Absorption of Minerals and Metals
2012
2011
2010
2009
Stontium
Biphosphonates 9/21
Hair loss after weight loss surgery! 5/18
Drug interactions with herbal remedies 5/4
Exercise habit
Pregnancy after duodenal switch 4/27
Calorie calculation 4/13
Cells found in bones 3/11
Calorie predictive relations in energy regulation by rats3/9
2/2
Am I going Bald
Trans Fatty Acids 1/7
2008
Olive oil 12/30
Bariatric surgery before pregnancy 12/5
Antioxidant effects of almonds 10/20
Moderate Exercise Yields Big Benefits 6/1
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.
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 voltageinsensitive 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 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 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.
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 olybdenum can
induce secondary copper deficiency
states.
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