Significance of mineral absorption

The small intestine is responsible for the vast majority of mineral absorption. Mineral absorption mechanisms have clearly been studied most thoroughly for calcium and iron, deficiencies of which are associated with significant health problems throughout the world.

Minerals are unquestionably necessary for health, but many of them are also extremely toxic when present in concentrations greater than normal. In order to maintain efficient but limited absorption, there is a physiologic challenge to overcome. In many cases, intestinal absorption is a critical regulatory step in the maintenance of mineral homeostasis.

Calcium

There are two distinct mechanisms that cause calcium to be absorbed from the intestinal lumen, and their relative importance is determined by the amount of free calcium available for absorption:

The duodenum is the site of active, transcellular calcium absorption only when the calcium intake is low. During this process, calcium is brought into the enterocyte, transported across the cell, and then expelled into the extracellular fluid and the bloodstream. Intestinal epithelial cells receive calcium from the bloodstream through voltage-insensitive (TRP) channels, which are then expelled by a calcium-ATPase.

The transport of calcium across the epithelial cell is the rate-limiting step in transcellular calcium absorption. The transport of calcium across the epithelial cell is greatly enhanced by the carrier protein calbindin, whose synthesis is completely dependent on vitamin D.

2. When dietary calcium levels are moderate or high, passive, paracellular absorption occurs in the jejunum and ileum, as well as, to a lesser extent, in the colon. Here, ionised calcium diffuses into the basolateral spaces surrounding enterocytes, and then into the bloodstream through tight junctions. It is this pathway, which is responsible for the majority of calcium absorption during times of high calcium availability, because active transport in the duodenum takes place in a very short amount of time.

Phosphorus

Phosphorus is primarily absorbed as inorganic phosphate in the upper small intestine, where it is converted to phosphorus. When phosphate and sodium are transported together into epithelial cells, the expression of this (or these) transporters is increased, and vitamin D helps to promote the expression of these transporters.

Iron

Due to the fact that iron homeostasis is controlled at the level of intestinal absorption, it is critical that sufficient but not excessive amounts of iron be absorbed from the diet. It is possible to develop iron-deficiency disorders such as anaemia as a result of insufficient absorption. Excessive iron, on the other hand, is toxic to mammals because they lack a physiologic pathway for excretion of the metal in their bodies.

The proximal duodenum contains villus enterocytes, which are responsible for iron absorption. An acidic environment is required for efficient absorption, and antacids or other conditions that interfere with gastric acid secretion can cause iron absorption to be reduced or inhibited.

The action of a brush border ferrireductase in the duodenal lumen results in the reduction of ferric iron (Fe+++) to ferrous iron. Divalent metal transporter-1 (DMT-1) is responsible for the cotransportation of iron and a proton into the enterocyte. This transporter is not only capable of transporting iron ions, but it is also capable of transporting many other divalent metal ions.

Once inside the enterocyte, iron travels through the body in one of two major ways. How the cell chooses to proceed is determined by a complex programming process that takes into account dietary and systemic iron loads:

If you have a high concentration of iron in your enterocyte, it is trapped by incorporation into ferritin and is not transported into the bloodstream. This iron is lost when the enterocyte dies and is shed from the body.

For enterocytes in iron-limiting states, a transporter (ferroportin) located in the basolateral membrane exports iron from the cell. It then forms a bond with the iron-transporting protein transferrin, which allows it to be transported throughout the body.

In addition, iron in the form of heme, obtained through the ingestion of haemoglobin or myoglobin, is readily absorbed. Endocytosis appears to be responsible for the uptake of intact heme by the small intestinal enterocyte in this instance. Once inside the enterocyte, iron is liberated and essentially follows the same path to the colon as absorbed inorganic iron in terms of transport. Some heme may be transported into the circulation in an intact state.

Copper

In terms of copper absorption, it appears that two processes are involved: a fast, low-capacity system and a slower, high-capacity system, which may be similar to the two processes involved in calcium absorption. It is still unclear how copper absorbs light at the molecular level in many situations. The presence of inactivating mutations in the gene encoding an intracellular copper ATPase has been demonstrated to be responsible for the failure of intestinal copper absorption observed in Menkes disease patients.

Copper absorption has been shown to be influenced by a variety of dietary factors. If you consume too much zinc or molybdenum, you can develop secondary copper deficiency states, which are dangerous.

Zinc

Zinc homeostasis is largely controlled by the amount of zinc that is absorbed and excreted through the small intestine. Despite the identification of a number of zinc transporters and binding proteins in villus epithelial cells, a comprehensive picture of the molecules involved in zinc absorption is still lacking.

Zinc is excreted from the intestinal tract through the shedding of epithelial cells as well as through pancreatic and biliary secretions.

Zinc absorption is modulated by a number of nutritional factors, which have been identified so far. The consumption of certain animal proteins in the diet can help to increase zinc absorption. Phytates derived from dietary plant material (such as cereal grains, corn, and rice) chelate zinc and prevent it from being absorbed. It is believed that human zinc deficiency is caused by a significant portion of the population’s resistance to phytate-rich diets.

CONCLUSION:

Generally speaking, mineral absorption is proportional to dietary intake, with two notable exceptions: the absorption of iron and calcium, both of which can be controlled to meet specific needs of the body, and vitamin D absorption. The amount of specific binding protein present in the enterocyte is related to the amount of calcium absorbed. In the absence of sufficient vitamin D levels, the concentration of calcium binding protein, which regulates calcium absorption from the gut, is secondary.

The duodenum and proximal jejunum are the organs responsible for iron absorption. Following digestion, iron can be found in two forms: ferrous and nonferrous. The first is haem iron, which is bound to haemoglobin and myoglobin in haemoglobin and myoglobin. Alternatively, free ionised iron in the ferrous and ferric states can be found as the second form. In contrast to free iron, which is likely to be absorbed by a specific carrier protein, hem iron is taken up through binding to a probable haemoglobin receptor. Iron is cytotoxic when present in free form, so it is bound inside enterocytes to the large storage protein apoferritin or bound to transferrin for transport to the bloodstream.