Digestion and Absorption

Dr. Mir abdul munif

UIMS,PRAYAGRAJ
 introduction
Digestion and absorption are the ultimate functions
of the gastrointestinal tract.

Digestion is the chemical breakdown of ingested

foods into absorbable molecules.

The digestive enzymes are secreted in salivary, gastric,

and pancreatic juices and also are present on the
apical membrane of intestinal epithelial cells.
Absorption is the movement of nutrients, water,
and electrolytes from the lumen of the intestine
into the blood.

There are two paths for absorption, a cellular path

and a paracellular path.
In the cellular path, the substance must cross the
apical membrane, enter the intestinal epithelial
cell, and then be extruded from the cell across the
basolateral membrane into blood.

 Transporters in the apical and basolateral

membranes are responsible for the absorptive
processes.
In the paracellular path, substances move across
the tight junctions between intestinal epithelial
cells, through the lateral intercellular spaces, and
into the blood.
 CARBOHYDRATES

Carbohydrates constitute about 50% of the diet.

 Ingested carbohydrates are polysaccharides,

disaccharides (sucrose, lactose, maltose and
trehalose), and small amounts of monosaccharides
(glucose and fructose).
 Digestion of Carbohydrates
Only monosaccharides are absorbed by the
intestinal epithelial cells.

Therefore, to be absorbed, all ingested

carbohydrates must be digested to
monosaccharides: glucose, galactose, or fructose.

 Starch is first digested to disaccharides, and then

disaccharides are digested to monosaccharides.
Digestion of starch begins with α-amylase.

 Salivary amylase starts the process of starch

digestion in the mouth.

 Pancreatic amylase digests 1,4-glycosidic bonds

in starch, yielding three disaccharides, α-limit
dextrins, maltose, and maltotriose.
These disaccharides are further digested to
monosaccharides by the intestinal brush-border
enzymes, α-dextrinase, maltase, and sucrase.

The product of each of these final digestive steps is

glucose.

So there are three end products of carbohydrate

digestion: glucose, galactose, and fructose; each is
absorbable by intestinal epithelial cells
 Absorption of Carbohydrates

Glucose and galactose are absorbed by

mechanisms involving Na+-dependent cotransport.

Fructose is absorbed by facilitated diffusion

Glucose and galactose are absorbed across the
apical membrane by secondary active transport
mechanisms.

Glucose and galactose are actively taken up by the

brush border epithelial cells by a transport protein
called SGLT1.

 SGLT1 uses the energy of the Na+ gradient to

actively transport glucose and galactose into the
intestinal epithelial cells.
The active entry of glucose and galactose into the
intestinal epithelial cells is stimulated by the
presence of Na+ in the lumen.

Similarly, the entry of Na+ into the epithelial cell

across the brush border membrane is stimulated
by glucose or galactose in the lumen.
SGLT1 transports two Na+ ions and one glucose or
galactose molecule across the brush border
membrane.

The electrochemical potential gradient for Na+ is

created by Na+-K+ATPase pumps present in the
basolateral plasma membranes of the intestinal
epithelial cells.
Glucose and galactose leave the intestinal
epithelial cell at the basal and lateral plasma
membranes via facilitated transport, and they then
diffuse into the mucosal capillaries.

The transport protein responsible for efflux of

glucose and galactose across the basolateral
membrane is GLUT2.
Fructose is transported across both the apical and
basolateral membranes by facilitated diffusion;

In the apical membrane, the fructose-specific

transporter is called GLUT 5, and in the basolateral
membrane, fructose is transported by GLUT 2.
Factors affecting rate of glucose absorption from
the intestine
State of mucous membrane:
-in enteritis and coeliac disease: absorption
decreases

Duration of contact of carbohydrate with mucous

membrane:
-diarrhoea,excision of small intestine,gastro-colic
fistula: absorption decreases.
Thyroid hormone: thyroxine acting directly on
intestinal mucosa,increases the absorption.

Anterior pituitary: by influencing thyroid

Adrenal cortex defeciency: decreased aldosterone

Insulin: no effect on absorption.

