Ursodeoxycholic acid decreases bilirubin‐induced osteoblast apoptosis

Ruiz-Gaspà, Sílvia; Dubreuil, Marta; Guañabens, Núria; Combalía, Andrés; Peris, Pilar; Monegal, Ana; Parés, Albert

doi:10.1111/eci.12355

Cited by 28 publications

(30 citation statements)

References 46 publications

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“…However, accumulating evidence confirmed that UDCA could act as pleiotropic agents and is effective in ameliorating non-hepatic ailments. UDCA protects neurons and osteoblasts from unconjugated bilirubin toxicity [66,67]. Glycoursodeoxycholic acid counteracts bilirubin-induced neuronal death and synaptic changes [68].…”

Section: Discussionmentioning

confidence: 99%

Testicular immunohistochemical and Ultrastructural changes associated with chronic cholestasis in rats: Effect of ursodeoxycholic acid

Mahmoud

2015

Life Sciences

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Section: Discussionmentioning

confidence: 99%

Testicular immunohistochemical and Ultrastructural changes associated with chronic cholestasis in rats: Effect of ursodeoxycholic acid

Mahmoud

2015

Life Sciences

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“…70 Interestingly, ursodeoxycholic acid counteracts the damaging effects of these agents on osteoblast viability, proliferation, mineralization and apoptosis. 71 Our hypothesis is that sclerostin may have a main role in the low bone formation in early stages of PBC when inflammation surrounding the bile ducts is apparent in the liver. Later, in more advanced liver disease, there is a progressive lack of bile ducts, and the accumulation of retained substances of cholestasis such as bile acids and bilirubin induce low bone formation, as has been established in in vitro studies.…”

Section: Ris K Fac Tor S For Os Teop Oros Is and Fr Ac Ture Smentioning

confidence: 96%

“…Both bilirubin and lithocholic acid induce apoptosis in osteoblastic cells as well . Interestingly, ursodeoxycholic acid counteracts the damaging effects of these agents on osteoblast viability, proliferation, mineralization and apoptosis …”

Section: Pathogenesis Of Osteopororosis In Liver Diseasesmentioning

confidence: 99%

Osteoporosis in chronic liver disease

Guañabens

Parés

2018

Liver International

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Osteoporosis is a frequent complication in patients with chronic liver disease, especially in end-stages and in chronic cholestasis, in addition to non-alcoholic fatty liver disease, haemochromatosis and alcoholism. Mechanisms underlying osteoporosis are poorly understood, but osteoporosis mainly results from low bone formation. In this setting, sclerostin, a key regulator of the Wnt/β-catenin signalling pathway which regulates bone formation, in addition to the effects of the retained substances of cholestasis such as bilirubin and bile acids on osteoblastic cells, may influence the decreased bone formation in chronic cholestasis. Similarly, the damaging effects of iron and alcohol on osteoblastic cells may partially explain bone disease in haemochromatosis and alcoholism. A role for proinflammatory cytokines has been proposed in different conditions. Increased bone resorption may occur in cholestatic women with advanced disease. Low vitamin D, poor nutrition and hypogonadism, may be contributing factors to the full picture of bone disorders in chronic liver disease.

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“…The explanation for these findings may be attributable to decreased osteoblastic function or increased osteoclastic resorption in BA patients. It has been documented that osteoblast proliferation was inhibited by unconjugated bilirubin in vitro and by the serum of jaundiced patients, indicating that bilirubin might have a direct effect on bone metabolism[14,15]. A number of BA cases eventually become advanced stage of liver disease and pediatric liver transplantation is the treatment strategy of choice for improving quality of life in BA children.…”

Section: Discussionmentioning

confidence: 99%

Low bone mineral density and the severity of cholestasis in biliary atresia

Homchan

Chaiwatanarat

Udomsinprasert

et al. 2017

WJH

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AIMTo investigate the prevalence of osteopenia and osteoporosis in postoperative biliary atresia (BA) children and the association of bone mineral density (BMD) and biochemical parameters in postKasai BA subjects.METHODSA total of 70 patients with postKasai BA were enrolled in this prospective study. The patients were classified into two groups according to their jaundice status. BMD of the lumbar spine was analyzed using dual energy X-ray absorptiometry.RESULTSThe prevalence of low bone mass (osteopenia and osteoporosis) in BA patients were 51.4% (36 out of 70). Ten patients (35.7%) in the jaundice group and 8 patients (19.0%) in the non-jaundice group had osteopenia. Sixteen patients (57.1%) in the jaundice group and 2 patients (4.8%) in the no jaundice group had osteoporosis. In addition, lumbar spine BMD Z-score was substantially lower in the jaundice BA patients compared with non-jaundice patients. BA subjects with persistent jaundice had significantly lower serum 25-hydroxyvitamin D than those without jaundice. Further analysis revealed that lumbar spine BMD was correlated with age (r = 0.774, P < 0.001), serum albumin (r = 0.333, P = 0.005), total bilirubin (r = -0.476, P < 0.001), aspartate aminotransferase (r = -0.583, P < 0.001), alanine aminotransferase (r = -0.428, P < 0.001), and alkaline phosphatase(r = -0.456, P < 0.001).CONCLUSIONLow BMD was associated with biochemical parameters reflecting the severity of cholestasis in postKasai BA patients.

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Ursodeoxycholic acid decreases bilirubin‐induced osteoblast apoptosis

Abstract: Bilirubin and LCA induce apoptosis in osteoblastic cells. UDCA counteracts the apoptotic consequences of these two substances, and therefore, it may have further beneficial effects on the decreased bone formation in the cholestasis.

Cited by 28 publications

References 46 publications

Testicular immunohistochemical and Ultrastructural changes associated with chronic cholestasis in rats: Effect of ursodeoxycholic acid

Testicular immunohistochemical and Ultrastructural changes associated with chronic cholestasis in rats: Effect of ursodeoxycholic acid

Osteoporosis in chronic liver disease

Low bone mineral density and the severity of cholestasis in biliary atresia

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