In a physiological axis of bone-fat-energy metabolism, exercise-induced body fat reduction and improved insulin sensitivity were accompanied by an increase in serum osteocalcin and leptin levels, but other factors also seem to be involved in this interrelationship.

The prevailing model of osteology is that bones constantly undergo a remodeling process, and that the differentiation and functions of osteoblasts are partially regulated by leptin through different central hypothalamic pathways. The finding that bone remodeling is regulated by leptin suggested possible endocrinal effects of bones on energy metabolism. Recently, a reciprocal relationship between bones and energy metabolism was determined whereby leptin influences osteoblast functions and, in turn, the osteoblast-derived protein osteocalcin influences energy metabolism. The metabolic effects of bones are caused by the release of osteocalcin into the circulation in an uncarboxylated form due to incomplete γ-carboxylation. In this regard, the Esp gene encoding osteotesticular protein tyrosine phosphatase is particularly interesting because it may regulate γ-carboxylation of osteocalcin. Novel metabolic roles of osteocalcin have been identified, including increased insulin secretion and sensitivity, increased energy expenditure, fat mass reduction, and mitochondrial proliferation and functional enhancement. To date, only a positive correlation between osteocalcin and energy metabolism in humans has been detected, leaving causal effects unresolved. Further research topics include: identification of the osteocalcin receptor; the nature of osteocalcin regulation in other pathways regulating metabolism; crosstalk between nutrition, osteocalcin, and energy metabolism; and potential applications in the treatment of metabolic diseases.

Over the past three decades, human pancreatic islet isolation and transplantation techniques have developed as a routine clinical procedure for selected patients with type 1 diabetes mellitus. However, due to the donor shortage and required chronic systemic immunosuppression, the widespread application of islet transplantation is limited. To overcome these limitations, providing a physical barrier to transplanted islet cells with encapsulating biomaterial has emerged as a promising approach to enhance engraftment and promote islet survival post-transplantation. Alginate has been considered to be a reliable biomaterial, as it enhances islet survival and does not hamper hormone secretion. Alginate-catechol (Al-CA) hydrogel was reported to provide high mechanical strength and chemical stability without deformation over a wide range of pH values. In this study, we, demonstrated, for the first time in the literature, that encapsulation of murine pancreatic islet cells with Al-CA hydrogel does not induce cytotoxicity ex vivo for an extended period; however, it does markedly abate glucose-stimulated insulin secretion. Catechol should not be considered as a constituent for alginate gelation for encapsulating islet cells in the application of islet transplantation.

Objective: FSTL1, an extracellular glycoprotein, is a novel myokine that is secreted by skeletal muscle. However, its functions in metabolism remain unclear, Adipose tissue is one of the important organs for maintaining energy homeostasis. FSTL1 is known to induce inflammatory response and inhibit insulin-mediated Akt signaling pathway, we aimed to investigate whether FSTL1 play metabolic roles in human adipose tissue. We hypothesized that FSTL1 increases lipolysis through its putative receptor DIP2A (Disco interacting protein 2 homolog A). Methods: Human primary adipocytes were treated with recombinant FSTL1 in dose and time dependent manner. To determine its lipolytic activity, pHSL ser563,565,660, perilipin, AMPK, PKA were determined by western blot and the rate of free fatty acid was assessed. Expression of DIP2A was determined by PCR and western blot. DIP2A was knocked-down to examine whether it mediates metabolic effects of FSTL1. Results: FSTL1 did not affect catecholamine-induced lipolysis via PKA. FSTL1, however, increased lipolysis through AMPK activation and, subsequently, HSL ser565 phosphorylation in dose dependent manner. It was found that DIP2A expression did not change during differentiation of human primary adipocyte, suggesting that it is not involved in adipocyte maturation. Conclusion: FSTL1 increased basal lipolysis through AMPK activation. AMPK is well known sensor of the intracellular energy state and serves to regulate various signals. Its activation provides ATP by FA oxidation. Therefore, FSTL1 may play an important in the regulation of energy homeostasis. FSTL1 also has effect through DIP2A. These findings suggest that DIP2A plays important roles in FSTL1 mediated lipolysis. Disclosure C. Ahn: None. A. Choi: None. J. Kim: None. K. Park: None. S. Lee: None. J. Nam: None. S. Park: None. M. Kim: None. Y. Kim: None. J. Nam: None. S. Kang: None. J. Park: None.