Animal Study: Lycopene Restores Bone Strength After Menopause?
A preliminary animal study suggests lycopene may help prevent bone loss associated with aging.
Photo © iStockphoto.com/Jasmina007
Researchers have found that lycopene supplementation may help restore bone strength caused by post-menopausal osteoporosis. The findings come out of a new preliminary animal study from Saudi Arabia.
The study included 264 Wistar rats aged six months that were either sham-operated (SHAM) or ovariectomized (OVX) to simulate post-menopausal osteoporosis symptoms. The SHAM group served as a control while the OVX group was randomized to receive oral daily lycopene treatments of 0, 15, 30, or 45 mg/kg body weight per day, or alendronate at 2µg/kg of body weight per day. The supplementation period lasted for 12 weeks.
Researchers measured lycopene’s effect on the rats’ bones by bone densitometry measurements, bone turnover markers, biomechanical testing, histomorphometric analysis, and micro computed tomography (to evaluate changes in microarchitecture).
Lycopene treatment was found to suppress the OVX-induced increase in bone turnover, as evidenced by changes in biomarkers of bone metabolism, including serum osteocalcin, serum N-terminal propeptide of type 1 collagen, serum crosslinked carboxyterminal telopeptides, and urinary deoxypridinoline.
“Significant improvement in OVX-induced loss of bone mass, bone strength, and microarchitectural deterioration was observed in lycopene-treated OVX animals,” wrote the researchers. They also noted that the observed beneficial effects of lycopene supplementation were especially pronounced at sites rich in trabecular bone, and less pronounced in cortical bone.
“These findings demonstrate that lycopene treatment in OVX rats primarily suppressed bone turnover to restore bone strength and microarchitecture,” researchers concluded.
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Michael Crane
Associate Editor
Nutritional Outlook Magazine
michael.crane@ubm.com
References:
Ardawi MS et al., “Lycopene treatment against loss of bone mass, microarchitecture and strength in relation to regulatory mechanisms in a postmenopausal osteoporosis model,” Bone, vol. 83 (February 2016): 127-140
