Biochemistry for Nurses Absorption of Carbohydrates
Absorption Of Carbohydrates
It is observed from carbohydrate digestion is complete when the food materials reach small intestine and all complex dietary carbohydrates like starch and glycogen and the disaccharides are ultimately converted to simpler monosaccharides.
All monosaccharides, products of digestion of dietary carbohydrates, are practically completely absorbed almost entirely from the small intestine.
Absorption Rate in Small Intestine
Rate of absorption diminishes from above downwards; proximal jejunum three times greater than that of distal ileum.
Absorption of Disaccharides
It is also proved that some disaccharides, which escape digestion, may enter the cells lining the intestinal lumen may be by pinocytosis; and are hydrolysed within these cells.
No carbohydrates higher than the monosaccharides can be absorbed directly into
the bloodstream in normal health and if administered parenterally, they are
eliminated as foreign bodies.
Cori Theory About The Rate of Absorption for Diffrent Carbohydrates
Cori studied
the rate of absorption of different sugars from small intestine in rat. Taking
glucose absorption as 100, comparative rate of absorption of other sugars were
found as follows:
Galactose(110) >
Glucose (100) > Fructose (43) > Manose (19) > Xylose (15) > Arabinose
(9)
The above study
proves that glucose and galactose are absorbed very fast; fructose and mannose
intermediate rate and the pentoses are absorbed slowly. Galactose is absorbed
more rapidly than glucose.
Mechanisms Of Absorption
Two mechanisms
are suggested:
1. Simple diffusion: This is dependent on sugar concentration gradients between the intestinal lumen, mucosal cells and blood plasma. All the monosaccharides are probably absorbed to some extent by simple ‘passive’ diffusion.
2. “Active” Transport Mechanisms
• Glucose and
galactose are absorbed very rapidly and hence it has been suggested that they
are absorbed actively and it requires energy.
• Fructose
absorption is also rapid but not so much as compared to glucose and galactose,
but it is definitely faster than pentoses. Hence fructose is not absorbed by
simple diffusion alone and it is suggested that some mechanism facilitates its
transport, called as facilitated transport.
Wilson and Crane’s Hypothesis of Active Transport :Wilson and Crane have shown that sugars which are ‘actively’ transported have several chemical features in common. They suggested that to be actively transported sugar must have the following:
1:They must
have a six-membered ring,
2:Secondly, they must have one or more carbon atoms attached to C 5
3:Thirdly, they
must have a –OH group at C-2 with the same stereo configuration as occurs in
D-glucose. –OH group and 5 hydroxymethyl or methyl group on the pyranose ring
appear to be essential structural requirements for the active transport
mechanism.
Energy: It is provided by ATP, by the interaction of the sodium dependent sugar carrier and the sodium pumps, actively transported sugars are concentrated within the cell without any back leakage of the sugar into the lumen.
It is believed that sodium binding by the carrier-protein is pre-requisite for glucose binding. Sodium binding changes the conformation of the protein molecule, enabling the binding of glucose to take place and thus the absorption to occur.
It is presumed that analogous “carrier protein” exists for D-galactose also. This is a cotransport system Glucose Transporters (GLUT) Several glucose transporters GLUT-1 to 7 have been described in various tissues
Evidences in
favour of the cotransport system of glucose absorption:
• The
dependence of the active transport of glucose upon the presence of sodium ions
has been demonstrated in isolated loops of rat intestine by replacing the
sodium of bathing fluid by K+ and lithium. Under these circumstances, the rate
of glucose transport is markedly reduced and ultimately stopped.
• Drugs such as
strophanthin and ouabain which inhibit sodium pump also inhibit active
transport of sugars.
• Substances
preventing the liberation of metabolic energy, such as dinitrophenol (DNP),
also inhibits active transport of sugars.
• Phloridzin, a
glycoside inhibits glucose transport by probably displacing sodium from its
binding site, as a result glucose cannot be bound and transported.
Absorption of
Other Sugars
• Sugars like
D-fructose and D-mannose are probably absorbed by facilitated transport which
requires the presence of carrier protein but does not require energy.
• Other sugars
like pentoses and L-isomers of glucose and galactose are absorbed passively by
simple diffusion. Facilitated Transport Vs Active Transport Similarities
• Both appear
to involve carrier proteins.
• Both show
specificity.
• Both resemble
a substrate-enzyme type of reaction.
• Both have
specific binding sites for solutes.
• ‘Carrier’ is
saturable so it has maximum rate of transport.
• There is a
binding constant for solute.
• Structurally
similar competitive inhibitors block transport. Differences
• Facilitated
transport can act bi-directionally, whereas active transport is unidirectional.
