Intestinal mineral absorption pathway

The intestinal mineral absorption pathway refers collectively to the physiological and molecular processes by which dietary minerals—including but not limited to calcium, iron, zinc, copper, and phosphate—are absorbed from the intestinal lumen into enterocytes and then transported into systemic circulation. This process is highly regulated due to both the essential nature and potential toxicity of many minerals at high concentrations[2][4]. Absorption occurs primarily in the small intestine via two main routes: transcellular (active) transport involving specific membrane proteins such as channels or pumps—often regulated by hormones like vitamin D—and paracellular (passive) diffusion through tight junctions between epithelial cells[1][2][3][5]. For example, active transcellular calcium uptake is upregulated by vitamin D via increased expression of calbindin and other related proteins[3], while passive paracellular movement predominates when luminal concentrations are high. Iron is actively transported into enterocytes where it binds ferritin before being released according to systemic needs[1]. The efficiency and selectivity of these pathways are critical for maintaining overall mineral homeostasis. Note: "Intestinal mineral absorption pathways" does not refer to a single molecule or receptor but rather an ensemble of physiological processes involving multiple distinct molecular targets. Therefore this entry should be flagged as not a canonical therapeutic target but rather a functional category encompassing several targets such as divalent metal transporter 1 (DMT1), TRP channels for calcium uptake, sodium-phosphate cotransporters etc.[2][4].

Other names

Mineral absorption pathwaysIntestinal mineral transport mechanismsMineral uptake in intestine