Intestinal Ca2+ absorption revisited: A molecular and clinical approach

Figure 1 Effects of hormones on intestinal Ca²⁺ absorption. Calcitriol stimulates the transcellular and paracellular absorptive pathways by inducing the expression of genes and proteins involved in Ca²⁺ transport and modifying the permeability of tight junctions. Thyroid hormones enhance the genomic actions of calcitriol whereas glucocorticoids inhibit the transcellular pathway by affecting the expression of Ca²⁺ transporting proteins. Fibroblast growth factor inhibits the intestinal Ca²⁺ absorption antagonizing 1,25(OH)₂D₃ action. Growth hormone enhances the intestinal Ca²⁺ absorption through vitamin D dependent and independent mechanisms. PMCA_1b: Plasma membrane Ca²⁺-ATPase; CB_9k: Calbindin 9k; Ca_v1.3: Ca²⁺ channel voltage-dependent L type alpha 1D subunit; TRPV5: Transient receptor potential vanilloid 5; TRPV6: Transient receptor potential vanilloid 6; CLDNs 2, 12 and 15: Claudins 2, 12 and 15; NCX1: Na⁺/Ca²⁺ exchanger; 1,25(OH)₂D3: Calcitriol; FGF-23: Fibroblast growth factor; GH: Growth hormone; GC: Glucocorticoids; T4: Thyroxine; TJ: Tight junction; VDR: Vitamin D receptor.