Piper sarmentosum prevents glucocorticoid-induced osteoporotic bone resorption by increasing 11β-hydroxysteroid dehydrogenase type 1 activity

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Abstract

Aims. Osteoporosis is a proven complication of long-term glucocorticoid therapy. Concern on glucocorticoid induced osteoporosis has increased dramatically in recent years with the widespread use of synthetic glucocorticoids. Glucocorticoid action in bone depends upon the activity of 11β-hydroxysteroid dehydrogenase type 1 enzyme (11β-HSD1). This enzyme plays an important role in regulating corticosteroids by locally interconverting cortisone into active cortisol. This has been demonstrated in primary cultures of human, mouse or rat osteoblasts. Therefore, inhibition of this enzyme may reduce bone resorption markers. Piper sarmentosum (Ps) is a potent inhibitor of 11β-HSD1 in liver and adipose tissue. In this study we determined the effect of Ps on 11β-HSD1 activity in bones of glucocorticoid-induced osteoporotic rats. Materials and Methods. Three-month old male Sprague-Dawley rats were adrenalectomised to remove the main source of circulating glucocorticoids. The animals were administered with dexamethasone 120 μg/kg body weight/day. Treatment with Ps 125 mg/kg body weight and glycirrhizic acid (GCA) 120 mg/kg body weight were given simultaneously. Results. The results showed that Ps extract reduced plasma corticosterone concentration (1.05+0.02μg/ml) and induced 11β-HSD1 dehydrogenase activity in bone (87.69+1.41%). Consequently, it also reduced the bone resorption marker, pyridinoline, in dexamethasonetreated adrenalectomised rats (2.07+0.62/L). Despite that, our data showed an inverse relationship between the plasma corticosterone level and the dehydrogenase activity of 11β-HSD1 in the bone. Conclusions. This suggests that 11β-HSD1 acts as the local regulator of glucocorticoid and its activity in bone was not correlated to systemic corticosterone level.

Original languageEnglish
Pages (from-to)313-318
Number of pages6
JournalClinica Terapeutica
Volume162
Issue number4
Publication statusPublished - 2011

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11-beta-Hydroxysteroid Dehydrogenases
Piper
Bone Resorption
Glucocorticoids
Enzymes
Bone and Bones
Corticosterone
Body Weight
Osteoporosis
Oxidoreductases
Cortisone
Osteoblasts
Dexamethasone
Sprague Dawley Rats
Hydrocortisone
Adipose Tissue
Adrenal Cortex Hormones
Acids
Liver

Keywords

  • 11β-hydroxysteroid dehydrogenase type 1
  • Dexamethasone
  • Glucocorticoids
  • Osteoporosis
  • Piper sarmentosum

ASJC Scopus subject areas

  • Medicine(all)

Cite this

@article{61b1fa8e4033413d9ccd70f86baf0394,
title = "Piper sarmentosum prevents glucocorticoid-induced osteoporotic bone resorption by increasing 11β-hydroxysteroid dehydrogenase type 1 activity",
abstract = "Aims. Osteoporosis is a proven complication of long-term glucocorticoid therapy. Concern on glucocorticoid induced osteoporosis has increased dramatically in recent years with the widespread use of synthetic glucocorticoids. Glucocorticoid action in bone depends upon the activity of 11β-hydroxysteroid dehydrogenase type 1 enzyme (11β-HSD1). This enzyme plays an important role in regulating corticosteroids by locally interconverting cortisone into active cortisol. This has been demonstrated in primary cultures of human, mouse or rat osteoblasts. Therefore, inhibition of this enzyme may reduce bone resorption markers. Piper sarmentosum (Ps) is a potent inhibitor of 11β-HSD1 in liver and adipose tissue. In this study we determined the effect of Ps on 11β-HSD1 activity in bones of glucocorticoid-induced osteoporotic rats. Materials and Methods. Three-month old male Sprague-Dawley rats were adrenalectomised to remove the main source of circulating glucocorticoids. The animals were administered with dexamethasone 120 μg/kg body weight/day. Treatment with Ps 125 mg/kg body weight and glycirrhizic acid (GCA) 120 mg/kg body weight were given simultaneously. Results. The results showed that Ps extract reduced plasma corticosterone concentration (1.05+0.02μg/ml) and induced 11β-HSD1 dehydrogenase activity in bone (87.69+1.41{\%}). Consequently, it also reduced the bone resorption marker, pyridinoline, in dexamethasonetreated adrenalectomised rats (2.07+0.62/L). Despite that, our data showed an inverse relationship between the plasma corticosterone level and the dehydrogenase activity of 11β-HSD1 in the bone. Conclusions. This suggests that 11β-HSD1 acts as the local regulator of glucocorticoid and its activity in bone was not correlated to systemic corticosterone level.",
keywords = "11β-hydroxysteroid dehydrogenase type 1, Dexamethasone, Glucocorticoids, Osteoporosis, Piper sarmentosum",
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",
language = "English",
volume = "162",
pages = "313--318",
journal = "Clinica Terapeutica",
issn = "0009-9074",
publisher = "Societa Editrice Universo",
number = "4",

