ECTS2016 Poster Presentations Bone Marrow (4 abstracts)
Increased bone marrow adiposity in energy deficit context: tip of the iceberg?
Olfa Ghali 1 , Damien Leterme 1 , Xavier Coutel 2 , Anne Résonet 1 , Pierre Marchandise 2 , Flore Miellot 1 , Guillaume Penel 2 , Pierre Hardouin 1 & Christophe Chauveau 1
1Pathophysiology of Inflammatory Bone Diseases, Université du Littoral Côte d’Opale, Boulogne/mer, France; 2Pathophysiology of Inflammatory Bone Diseases, UniversitY of Lille, Lille, France.
Context: An increase in bone marrow adiposity (BMA) is usually described in anorexia nervosa (AN) patients and in calorie restriction models. This induced BMA could be involved in the development of the osteoporosis often described in AN. However, BMA increase is not always observed and could be depending on the severity of the deficit.
We previously developed the separation-based anorexia mouse model (SBA)1 (Ethical approval CEEA #022012). SBA mice displayed a severe body weight loss and a low bone mass, but no obvious increase in BMA.
Objectives: To determine the potential association between body weight loss, bone mass and BMA in a calorie deficit context.
Methods: The SBA model was adapted to target various levels of body weight loss. At the end of the 10 week protocol, we assessed tibia and vertebral bone parameters using microCT. We determined changes in volume and location of BMA after osmium staining. The capability of bone marrow stromal cells (BMSCs) to differentiate in adipocytes and osteoblasts was also determined in our co-differentiation medium2.
Results: First results showed that bone alterations take place without increase in BMA. But, 48 h after plating, PPARγ expression was only found in BMSCs from SBA mice. BMSCS from each SBA group displayed an increase in the adipocyte differentiation capabilities at the expense of osteoblastic differentiation. Lipid storage in adipocytes was detected as soon as 3 days after induction of differentiation vs 10 days for BMSCs from control mice. The expression of adipocyte markers was increased and that of the osteoblastic markers reduced in cells from SBA mice.
Conclusions: These results suggest that BMA could be a late marker of early changes responsible for alterations of bone phenotype.
1 Zgheib S, et al., 2014 PLoS ONE 9(8): e103775.
2 Ghali O, et al., 2015. BMC Cell Biol 16:9, DOI 10.1186/s12860-015-0056-6.
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