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Osteocalcin: a pivotal mediator or an innocent bystander in energy metabolism?

The importance of the bone–kidney axis in physiologic regulation of mineral ion homeostasis has been extensively studied and documented. Numerous research studies have convincingly shown that pathology in one organ can affect the functionality of the other organ. For instance, chronic kidney disease (CKD) patients usually present with complications of bone anomalies that vary from fractures (due to increased bone fragility) to extraskeletal calcification (due to mineral ion dysregulation). These skeletal anomalies in CKD–mineral bone disorder (CKD–MBD) are partly related to decreased osteoblastic differentiation that impairs the anabolic responses of the bone [1]. CKD patients in their forties who are undergoing dialysis treatment are 80 times more likely to acquire hip fractures than age- and sex-matched controls [2]. Furthermore, studies have documented a linear correlation between insulin resistance and the decline of renal functions [3]. In a large cohort of > 6000 non-diabetic individuals, insulin resistance and concomitant hyperinsulinemia were detected in CKD patients [4]. Why CKD patients are more likely to develop insulin resistance is not yet clear, and carefully designed studies are needed to determine whether impaired osteoblastic activity in CKD may induce such resistance. Such possibilities arise from the recent discoveries that have shown that osteoblast-derived factor can affect energy metabolism by influencing insulin secretion [5,6].