Absorption of Minerals & Metals (Info from Colorado State University)

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Absorption of Minerals and Metals

The vast bulk of mineral absorption occurs in the small intestine. The

best-studied mechanisms of absorption are clearly for calcium and iron,

deficiencies of which are significant health problems throughout the world.

Minerals are clearly required for health, but most also are quite toxic

when present at higher than normal concentrations. Thus, there is a

physiologic challenge of supporting efficient but limited absorption. In

many cases intestinal absorption is a key regulatory step in mineral

homeostasis.

Calcium

The quantity of calcium absorbed in the intestine is controlled by how much

calcium has been in the diet during recent periods of time. Calcium is

absorbed by two distinct mechanims, and their relative magnitude of

importance is set by dietary calcium " history " :

* Active, transcellular absorption occurs only in the duodenum when

calcium intake has been low. This process involves import of calcium into

the enterocyte, transport across the cell, and export into extracellular

fluid and blood. Calcium enters the intestinal epithelial cells through

voltage-insensitive channels and is pumped out of the cell via a

calcium-ATPase.

The rate limiting step in transcellular calcium absorption is

transport across the epithelial cell, which is greatly enhanced by the

carrier protein calbindin, the synthesis of which is totally dependent on

vitamin D.

* Passive, paracellular absorption occurs in the jejunum and ileum,

and, to a much lesser extent, in the colon when dietary calcium levels have

been moderate or high. In this case, ionized calcium diffuses through tight

junctions into the basolateral spaces around enterocytes, and hence into

blood. Such transport depends on having higher concentrations of free

calcium in the intestinal lumen than in blood.

Phosphorus

Phosphorus is predominantly absorbed as inorganic phosphate in the upper

small intestine. Phosphate is transported into the epithelial cells by

contransport with sodium, and expression of this (or these) transporters is

enhanced by vitamin D.

Iron

Iron homeostasis is regulated at the level of intestinal absorption, and it

is important that adequate but not excessive quantities of iron be absorbed

from the diet. Inadequate absorption can lead to iron-deficiency disorders

such as anemia. On the other hand, excessive iron is toxic because mammals

do not have a physiologic pathway for its elimination.

Iron is absorbed by villus enterocytes in the proximal duodenum. Efficient

absorption requires an acidic environment, and antacids or other conditions

that interfere with gastric acid secretion can interfere with iron absorption.

Ferric iron (Fe+++) in the duodenal lumen is reduced to its ferrous form

through the action of a brush border ferrireductase. Iron is the

cotransported with a proton into the enterocyte via the divalent metal

transporter DMT-1. This transporter is not specific for iron, and also

transports many divalent metal ions.

Once inside the enterocyte, iron follows one of two major pathways. Which

path is taken depends on a complex programming of the cell based on both

dietary and systemic iron loads:

* Iron abundance states: iron within the enterocyte is trapped by

incorporation into ferritin and hence, not transported into blood. When the

enterocyte dies and is shed, this iron is lost.

* Iron limiting states: iron is exported out of the enterocyte via a

transporter (ferroportin) located in the basolateral membrane. It then

binds to the iron-carrier transferrin for transport throughout the body.

Iron in the form of heme, from ingestion of hemoglobin or myoglobin, is

also readily absorbed. In this case, it appears that intact heme is take up

by the small intestinal enterocyte by endocytosis. Once inside the

enterocyte, iron is liberated and essentially follows the same pathway for

export as absorbed inorganic iron. Some heme may be transported intact into

the circulation.

Copper

There appear to be two processes responsible for copper absorption - a

rapid, low capacity system and a slower, high capacity system, which may be

similar to the two processes seen with calcium absorption. Many of the

molecular details of copper absorption remain to be elucidated.

Inactivating mutations in the gene encoding an intracellular copper ATPase

have been shown responsible for the failure of intestinal copper absorption

in Menkes disease.

A number of dietary factors have been shown to influence copper absorption.

For example, excessive dietary intake of either zinc or molybdenum can

induce secondary copper deficiency states.

Zinc

Zinc homeostasis is largely regulated by its uptake and loss through the

small intestine. Although a number of zinc transporters and binding

proteins have been identified in villus epithelial cells, a detailed

picture of the molecules involved in zinc absorption is not yet in hand.

Intestinal excretion of zinc occurs via shedding of epithelial cells and in

pancreatic and biliary secretions.

A number of nutritional factors have been identified that modulate zinc

absorption. Certain animal proteins in the diet enhance zinc absorption.

Phytates from dietary plant material (including cereal grains, corn, rice)

chelate zinc and inhibit its absorption. Subsistance on phytate-rich diets

is thought responsible for a considerable fraction of human zinc deficiencies.

References and Reviews

* s NC: Disorders of iron metabolism. New Eng J Med 341:1986, 1999.

* Bronner F: Calcium absorption: A paraadigm for mineral absorption. J

Nutrition 128:917-920, 1998.

* Krebs NF: Overview of zinc absorption and excretion in the human

gastrointestinal tract. J Nutrition 130:1374S-1377S, 2000.

* Lonnerdal B: Dietary factors influencing zinc absorption. J

Nutrition 130:1378S-1385S, 2000.

* Miret S, Simpson RJ, McKie AT: Physiology and molecular biology of

iron absorption. Ann Rev Nutr 23:283-301, 2003.

* Wessling-Resnick M: Iron transport. Annu Rev Nutr 20:129-151, 2000.

Index of: The Small Intestine: Introduction and Index

Last updated on March 7, 2004

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