Effect of IIβ-HSD1 dehydrogenase activity on bone histomorphometry of glucocorticoid-induced osteoporotic male Sprague-Dawley rats

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Abstract

Introduction: Glucocorticoids cause osteoporosis by decreasing bone formation and increasing bone resorption activity. Glucocorticoid action in bones depends on the activity of 11-betahydroxysteroid dehydrogenase type 1 (11β- HSD1) enzyme, which plays an important role in regulating corticosteroids. 11β-HSD1 is expressed by human and rat osteoblasts. We aimed to investigate the relationship between 11β-HSD1 dehydrogenase activity and bone histomorphometric changes in glucocorticoidinduced osteoporotic bone in rats. Methods: A total of 30 male Sprague-Dawley rats (aged three months, weighing 200-250 g) were divided into three groups of ten each. Group 1 rats were the baseline control, which were sacrificed untreated at the beginning of the study. Group 2 rats underwent sham operation and were administered with vehicle olive oil intramuscularly at 0.05 ml /kg. Group 3 rats were adrenalectomised and administered with an intramuscular injection of dexamethasone 120 mu;g/kg body weight/day. The treatment was started two weeks after the operation, for a duration of two months. Plasma osteocalcin, plasma pyrodinoline, plasma corticosterone and 11β-HSD1 were measured, and bone histomorphometry analysis was performed. Results: Dexamethasone treatment caused an increase in plasma corticosterone level, together with a significant reduction in 11β-HSD1 dehydrogenase activity of the bone, along with a higher plasma level of the bone resorption marker, pyridinoline. Dexamethasone treatment also caused a reduction in trabecular volume, number and thickness, and an increase in trabecular separation. Conclusion: Long-term glucocorticoid treatment reduces the 11β-HSD1 dehydrogenase activity in the bone, which can otherwise lead to bone loss due to the increased level of active glucocorticoids.

Original languageEnglish
Pages (from-to)786-793
Number of pages8
JournalSingapore Medical Journal
Volume52
Issue number11
Publication statusPublished - Nov 2011

Fingerprint

Glucocorticoids
Sprague Dawley Rats
Oxidoreductases
Bone and Bones
Dexamethasone
Bone Resorption
Corticosterone
Intramuscular Injections
Osteocalcin
Therapeutics
Osteoblasts
Osteogenesis
Osteoporosis
Adrenal Cortex Hormones
Body Weight
Enzymes

Keywords

  • Bone
  • Dexamethasone
  • Glucocorticoids
  • II-beta-hydroxysteroid dehydrogenase type 1
  • Osteoporosis

ASJC Scopus subject areas

  • Medicine(all)

Cite this

@article{3af1301bf2654328980379103b1d8cce,
title = "Effect of IIβ-HSD1 dehydrogenase activity on bone histomorphometry of glucocorticoid-induced osteoporotic male Sprague-Dawley rats",
abstract = "Introduction: Glucocorticoids cause osteoporosis by decreasing bone formation and increasing bone resorption activity. Glucocorticoid action in bones depends on the activity of 11-betahydroxysteroid dehydrogenase type 1 (11β- HSD1) enzyme, which plays an important role in regulating corticosteroids. 11β-HSD1 is expressed by human and rat osteoblasts. We aimed to investigate the relationship between 11β-HSD1 dehydrogenase activity and bone histomorphometric changes in glucocorticoidinduced osteoporotic bone in rats. Methods: A total of 30 male Sprague-Dawley rats (aged three months, weighing 200-250 g) were divided into three groups of ten each. Group 1 rats were the baseline control, which were sacrificed untreated at the beginning of the study. Group 2 rats underwent sham operation and were administered with vehicle olive oil intramuscularly at 0.05 ml /kg. Group 3 rats were adrenalectomised and administered with an intramuscular injection of dexamethasone 120 mu;g/kg body weight/day. The treatment was started two weeks after the operation, for a duration of two months. Plasma osteocalcin, plasma pyrodinoline, plasma corticosterone and 11β-HSD1 were measured, and bone histomorphometry analysis was performed. Results: Dexamethasone treatment caused an increase in plasma corticosterone level, together with a significant reduction in 11β-HSD1 dehydrogenase activity of the bone, along with a higher plasma level of the bone resorption marker, pyridinoline. Dexamethasone treatment also caused a reduction in trabecular volume, number and thickness, and an increase in trabecular separation. Conclusion: Long-term glucocorticoid treatment reduces the 11β-HSD1 dehydrogenase activity in the bone, which can otherwise lead to bone loss due to the increased level of active glucocorticoids.",
keywords = "Bone, Dexamethasone, Glucocorticoids, II-beta-hydroxysteroid dehydrogenase type 1, Osteoporosis",
author = "{Mohd Ramli}, {Elvy Suhana} and Farihah Suhaimi and Faizah Othman and Shuid, {Ahmad Nazrun} and Norazlina Mohamed and Norliza Muhammad and Soelaiman, {Ima Nirwana}",
year = "2011",
month = "11",
language = "English",
volume = "52",
pages = "786--793",
journal = "Singapore Medical Journal",
issn = "0037-5675",
publisher = "Singapore Medical Association",
number = "11",

