Gastric Acid, Calcium Absorption, and Their Impact on Bone Health

Abstract

Calcium balance is essential for a multitude of physiological processes, ranging from cell signaling to maintenance of bone health. Adequate intestinal absorption of calcium is a major factor for maintaining systemic calcium homeostasis. Recent observations indicate that a reduction of gastric acidity may impair effective calcium uptake through the intestine. This article reviews the physiology of gastric acid secretion, intestinal calcium absorption, and their respective neuroendocrine regulation and explores the physiological basis of a potential link between these individual systems.

Vitamin D-Enhanced Duodenal Calcium Transport

“…3B). Recently, another family of the basolateral calcium transporters, namely potassium-dependent sodium calcium exchangers (e.g., NCKX3 and 4), has been suggested to contribute to calcium extrusion (Kopic & Geibel, 2013), but whether 1,25(OH) 2 D 3 is capable of stimulating these transporters in the small intestine is not known. A study in mouse dendritic cells indicated that 1,25(OH) 2 D 3 could increase the membrane abundance of NCKX proteins as well as their activities (Shumilina et al, 2010).…”

“…Such transient change of plasma calcium is recovered by an integrative response of three calcium-regulating organs organized as the parathyroid-kidney-intestinal axis (Fig. 4) (Kopic & Geibel, 2013;Peacock, 2010). PTH secretion from the parathyroid gland is inhibited after calcium binds to calcium sensing receptor (CaSR) in the plasma membrane of parathyroid chief cells.…”

“…In a classical loop of regulation, low plasma calcium level curtails this CaSR-induced suppression, thereby increasing PTH secretion. PTH, in turn, raises plasma calcium level by (i) enhancing calcium reabsorption in the thick ascending limb of the Henle's loop and distal renal tubule, which occurs within minutes, and (ii) stimulating osteoblasts to secrete RANKL, which activates osteoclastmediated bone resorption within minutes to hours (Favus, Bushinsky, & Lemann, 2006;Kopic & Geibel, 2013). PTH can further induce bone calcium release by osteocytes through a poorly defined mechanism, known as osteocytic osteolysis (Tazawa et al, 2004).…”

“…Paracellular calcium transport, on the other hand, is present along the entire length of the small intestine. However, it is believed that a considerable amount of lumen-to-plasma paracellular calcium flux also occurs in the duodenum since it is exposed to high luminal concentration of free-ionized calcium, which is liberated from insoluble complexes by gastric acidic environment (Kopic & Geibel, 2013), especially after high-calcium meal or oral calcium supplementation. Our investigation has provided evidence that the paracellular calcium flux in the rat duodenum is much greater than the transcellular calcium flux (up to 10:1 when luminal calcium >5 mmol/L) (Charoenphandhu, Tudpor, Pulsook, & Krishnamra, 2006).…”

Functional hypoparathyroidism secondary to magnesium deficiency in long-term users of proton pump inhibitor

“…Лечение ГЭРБ включает рекомендации по изменению образа жизни пациента и медикаментоз-ную терапию -первоначально ингибиторов протонной помпы (ИПП), которые блокируют H+-K+-АТФазу парие-тальных клеток желудка. Немаловажную роль в образо-вании соляной кислоты и гастрина (G-клетки) в желудке играет Ca2+/Mg2+-чувствительный рецептор за счет ак-тивации Н+-К+-АТФазы [3].…”