Staff Members - Benha University
Leptin exerts a bone protective effect in ovariectomized rats via inhibiting osteoclastogenesis
• 2020
Publication Information
Authors
Mona A. Said 1
, Heba M. Abdel-Kareem 2 and Hend A. Abdallah 1
Keywords
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publication.type
Local
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Supplementary Materials
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Abstract
Osteoporosis is one of the most prevalent bone diseases especially
among postmenopausal women. This study was conducted on 36 female rats
divided into three equal groups; i) Sham-operated, ii) Ovariectomized (OVX), iii)
Leptin treated ovariectomized group. At the end of experiment, blood was
collected for measurement of serum alkaline phosphate (ALP), calcium (Ca),
phosphorus (P), osteocalcin, receptor activator of nuclear factor κB ligand
(RANKL) and osteoprotegerin (OPG). Urine was collected for measurement of
urinary deoxypyridoline/creatinine (DPY/Cr). After eight weeks of treatment,
administration of leptin inhibited OVX-induced weight gain with uterotrophic
effect, decreased bone turnover markers (urinary DPY/Cr, serum osteocalcin and
serum ALP) and serum RANKL while it resulted in significant increase in serum
calcium and OPG. Moreover, it markedly decreased expression of RANKL and
increased expression of OPG in proximal femur, and thus lowered the
RANKL/OPG ratio. These findings suggests that the anti-osteoporotic effect of
leptin was by inhibiting osteoclastogenesis via modulating RANKL/OPG ratio.
Leptin had potential to be developed as alternative therapeutic agents of
osteoporosis induced by postmenopause
among postmenopausal women. This study was conducted on 36 female rats
divided into three equal groups; i) Sham-operated, ii) Ovariectomized (OVX), iii)
Leptin treated ovariectomized group. At the end of experiment, blood was
collected for measurement of serum alkaline phosphate (ALP), calcium (Ca),
phosphorus (P), osteocalcin, receptor activator of nuclear factor κB ligand
(RANKL) and osteoprotegerin (OPG). Urine was collected for measurement of
urinary deoxypyridoline/creatinine (DPY/Cr). After eight weeks of treatment,
administration of leptin inhibited OVX-induced weight gain with uterotrophic
effect, decreased bone turnover markers (urinary DPY/Cr, serum osteocalcin and
serum ALP) and serum RANKL while it resulted in significant increase in serum
calcium and OPG. Moreover, it markedly decreased expression of RANKL and
increased expression of OPG in proximal femur, and thus lowered the
RANKL/OPG ratio. These findings suggests that the anti-osteoporotic effect of
leptin was by inhibiting osteoclastogenesis via modulating RANKL/OPG ratio.
Leptin had potential to be developed as alternative therapeutic agents of
osteoporosis induced by postmenopause