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TY - JOUR

T1 - Effect of IIβ-HSD1 dehydrogenase activity on bone histomorphometry of glucocorticoid-induced osteoporotic male Sprague-Dawley rats

AU - Mohd Ramli, Elvy Suhana

AU - Suhaimi, Farihah

AU - Othman, Faizah

AU - Shuid, Ahmad Nazrun

AU - Mohamed, Norazlina

AU - Muhammad, Norliza

AU - Soelaiman, Ima Nirwana

PY - 2011/11

Y1 - 2011/11

N2 - Introduction: Glucocorticoids cause osteoporosis by decreasing bone formation and increasing bone resorption activity. Glucocorticoid action in bones depends on the activity of 11-betahydroxysteroid dehydrogenase type 1 (11β- HSD1) enzyme, which plays an important role in regulating corticosteroids. 11β-HSD1 is expressed by human and rat osteoblasts. We aimed to investigate the relationship between 11β-HSD1 dehydrogenase activity and bone histomorphometric changes in glucocorticoidinduced osteoporotic bone in rats. Methods: A total of 30 male Sprague-Dawley rats (aged three months, weighing 200-250 g) were divided into three groups of ten each. Group 1 rats were the baseline control, which were sacrificed untreated at the beginning of the study. Group 2 rats underwent sham operation and were administered with vehicle olive oil intramuscularly at 0.05 ml /kg. Group 3 rats were adrenalectomised and administered with an intramuscular injection of dexamethasone 120 mu;g/kg body weight/day. The treatment was started two weeks after the operation, for a duration of two months. Plasma osteocalcin, plasma pyrodinoline, plasma corticosterone and 11β-HSD1 were measured, and bone histomorphometry analysis was performed. Results: Dexamethasone treatment caused an increase in plasma corticosterone level, together with a significant reduction in 11β-HSD1 dehydrogenase activity of the bone, along with a higher plasma level of the bone resorption marker, pyridinoline. Dexamethasone treatment also caused a reduction in trabecular volume, number and thickness, and an increase in trabecular separation. Conclusion: Long-term glucocorticoid treatment reduces the 11β-HSD1 dehydrogenase activity in the bone, which can otherwise lead to bone loss due to the increased level of active glucocorticoids.

AB - Introduction: Glucocorticoids cause osteoporosis by decreasing bone formation and increasing bone resorption activity. Glucocorticoid action in bones depends on the activity of 11-betahydroxysteroid dehydrogenase type 1 (11β- HSD1) enzyme, which plays an important role in regulating corticosteroids. 11β-HSD1 is expressed by human and rat osteoblasts. We aimed to investigate the relationship between 11β-HSD1 dehydrogenase activity and bone histomorphometric changes in glucocorticoidinduced osteoporotic bone in rats. Methods: A total of 30 male Sprague-Dawley rats (aged three months, weighing 200-250 g) were divided into three groups of ten each. Group 1 rats were the baseline control, which were sacrificed untreated at the beginning of the study. Group 2 rats underwent sham operation and were administered with vehicle olive oil intramuscularly at 0.05 ml /kg. Group 3 rats were adrenalectomised and administered with an intramuscular injection of dexamethasone 120 mu;g/kg body weight/day. The treatment was started two weeks after the operation, for a duration of two months. Plasma osteocalcin, plasma pyrodinoline, plasma corticosterone and 11β-HSD1 were measured, and bone histomorphometry analysis was performed. Results: Dexamethasone treatment caused an increase in plasma corticosterone level, together with a significant reduction in 11β-HSD1 dehydrogenase activity of the bone, along with a higher plasma level of the bone resorption marker, pyridinoline. Dexamethasone treatment also caused a reduction in trabecular volume, number and thickness, and an increase in trabecular separation. Conclusion: Long-term glucocorticoid treatment reduces the 11β-HSD1 dehydrogenase activity in the bone, which can otherwise lead to bone loss due to the increased level of active glucocorticoids.

KW - Bone

KW - Dexamethasone

KW - Glucocorticoids

KW - II-beta-hydroxysteroid dehydrogenase type 1

KW - Osteoporosis

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M3 - Article

VL - 52

SP - 786

EP - 793

JO - Singapore Medical Journal

JF - Singapore Medical Journal

SN - 0037-5675

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