Autophagy is an evolutionarily conserved intracellular process and is considered one of the main catabolism pathways. In the process of autophagy, cells are digested nonselectively or selectively to recover nutrients and energy, so it is regarded as an antiaging process. In addition to the essential role of autophagy in cellular homeostasis, autophagy is a stress response mechanism for cell survival. Here, we review recent literature describing the pathway of autophagy and its role in different bone cell types, including osteoblasts, osteoclasts, and osteocytes. Also discussed is the mechanism of autophagy in bone diseases associated with bone homeostasis, including osteoporosis and Paget's disease. Finally, we discuss the application of autophagy regulators in bone diseases. This review aims to introduce autophagy, summarize the understanding of its relevance in bone physiology, and discuss its role and therapeutic potential in the pathogenesis of bone diseases such as osteoporosis.

Objectives Hypothalamic dysfunction leads to glucose metabolic imbalance; however, the mechanisms still need clarification. Our current study was to explore the role of hypothalamic Hnscr in glucose metabolism. Materials and Methods Using Hnscr knockout or htNSC‐specific Hnscr overexpression mice, we evaluated the effects of Hnscr on glucose metabolism through GTTs, ITTs, serum indicator measurements, etc. Immunofluorescence staining and Western blotting were performed to test inflammation levels and insulin signalling in hypothalamus. Conditioned medium intervene were used to investigate the effects of htNSCs on neuronal cell line. We also detected the glucose metabolism of mice with htNSCs implantation. Results Hnscr expression decreased in the hypothalamus after high‐fat diet feed. Hnscr‐null mice displayed aggravated systematic insulin resistance, while mice with htNSC‐specific Hnscr overexpression had the opposite phenotype. Notably, Hnscr‐null mice had increased NF‐κB signal in htNSCs, along with enhanced inflammation and damaged insulin signal in neurons located in arcuate nucleus of hypothalamus. The secretions, including sEVs, of Hnscr‐deficient htNSCs mediated the detrimental effects on the CNS cell line. Locally implantation with Hnscr‐depleted htNSCs disrupted glucose homeostasis. Conclusions This study demonstrated that decreased Hnscr in htNSCs led to systematic glucose imbalance through activating NF‐κB signal and dampening insulin signal in hypothalamic neurons.