This study aimed to determine the effects and mechanisms of glucosamine on senile osteoporosis and osteogenic differentiation in vivo.

One of the most common conditions in the elderly population is osteoporosis. Based on available epidemiological data, one-third of the world’s elderly suffer from osteoporosis, which makes them susceptible to brittle fractures and decreases their quality of life.

The loss of bone mass and destruction of bone microstructure in senile osteoporosis (SOP) is due to an imbalance between bone formation and bone resorption, primarily due to an impaired osteogenic ability. However, the cause is unclear, and it may be associated with malnutrition, low sex hormone levels, high endogenous glucocorticoids, and accumulations of harmful substances.

In addition to being an essential component of the cartilage matrix, glucosamine (GlcN) is used as an over-the-counter dietary supplement to help treat osteoarthritis and improve joint function.

A few studies also indicated that GlcN promoted osteogenesis; Jiang et al. reported that GlcN protected osteoblasts from oxidative damage in vitro. In addition, Ali et al. said that feeding GlcN to ovariectomized rats preserved bone mass and biomechanical properties.

GlcN has been shown to accelerate early fracture repair in rats by increasing the activity of osteoblasts and promoting new bone formation, according to Kalbe et al. Hence; it is crucial to investigate if GlcN has a therapeutic effect on osteoporosis caused by reduced osteogenesis in senile age.

What Did The Study Reveal?

Aging was induced by subcutaneous injection of D-galactose (D-Gal), treated with GlcN or a vehicle. The researchers examined the anti-senile-osteoporosis effects of GlcN with micro-CT, serum indicators, body weight, protein, and gene expression of aging and apoptosis. 

Further, by inhibiting autophagy with 3-methyladenine (3-MA), the effects of GlcN on osteogenesis and autophagy were observed.

For studying GlcN on D-Gal-induced osteoporosis in vivo, the experts established the senile osteoporosis model in mice by chronically administering D-Gal (125 mg/kg/day) for 12 weeks, followed by GlcN (9 mg/kg/day) for 12 weeks.

In D-Gal-induced osteoporotic mice, GlcN significantly increased bone mineral density (BMD) and bone microarchitecture, reduced skeletal senescence and apoptosis, and increased osteogenesis. At the same time, all effect was reversed with 3-MA.

GLCN significantly delayed the progression of osteoporosis in senile osteoporotic mice by promoting osteoblast autophagy. This suggests that it may be a prospective candidate drug for treating SOP.

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