• Active
transport always occurs against an electrical or chemical gradient and hence
requires energy. Facilitated transport does not require energy. Mechanism of
Facilitated Transport Ping-Pong’ mechanism explains facilitated transport.
• Carrier
Protein exists in two principal conformations depending on the solute
concentration. Two forms are: – Pong state, and – Ping state.
• In the Pong
state, it is exposed to high concentrations of solutes, and molecules of
solutes bind to specific sites on the ‘carrier protein’. This occurs in lipid
bilayer of the cell with high solute concentration.
• In inner
side, a conformational change occurs to Ping state and the solute is discharged
to the side favouring new equilibrium.
• The empty
carrier protein then reverts to the original conformation “Pong” state to
complete the cycle. Factors determining facilitated transport: Rate at which
solutes enter a cell by facilitated transport is determined by the following
factors:
• Concentration
gradient across the membrane.
• The amount of
“Carrier protein” available (key control system).
• Rapidity of
solute-carrier interaction.
• Rapidity of conversion of conformation state from ‘Pong’ to ‘Ping’ and vice versa.
Factors Influencing Rate of Absorption
1. State of mucous membrane and length of time of contact:
If mucous membrane is not healthy, absorption will suffer.
Similarly in hurried bowel, length of contact is less and as such absorption
will be less.
2. Hormones
• Thyroid
hormones: These increase absorption of hexoses and act directly on intestinal
mucosa.
• Adrenal
cortex: Absorption decreases in adrenocortical deficiency, mainly due to
decreased concentration of sodium in body fluids
• Anterior
pituitary: This affects absorption mainly through its influence on thyroids.
Hyperpituitarism induces thyroid overactivity and vice versa.
• Insulin: This
has no effect on absorption of glucose.
3. Vitamins:
Absorption is
diminished in states of deficiency of B-vitamins, viz, thiamine, pyridoxine and
pantothenic acid.
4. Inherited enzyme deficiencies:
Inherited
enzyme deficiencies like sucrase and lactase can interfere with hydrolysis of
corresponding disaccharides and their absorption.
Clinical Aspect
Defects In Digestion And Absorption Of Carbohydrates (including inherited
disorders)
1. Lactase
Deficiency
Some infants
may have deficiency of the enzyme lactase and they show intolerance to lactose,
the sugar of milk. Symptoms and signs seen in affected infants include:
• Diarrhea and
flatulence
• Abdominal
cramps
• Distension.
Explanation: The above features are explained as follows:
• As lactose of
milk cannot be hydrolyzed due to deficiency of lactase enzyme, there occurs
accumulation of lactose in intestinal tract, which is osmotically active and
holds water, producing diarrhea.
• Accumulated
lactose is also fermented by intestinal bacteria which produce gas and other
products, producing flatulence, distension and abdominal cramps. Types: Lactase
deficiency can be of 3 types. Inherited Lactase Deficiency
• Rare disorder
• Symptoms of
intolerance to milk such as diarrhea and wasting incident to fluid and
electrolyte disturbances as well as inadequate nutrition, all develop very soon
after birth • Urine: Presence of lactose in urine is a prominent feature
(lactosuria)
• Treatment: Feeding of lactose-free diet results in disappearance of the
symptoms and marked improvement.
Low Lactase Activity
a. Primary low lactase activity: It is relatively a common syndrome. It is seen particularly among non-white population in USA as well as other parts of the world specially South East Asia including India.
Intolerance to lactose is not a feature in
early life and appears later in life. It is presumed to represent a gradual
decline in the activity of the enzyme lactase in susceptible individuals.
b. Secondary
low lactase deficiency: This is secondary to many GI conditions prevalent in
tropics and non-tropical countries like:
• Tropical and
nontropical sprue (Celiac disease)
• Kwashiorkor
• Colitis and chronic gastroenteritis Also can occur after surgery of peptic ulcer.
2.
Sucrase Deficiency Inherited deficiency of sucrase and isomaltase have been
reported. Symptoms occur in early childhood with ingestion of sugars (cane
sugar and table sugar) sucrose, a disaccharide. Symptoms and signs as in
lactase deficiency.
3.
Disacchariduria An increase in the excretion of disaccharides may be observed
in some patients with disaccharidase deficiency. As much as 300 mg or more of
disaccharides may be excreted in those people and in patients with intestinal
damage (e.g. sprue and celiac disease).
4.
Monosaccharide Malabsorption Inherited disorders in which glucose and/or
galactose are absorbed very slowly have been reported. The reason probably is
absence of “carrier protein” necessary for absorption of
glucose/galactose.
Give your opinion if have any.