Obesity, type 2 diabetes, and osteoporosis are metabolic diseases often accompanied by increased bone marrow adipose tissue (BMAT), which is closely linked to complications in both fat and bone metabolism. Bone and BMAT share the common precursor of the origin, bone marrow stromal cells (BMSCs), whose differentiation potential and metabolic function are affected by nutrient overload and metabolic stress. Insulin signalling, lipid handling, and oxidoreductase activity are nutrient-sensing pathways that are affected by metabolic disturbances and play a critical role in regulating glucose metabolism and bone homeostasis. In this presentation, I will highlight recent findings on how metabolic diseases and dietary interventions modulate bone and adipose cell metabolism, and discuss emerging data on BMAT phenotypic changes in diverse mouse models. Finally, I will explore how targeting metabolic enzymes relevant to bone–fat interactions may offer new strategies for treating metabolic and bone disorders.

IPHYS contact: Michaela Tencerová, PhD., the Head of Laboratory of Molecular Physiology of Bone, IPHYS, michaela.tencerova@fgu.cas.cz

Funding: Output of project no. LX22NPO5104 „Funded by the European Union – Next Generation EU“