Activation of calcium-sensing receptor by allosteric agonists cinacalcet and AC-265347 abolishes the 1,25(OH)2 D3 -induced Ca2+ transport: Evidence that explains how the intestine prevents excessive Ca2+ absorption

Archives of Biochemistry and Biophysics
Kannikar WongdeeNarattaphol Charoenphandhu

Abstract

Long-term high-calcium intake and intestinal calcium hyperabsorption are hazardous to the body. It is hypothesized that enterocytes possess mechanisms for preventing superfluous calcium absorption, including secretion of negative regulators of calcium absorption and utilization of calcium-sensing receptor (CaSR) to detect luminal calcium. Herein, Caco-2 monolayers were treated with high doses of 1,25(OH)2D3 to induce calcium hyperabsorption or directly exposed to high apical calcium. The expression of counterregulatory factor of calcium absorption, fibroblast growth factor (FGF)-23, was also investigated in the intestine of lactating rats, which physiologically exhibit calcium hyperabsorption. We found that FGF-23 expression was enhanced in all intestinal segments of lactating rats. In Caco-2 monolayers, high apical calcium and 1,25(OH)2D3 induced FGF-23 secretion into culture media. FGF-23 antagonized 1,25(OH)2D3-induced calcium transport and led to a significant, but small, change in paracellular permeability. Furthermore, high-dose 1,25(OH)2D3 upregulated FGF-23 expression, which was prevented by CaSR inhibitors. Activation of apical CaSR by cinacalcet and AC-265347 abolished 1,25(OH)2D3-induced calcium transport in a dose-d...Continue Reading

Citations

Aug 9, 2020·Medical Hypotheses·Michael T SheehanAdedayo A Onitilo
Dec 29, 2020·American Journal of Physiology. Cell Physiology·Krittikan ChanpaisaengNarattaphol Charoenphandhu
May 1, 2021·Experimental Biology and Medicine·Rebecca Siu Ga TanR Todd Alexander

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