Figure 2.

Schematic representation of hyperinsulinaemia effects on cellular oxidative state, and bone homeodynamics. Acetoacetate (AcAc), adenosine triphosphate (ATP), advanced glycation end-products (AGE), beta-adrenergic receptor 2 (AdrB2), beta-hydroxybutyrate (BHB), heparan sulphate (HS), heparan sulphate proteoglycan (HSPG), hydrogen peroxide (H₂O₂), hyperinsulinaemia (HI), insulin receptor (InsR), isocitrate dehydrogenase 2 (Idh2), forkhead box O1 (FoxO1), glutathione oxidised form (GSSG), glutathione reduced form (GSH), lysine 68 (K68), magnesium (Mg), manganese superoxide dismutase 2 (MnSOD2), nicotinamide adenine dinucleotide (NAD+), nicotinamide adenine dinucleotide phosphate (NADP+), nuclear factor-kB (NF-kB), osteocalcin carboxylated (Gla-OCN or cOCN), osteocalcin un(der)carboxylated (Glu-OCN or ucOCN), osteoprotegerin (OPG), oxidative phosphorylation (OxPhos), receptor activator of nuclear factor-kB ligand (RANKL), reactive oxygen species (ROS), sirtuin 3 (SIRT3), superoxide (O₂⁻), tumour necrosis factor α (TNFα), T cell immune regulator 1 (Tcirg1), tryptophan hydroxylase (Tph), vitamin D (D₃), and vitamin K (K).