Changes in bone tissue energy metabolism in diabetes mellitus and aging as a cause of increased skeletal fragility

Interest in studying intermediary metabolic products and cellular bioenergetics is driven by the global increase in the prevalence of metabolic diseases. Structural features of bone tissue associated with an increased risk of fragility fractures in diabetes mellitus are associated with complex disorders of bone metabolism, including the accumulation of advanced glycation end products, suppression of osteoblastogenesis, increased sclerostin expression, development of oxidative stress and enhancement of catabolic processes under the influence of hyperglycemia. Pathogenetic changes in osteoporosis, in turn, are associated with complex alterations in cellular energy metabolism, mitochondrial function, and purine homeostasis, which contribute to a progressive imbalance in bone remodeling and a decrease in the biomechanical properties of bone tissue. This literature review provides information on the main sources and pathways of adenosine triphosphate synthesis in bone cells, the mechanisms of energy metabolism regulation under normal conditions, as well as under conditions of hyperglycemia in diabetes mellitus and under conditions of age-related changes in the body with the development of osteoporosis. The presented data reveal promising prospects for the development of targeted therapies aimed at the described metabolic alterations, offering a potential approach for the prevention and management of bone disorders.

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