Liraglutide increases bone formation and inhibits bone resorption in rats with glucocorticoid-induced osteoporosis.

Abstract

This study aimed to investigate the effects of liraglutide on bone metabolism markers in rat models with glucocorticoid-induced osteoporosis (GIOP), including the effects on bone mass, bone tissue microstructure, bone biomechanics, and bone turnover markers. Thirty male Sprague-Dawley rats aged 8weeks were randomly divided into three groups: the control group (n = 10) was intramuscularly injected with an equal volume of 0.9% sodium chloride, the dexamethasone group (n = 10) was intramuscularly injected with dexamethasone at 1mg/kg (twice a week) to induce GIOP, the dexamethasone plus liraglutide group (n = 10) was subcutaneously injected with liraglutide at 200μg/kg daily, simultaneously. The bilateral femurs and the fifth lumbar vertebrae were collected after 12weeks to perform micro-computed tomography and bone biomechanical examinations. Also, tartrate-resistant acid phosphatase (TRACP), cross-linked carboxy-terminal telopeptide of type I collagen (CTX-I), alkaline phosphatase (ALP), and osteocalcin (OC) were tested. The bone mineral density (BMD), bone microstructure, and bone biomechanical markers reduced significantly in the dexamethasone group compared with the control group. The bone resorption indicators (TRACP and CTX-I) increased, while the bone formation indicators (ALP and OC) decreased. After liraglutide treatment, BMD, bone microstructure, and bone biomechanical markers improved significantly. Moreover, TRACP and CTX-I decreased significantly, while ALP and OC increased compared with the dexamethasone group. Liraglutide improved BMD, bone microstructure, and bone strength and reversed GIOP, primarily through the reduction of bone resorption and promotion of bone formation.