 Carbohydrate Malabsorption Syndromes

Malabsorption of carbohydrates is usually caused

by a deficiency in one of the oligosaccharidases of
the brush border.
Lactose intolerance, which is caused by lactase
deficiency.

 In this disorder, the brush-border lactase is

deficient or lacking, and lactose is not digested to
glucose and galactose.
If lactose is ingested in milk or milk products, the
lactose remains undigested in the lumen of the
intestine.

 Lactose is nonabsorbable, holds water in the

lumen, and causes osmotic diarrhea.
Persons with lactose intolerance either may avoid
ingesting milk products or may ingest milk
products supplemented with lactase .
Glucose-galactose malabsorption syndrome is
a very rare hereditary disorder caused by a
missense mutation in SGLT1.
PROTEINS
Dietary proteins are digested to absorbable forms
(i.e., amino acids, dipeptides, and tripeptides) by
proteases in the stomach and small intestine .

 The proteins contained in gastrointestinal

secretions and proteins in exfoliated epithelial
cells are similarly digested and absorbed.

In humans, ingested protein is almost completely

absorbed by the time the meal has traversed the
jejunum.
Digestion of Proteins
Digestion of protein begins in the stomach with
the action of pepsin and is completed in the small
intestine with pancreatic and brush-border
proteases.

 The two classes of proteases are endopeptidases

and exopeptidases.
Endopeptidases hydrolyze the interior peptide
bonds of proteins.

The endopeptidases of the gastrointestinal tract

are pepsin, trypsin, chymotrypsin, and elastase.

Exopeptidases hydrolyze one amino acid at a

time from the C-terminal ends of proteins and
peptides.

 The exopeptidases of the gastrointestinal tract are

carboxypeptidases A and B.
protein digestion begins with the action of pepsin
in the stomach.

 There are three isozymes of pepsin, each of which

has a pH optimum ranging between pH 1 and 3;
above pH 5, pepsin is denatured and inactivated.

its actions are terminated in the duodenum, where

pancreatic HCO3- secretions neutralize gastric H+
and increase the pH.
The first step in intestinal protein digestion is the
activation of trypsinogen to its active form,
trypsin, by the brush-border enzyme
enterokinase.

Initially, a small amount of trypsin is produced,

which then catalyzes the conversion of all of the
other inactive precursors to their active enzymes.

 Even the remaining trypsinogen is autocatalyzed

by trypsin to form more trypsin.
Absorption of Proteins

The products of protein digestion are amino acids,

dipeptides, and tripeptides.

Each form can be absorbed by intestinal epithelial

cells.
The L-amino acids are absorbed by mechanisms
analogous to those for monosaccharide
absorption.

 The amino acids are transported from the lumen

into the cell by Na+-amino acid cotransporters in
the apical membrane, energized by the Na+
gradient.
There are four separate cotransporters: one each
for neutral, acidic, basic, and imino amino acids.

 The amino acids then are transported across the

basolateral membrane into the blood by facilitated
diffusion.
Disorders of Protein Digestion and
Absorption

Disorders of protein digestion or absorption occur

when there is a deficiency of pancreatic enzymes
or when there is a defect in the transporters of the
intestinal epithelial cells.
 chronic pancreatitis and cystic fibrosis:

There is a deficiency of all pancreatic enzymes,

including the proteases. Dietary protein cannot be
absorbed .

The absence of trypsin alone is very critical, since

trypsin is necessary for the activation of all
precursor enzymes to their active forms.
 Trypsinogen deficiency :

A rare congenital abnormality.

 Infants with this disease fail to thrive and have

low levels of plasma protein.

 Feeding partially hydrolyzed protein is effective

therapy.
Several diseases are caused by a defect in or
absence of an Na+-amino acid cotransporter.

 Cystinuria is a genetic disorder in which the

transporter for the dibasic amino acids cystine,
lysine, arginine, and ornithine is absent in both
the small intestine and the kidney.
As a result of this deficiency, none of these amino
acids is absorbed by the intestine or reabsorbed by
the kidney.

 The intestinal defect results in failure to absorb the

amino acids, which are excreted in feces.

The renal defect results in increased excretion of

these specific amino acids and gives the disease its
name, cystinuria .
Thank u