I n spite of its stagnant gross appearance, the skeleton is a highly metabolically active organ. The continuous process of bone remodeling, allowing homeostatic availability of calcium and renovation of the important structural material of bone, requires ample energy supply (1). Extreme examples of such energy demand had been noticed a long time ago in high bone turnover states, for instance in the cachexia accompanying severe hyperparathyroidism or in slender children with osteogenesis imperfecta, but lacked an explanation. Therefore, when the first mechanistic pieces of evidence linking bone and energy metabolism in animal models started arising (2), it not only made sense in physiological terms, but it was also felt as if by identifying these missing links we would potentially be able to tackle simultaneously two major health care concerns, adiposity and osteoporosis.It has now been more than 10 years since the paramount work of Lee and cols. placed osteocalcin (Oc) as the foremost bone-derived hormone to influence energy metabolism (3), rocketing Oc from its role as a (perhaps second rate) bone formation marker to a means by which bone, as an endocrine gland, would direct insulin sensitivity and production, and fat accumulation. From then onwards, subsequent evidence have solidified that, in mice, Oc favors glucose tolerance and insulin sensitivity (4,5). Its role as an energy metabolism effector in humans, however, remains elusive.Osteocalcin is produced by osteoblasts and secreted in a fully carboxylated form into the bone matrix, where it acts to regulate bone mineralization. Under acidic pH in the osteclastic resorption lacuna, it suffers decarboxylation generating undercarboxylated Oc -importantly, this is the form of Oc that has been chiefly linked to a metabolic role, but its determination in serum is not straightforward in clinical or even in research settings (5). Several studies in humans have investigated the relationship of total serum Oc and a variety of metabolic parameters, and results have been conflicting (6). Indeed, an effect, when seen, was considerably smaller in magnitude to what was observed in mice.Two articles in this issue of the Archives of Endocrinology and Metabolism (AE&M) have aimed to shed light on this topic through different approaches. Campos and cols. have analyzed clinical, laboratory and anthropometric and body composition parameters in a cohort of 34 obese adolescents submitted to a one-year interdisciplinary intervention including exercise, diet and psychological support (7). As expected, the intervention resulted in a reduction in body mass and fat was seen, accompanied by a significant increase in adiponectin and in lean mass. Even though an increase in bone mineral content was observed after the 1-year intervention, the expected progression of bone accretion during this period of life precludes ascertaining a positive effect of exercise on bone formation. The authors focused their analysis on the relation