Iepatic vitamin D 25-hydroxylase: Inhibition by bile duct ligation or bile salts

Bolt, Erry J. G.; Sitrin, Michael D.; Favus, Murray J.; Rosenberg, Irwin H.

doi:10.1002/hep.1840010512

Cited by 21 publications

(10 citation statements)

References 31 publications

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“…Impaired bone formation in chronic liver disease may be responsible for failure of osteomalacia to become apparent as mineralisation defects develop only in newly laid down osteoid. Earlier studies suggested that a decrease in 25-hydroxylase activity was responsible for the osteodystrophy found in bile duct ligated rats 30 This could not be confirmed in CCl 4 treated rats. 31 Vitamin D metabolism has not been studied in portacaval shunting.…”

Section: Discussionmentioning

confidence: 88%

Hepatic osteodystrophy in rats results mainly from portasystemic shunting

Merwe

Bogaerde²,

Goosen³

et al. 2003

Gut

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Background and aims: In chronic liver disease, bone disease frequently develops. The contributions of the different features of liver disease such as parenchymal inflammation, portal hypertension, and portasystemic shunting on bone metabolism have not been systematically studied. The aim of this study was to identify the features of liver disease contributing to bone disease using rat models. Methods: Parenchymal liver disease was induced by carbon tetrachloride administration, portal hypertension by partial portal vein ligation, and portasystemic shunting by end to side anastomosis of the portal vein to the inferior vena cava. Normal and sham operated surgical animals served as controls. Serum calcium, 25-hydroxy vitamin D (25-OH vit D), and osteocalcin levels, and urinary deoxypyridinoline excretion were analysed. Testosterone and oestradiol levels were determined in male and female rats, respectively. Interleukin 1, interleukin 6, and tumour necrosis factor α (TNF-α) were determined in serum. Bone density was measured in all groups and in addition, in the surgical groups, histomorphometry was performed on undecalcified specimens of the proximal tibia. The calcium content of the femurs, removed at termination and ashed, was determined. Results: Early parenchymal disease and portal hypertension did not affect bone metabolism or body mass. Portasystemic shunting increased bone resorption, decreased bone formation, bone density, and trabecular bone volume which were commensurate with a reduction in body mass. TNF-α levels were elevated and testosterone levels were low in male portasystemic shunted rats. Conclusions: Portasystemic shunting in the rat adversely affects bone metabolism as part of a generalised catabolic state where high TNF-α and low testosterone and 25-OH vit D levels may play a role.

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Section: Discussionmentioning

confidence: 88%

Hepatic osteodystrophy in rats results mainly from portasystemic shunting

Merwe

Bogaerde²,

Goosen³

et al. 2003

Gut

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“…The activation of hepatic stellate cells involves the increased cellular proliferation, increased synthesis of extracellular matrix proteins, and the expression of the activation marker a-SMA (Miyazaki et al 1993). Previous investigations have demonstrated that BDL cause progressive bile stasis, focal necrosis, bile ductular proliferations, and periportal inflammation in rats (Bolt et al 1981). Extracellular matrices in liver fibrosis are known to be produced by myofibroblasts that are transformed from fatstoring cells.…”

Section: Discussionmentioning

confidence: 98%

Protective effect of quercetin on liver damage induced by biliary obstruction in rats

Kanter

2010

J Mol Hist

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The aim of this study was to evaluate the possible protective effects of quercetin (QE) against cholestatic oxidative stress and liver damage in the common bile duct ligated rats. A total of 24 male Wistar albino rats were divided into three groups: control, bile duct ligation (BDL) and BDL + received QE; each group contain 8 animals. The rats in QE treated groups were given QE (15 mg/kg) once a day intraperitoneally for 4 weeks starting 3 days prior to BDL operation. The changes demonstrating the bile duct proliferation and fibrosis in expanded portal tracts include the extension of proliferated bile ducts into lobules, mononuclear cells, and neutrophil infiltration into the widened portal areas were observed in BDL group. Treatment of BDL with QE attenuated alterations in liver histology. The alpha smooth muscle actin (α-SMA), transforming growth factor beta (TGF-β1) positive cells and the activity of TUNEL in the BDL were observed to be reduced with the QE treatment. The data indicate that QE attenuates BDL-induced cholestatic liver injury, bile duct proliferation, and fibrosis. The hepatoprotective effect of QE is associated with antioxidative potential.

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“…The activation of hepatic stellate cells involves the increased cellular proliferation, increased synthesis of extracellular matrix proteins, and the expression of the activation marker α-SMA [49]. Previous investigations have demonstrated that BDL cause progressive bile stasis, focal necrosis, bile ductular proliferations, and periportal inflammation in rats [50]. Extracellular matrices in liver fibrosis are known to be produced by myofibroblasts that are transformed from fatstoring cells.…”

Section: Discussionmentioning

confidence: 98%