiol treatment of male rats. Ovariectomy, chemical castration of female rats with buserelin or treatment of female rats with the estrogen receptor antagonist ICI 182780 did not affect taurocholate uptake, but treatment of ovariectomized rats with ethinylestradiol decreased the taurocholate accumulation ratio by 53.7+/-15.8%. By determination of serum bile acids the possibility was excluded that this change was an indirect effect of cholestasis induced by ethinylestradiol. This study demonstrates gender differences in the renal handling of taurocholate in rats that may be related to an inhibitory effect of estrogens on taurocholate transport in proximal tubular cells. Since the ASBT protein content of the proximal tubular cells was found not to be different between male and female rats, a nongenomic mechanism may underly this estrogen effect.
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http://dx.doi.org/10.1007/s00210-005-1081-3 | DOI Listing |
J Am Soc Nephrol
January 2025
Centre de Recherche des Cordeliers, INSERM, Sorbonne Université, Université Paris Cité, F-75006 Paris, France.
The renal tubule and collecting duct express a large number of proteins, all having putative immunoreactive motives. Therefore, all can be the target of pathogenic autoantibodies. However, autoimmune tubulopathies seem to be rare and we hypothesize that they are underdiagnosed.
View Article and Find Full Text PDFJCI Insight
January 2025
Center for Precision Medicine, Department of Medicine, and.
The role played by anionic channels in diabetic kidney disease (DKD) is not known. Chloride channel accessory 1 (CLCA1) facilitates the activity of TMEM16A (Anoctamin-1), a Ca2+-dependent Cl- channel. We examined if CLCA1/TMEM16A had a role in DKD.
View Article and Find Full Text PDFFASEB J
January 2025
Department of Hematology, Nephrology, and Rheumatology, Graduate School of Medicine, Akita University, Akita, Japan.
Various tubular diseases in patients with multiple myeloma (MM) are caused by monoclonal immunoglobulin light chains (LCs). However, the physicochemical characteristics of the disease-causing LCs contributing to the onset of MM-associated tubular diseases remain unclear. We herein report a rare case of MM-associated combined tubulopathies: non-crystalline light chain proximal tubulopathy (LCPT) and crystalline light chain cast nephropathy (LCCN).
View Article and Find Full Text PDFInt J Biol Sci
January 2025
Division of Nephrology, Department of Medicine, University of Connecticut School of Medicine, Farmington, CT, USA.
Cisplatin is widely used for the treatment of solid tumors and its antitumor effects are well established. However, a known complication of cisplatin administration is acute kidney injury (AKI). In this study, we examined the role of TEA domain family member 1 (TEAD1) in the pathogenesis of cisplatin-induced AKI.
View Article and Find Full Text PDFZhonghua Wei Zhong Bing Ji Jiu Yi Xue
December 2024
Department of Emergency, Kweichow Moutai Hospital, Renhuai 564500, Guizhou, China. Corresponding author: Ou Renyang, Email:
Objective: To investigate the protective effect and mechanism of tumor necrosis factor receptor-associated factor 6 (TRAF6) inhibitor C25-140 on acute kidney injury (AKI) induced by acute diquat (DQ) poisoning in mice.
Methods: A total of 80 SPF grade healthy male C57BL/6 mice were randomly divided into the normal control group, DQ model group, C25-140 intervention group, and C25-140 control group, with 20 mice in each group. The DQ poisoning mouse model was established by using one-time intraperitoneal injection of 1 mL of 40 mg/kg DQ solution.
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