ECTS Abstracts (2015) 1 P58

Adiponectin deficiency in female mice leads to age-dependent changes in bone

Dorit Naot, Karen Callon, Maureen Watson, Jian-Ming Lin, Donna Tuary, Mei Lin Tay, Andrew Grey & Jillian Cornish

University of Auckland, Auckland, New Zealand.

Adiponectin, a peptide-hormone secreted from adipocytes, is involved in the regulation of energy homeostasis, glucose and lipid metabolism. Clinical studies show inverse relationships between circulating adiponectin concentrations and bone mineral density. Studies of the bone phenotype of adiponectin deficient mice (APN-KO) by different groups produced inconsistent results. The aim of our study was to conduct a systematic analysis of the bone phenotype of APN-KO mice, by adhering to strict experimental planning guidelines for in vivo studies. Groups of 10 WT C57BI/6J and 10 APN-KO (C57BI/6J background) female mice were culled at 8, 14, 21, 28 and 37 weeks of age. Bone architecture of femora was analysed by microCT (SkyScan 1172), and body composition was determined longitudinally by DEXA (Lunar PIXImus Densitometer). The WT and APN-KO animals had similar weights until week 37, when the WT mice were heavier (27.2±2.6g for WT and 24.63±1.9g for APN-KO, P<0.05). At 8 and 14 weeks, trabecular %BV/TV was lower in APN-KO mice (1.4-fold, P<0.001 and 1.3-fold, p<0.05 at 8 and 14 weeks, respectively), with no differences between the groups at later time points. Cortical %BV/TV was lower in the APN-KO groups at all the time points (P<0.001) and cortical thickness was lower from week 14 onwards (P<0.01). Analysis of body composition showed that from week 21 onwards, APN-KO animals had approximately 1.5-fold lower % fat (P<0.0001). Osteoclastogenesis assays in bone marrow cultures treated with 1,25(OH)2D3 showed increased numbers of TRAP+ multinucleated cells in cultures from APN-KO mice (>1.5-fold increase, P<0.01). Our results show a consistent reduction in cortical volume and thickness and reduced trabecular volume in young animals. The contribution of the increased osteoclastogenesis measured ex vivo to the phenotype requires further investigation. Analysis of bone strength is underway to determine the functional consequences of the changes in bone architecture.

Disclosure: The authors declared no competing interests. This work was supported by The Health Research Council of New Zealand.

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