In this abstract are reported some of the many works that emerged in the bone field last year. Two relevant article have been published about the role of osteocalcin on energy metabolism. Principal role as responsible of bone formation, the osteoblast is an endocrine cell that, by secreting the osteocalcin hormone, is able to increase insulin synthesis and sensitivity, leading to improved glucose homeostasis. However, the identification of bone as a regulator of glucose metabolism required, as premise, to define the function of glucose in the metabolism of osteoblast itself. Very recently, it has been found that glucose is the main nutrient of osteoblasts and it is transported in these cells in an insulin-independent manner through the Glut1 glucose transporter whose expression precedes that of Runx2 during skeletogenesis. Furthermore, there is a feed-forward regulation through which Runx2 increases Glut1 expression and this coupled mechanism orchestrates osteoblast differentiation during bone formation throughout life. With anabolic function also in skeletal muscle, insulin promotes glucose uptake in myofibers, although its circulating levels decline during exercise. This discrepancy suggested that the increase in nutrient uptake and catabolism in muscle, occurring during exercise, may be induced by other secreted molecules. Very recently, it has been showed that circulating levels of the bone-derived hormone osteocalcin are increased during aerobic exercise. Exploring these observations, authors showed that osteocalcin signaling in skeletal muscle fibers is required for adaptation to exercise by favoring uptake and catabolism of glucose and fatty acids. Still regarding skeletal muscle, cancer-associated muscle weakness has been for long time a poorly understood phenomenon. New research performed on seven different mouse models of human osteolytic bone metastases, all exhibiting impaired muscle function, showed that transforming growth factor (TGF)-b, released from the bone surface as a result of metastasis-induced bone destruction, was responsible for skeletal muscle weakness through the oxidation of RyR1 and the resultant Ca2+ leakage. This study suggests that targeting this pathway might help to ameliorate muscle weakness in cancer patients with bone metastases. Several line of evidence demonstrated that the gut microbiota influences not only the local immune response, but also contributes to immune responses in distant organs. In particular, microbiota has also been found to negatively influence bone homeostasis. New studies have shown that the intestinal microbiota modulates inflammatory responses caused by sex steroid deficiency in ovx mice, leading to trabecular bone loss. Estrogen deficiency increased gut permeability, expanded Th17 cells and upregulated the osteoclastogenic cytokines TNFα (TN F), RANKL, and IL-17 in the small intestine and bone marrow. The treatment of ovx mice with the probiotics Lactobacillus completely protects against bone loss by reducing gut permeability and intestinal and bone marrow inflammation, thus suggesting that probiotics might have potential as a therapeutic strategy for postmenopausal osteoporosis.