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TY - JOUR

T1 - Piper sarmentosum prevents glucocorticoid-induced osteoporotic bone resorption by increasing 11β-hydroxysteroid dehydrogenase type 1 activity

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

Y1 - 2011

N2 - Aims. Osteoporosis is a proven complication of long-term glucocorticoid therapy. Concern on glucocorticoid induced osteoporosis has increased dramatically in recent years with the widespread use of synthetic glucocorticoids. Glucocorticoid action in bone depends upon the activity of 11β-hydroxysteroid dehydrogenase type 1 enzyme (11β-HSD1). This enzyme plays an important role in regulating corticosteroids by locally interconverting cortisone into active cortisol. This has been demonstrated in primary cultures of human, mouse or rat osteoblasts. Therefore, inhibition of this enzyme may reduce bone resorption markers. Piper sarmentosum (Ps) is a potent inhibitor of 11β-HSD1 in liver and adipose tissue. In this study we determined the effect of Ps on 11β-HSD1 activity in bones of glucocorticoid-induced osteoporotic rats. Materials and Methods. Three-month old male Sprague-Dawley rats were adrenalectomised to remove the main source of circulating glucocorticoids. The animals were administered with dexamethasone 120 μg/kg body weight/day. Treatment with Ps 125 mg/kg body weight and glycirrhizic acid (GCA) 120 mg/kg body weight were given simultaneously. Results. The results showed that Ps extract reduced plasma corticosterone concentration (1.05+0.02μg/ml) and induced 11β-HSD1 dehydrogenase activity in bone (87.69+1.41%). Consequently, it also reduced the bone resorption marker, pyridinoline, in dexamethasonetreated adrenalectomised rats (2.07+0.62/L). Despite that, our data showed an inverse relationship between the plasma corticosterone level and the dehydrogenase activity of 11β-HSD1 in the bone. Conclusions. This suggests that 11β-HSD1 acts as the local regulator of glucocorticoid and its activity in bone was not correlated to systemic corticosterone level.

AB - Aims. Osteoporosis is a proven complication of long-term glucocorticoid therapy. Concern on glucocorticoid induced osteoporosis has increased dramatically in recent years with the widespread use of synthetic glucocorticoids. Glucocorticoid action in bone depends upon the activity of 11β-hydroxysteroid dehydrogenase type 1 enzyme (11β-HSD1). This enzyme plays an important role in regulating corticosteroids by locally interconverting cortisone into active cortisol. This has been demonstrated in primary cultures of human, mouse or rat osteoblasts. Therefore, inhibition of this enzyme may reduce bone resorption markers. Piper sarmentosum (Ps) is a potent inhibitor of 11β-HSD1 in liver and adipose tissue. In this study we determined the effect of Ps on 11β-HSD1 activity in bones of glucocorticoid-induced osteoporotic rats. Materials and Methods. Three-month old male Sprague-Dawley rats were adrenalectomised to remove the main source of circulating glucocorticoids. The animals were administered with dexamethasone 120 μg/kg body weight/day. Treatment with Ps 125 mg/kg body weight and glycirrhizic acid (GCA) 120 mg/kg body weight were given simultaneously. Results. The results showed that Ps extract reduced plasma corticosterone concentration (1.05+0.02μg/ml) and induced 11β-HSD1 dehydrogenase activity in bone (87.69+1.41%). Consequently, it also reduced the bone resorption marker, pyridinoline, in dexamethasonetreated adrenalectomised rats (2.07+0.62/L). Despite that, our data showed an inverse relationship between the plasma corticosterone level and the dehydrogenase activity of 11β-HSD1 in the bone. Conclusions. This suggests that 11β-HSD1 acts as the local regulator of glucocorticoid and its activity in bone was not correlated to systemic corticosterone level.

KW - 11β-hydroxysteroid dehydrogenase type 1

KW - Dexamethasone

KW - Glucocorticoids

KW - Osteoporosis

KW - Piper sarmentosum

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M3 - Article

VL - 162

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EP - 318

JO - Clinica Terapeutica

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