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Bone Abstracts (2013) 1 PP163 | DOI: 10.1530/boneabs.1.PP163

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1University Medical Center Hamburg-Eppendorf, Hamburg, Germany; 2University Medical Center, Freiburg, Germany.


Here we identify the lipolytic enzyme hepatic lipase (HL, encoded by Lipc) as a novel cell-autonomous regulator of osteoblast function. In an unbiased genome-wide expression analysis, we find Lipc – which was formerly thought to be expressed almost exclusively by the liver – to be highly induced upon osteoblast differentiation, as verified by quantitative Taqman analyses of primary osteoblasts in vitro and of bone samples in vivo. Functionally, loss of HL in vitro leads to increased expression and secretion of osteoprotegerin (OPG), while osteoblast differentiation is mildly impaired. When challenging energy metabolism in a diet-induced obesity (DIO) study, lack of HL leads to a significant increase in bone formation markers and a decrease in bone resorption markers. Accordingly, in the DIO setting, we observe in Lipc−/− animals but not in wild-type controls a significant increase in lumbar vertebral trabecular bone mass and an increase in bone formation rate. Taken together, here we demonstrate that HL expressed by osteoblasts has an impact on osteoblast OPG expression and that lack of HL leads to increased bone formation in DIO. These data provide a novel and completely unexpected molecular link in the ever more complex interplay of osteoblasts and systemic energy metabolism.

Volume 1

European Calcified Tissue Society Congress 2013

Lisbon, Portugal
18 May 2013 - 22 May 2013

European Calcified Tissue Society 

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