Hepatic lipase is expressed by osteoblasts and modulates bone remodeling in obesity
Standard
Hepatic lipase is expressed by osteoblasts and modulates bone remodeling in obesity. / Bartelt, Alexander; Beil, Timo; Müller, Brigitte; Koehne, Till; Yorgan, Timur A; Heine, Markus; Yilmaz, Tayfun; Ruether, Wolfgang; Heeren, Joerg; Schinke, Thorsten; Niemeier, Andreas.
in: BONE, Jahrgang 62, 01.05.2014, S. 90-98.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
Harvard
APA
Vancouver
Bibtex
}
RIS
TY - JOUR
T1 - Hepatic lipase is expressed by osteoblasts and modulates bone remodeling in obesity
AU - Bartelt, Alexander
AU - Beil, Timo
AU - Müller, Brigitte
AU - Koehne, Till
AU - Yorgan, Timur A
AU - Heine, Markus
AU - Yilmaz, Tayfun
AU - Ruether, Wolfgang
AU - Heeren, Joerg
AU - Schinke, Thorsten
AU - Niemeier, Andreas
N1 - Copyright © 2014 Elsevier Inc. All rights reserved.
PY - 2014/5/1
Y1 - 2014/5/1
N2 - A number of unexpected molecules were recently identified as products of osteoblasts, linking bone homeostasis to systemic energy metabolism. 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 to be highly induced upon osteoblast differentiation, 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 expression of some osteoblast differentiation makers is 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 formation rate as well as in femoral trabecular bone mass and cortical thickness. Taken together, we demonstrate that HL expressed by osteoblasts has an impact on osteoblast OPG expression and that lack of HL leads to increased bone mass in DIO. These data provide a novel and completely unexpected molecular link in the complex interplay of osteoblasts and systemic energy metabolism.
AB - A number of unexpected molecules were recently identified as products of osteoblasts, linking bone homeostasis to systemic energy metabolism. 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 to be highly induced upon osteoblast differentiation, 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 expression of some osteoblast differentiation makers is 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 formation rate as well as in femoral trabecular bone mass and cortical thickness. Taken together, we demonstrate that HL expressed by osteoblasts has an impact on osteoblast OPG expression and that lack of HL leads to increased bone mass in DIO. These data provide a novel and completely unexpected molecular link in the complex interplay of osteoblasts and systemic energy metabolism.
U2 - 10.1016/j.bone.2014.01.001
DO - 10.1016/j.bone.2014.01.001
M3 - SCORING: Journal article
C2 - 24440515
VL - 62
SP - 90
EP - 98
JO - BONE
JF - BONE
SN - 8756-3282
ER -