PPARGC1A and type 2 diabetes mellitus: The suggested mechanism behind that is; since SOST is produced mainly by osteocytes and blocks the Wnt signaling pathway that is responsible for the subsequent blocking of adipogenesis via suppressing both the peroxisome proliferator-activated receptor-γ (PPARγ) and CCAAT/enhancer-binding protein-α (CEBPα) and blocking the thermogenic program through suppression of PPARγ coactivator-1α (PGC-1α); consequently, SOST stimulates adipogenesis which enhances the progression to T2DM and its associated complications [10].