Trehalose delays postmenopausal osteoporosis by enhancing AKT/TFEB pathway-dependent autophagy flow in rats

Osteoporosis is a systemic bone metabolic disorder that plagues the health and quality of life of the elderly. Autophagy plays an important role in bone formation while maintaining the homeostasis of the body. Trehalose is a mTOR-independent autophagy inducer, but to the best of our knowledge, there is no rat model of postmenopausal osteoporosis. The present study found that trehalose can delay postmenopausal osteoporosis in rats, which may be achieved by inducing and enhancing AKT/transcription factor EB pathway-dependent autophagy flow. The specific mechanism of its occurrence needs to be further studied. Trehalose-containing drugs are promising for delaying postmenopausal osteoporosis. Hematoxylin and eosin (H&E) staining, western blotting, micro computerized tomography (CT) scanning and Transmission electron microscopy were used to investigate the role of trehalose in postmenopausal osteoporosis rat model at protein, cell and histology aspects. According to the H&E staining results, the bone trabecular histological structure of the trehalose group was superior to that of the model group. The Micro CT scanning indicated the imaging structure of bone trabeculae in the trehalose group was superior to than that in the model group. Western blotting indicated the activation of autophagic flow in trehalose group, the autophagy degree of the trehalose group is greater than that of the model group; Transmission electron microscopy indicated the autophagy degree of the Trehalose group was greater than that of the model group under electron microscopy. Trehalose can delay postmenopausal osteoporosis in rats, which may be achieved by inducing and enhancing Akt/TFEB pathway-dependent autophagy flow.

Automated summary

This study found that trehalose can delay the onset of postmenopausal osteoporosis in rats by inducing and enhancing autophagy flow through the Akt/TFEB pathway. The trehalose group showed better histological and cellular outcomes compared to the model group.