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Absorption of
carbohydrates
Clinical significance
Carbohydrates present in the
diet
Disaccharides Monosaccharides
Polysaccharides
Amylases Disaccharidases
Convert disaccharides to
convert polysaccharides to disaccharides
monosaccharides which are
finally absorbed
Salivary Maltase
Amylase
Sucrase-Isomaltase
Pancreatic
Amylase Lactase
Trehalase
Digestion in
mouth
Digestion in
stomach
Digestion
in small
intestine
Digestion in the Mouth
Digestion of Carbohydrate starts in the
mouth, upon contact with saliva during mastication.
Saliva contains a carbohydrate splitting enzyme called
salivary amylase , also known as ptylin.
Action of ptylin (salivary
amylase)
• Location: mouth
• It is α-amylase and requires Cl− ion for
activation with an optimum pH of 6.7 (Range
6.6 to 6.8).
• The enzyme hydrolyses α-1→ 4 glycosidic
linkages deep inside polysaccharide
molecules.
• However, ptylin action stops in the stomach
when the pH falls to 3.0.
Starch, Glycogen and dextrins
(Large polysaccharide molecules)
α- Amylase
HCl
Sucrose Fructose + Glucose
Digestion in Duodenum
• It is an α- Amylase
• Optimum pH=7.1
• Like ptylin, it requires Cl− ion for its activity.
• It hydrolyses α-1→ 4 glycosidic linkages
situated well inside polysaccharide molecules.
• Note: Pancreatic amylase, an isoenzyme of salivary
amylase, differs only in the optimum pH of action. Both
the enzymes require Chloride ions for their actions (Ion
activated enzymes).
Reaction catalyzed by pancreatic amylase
Starch/Glycogen
Pancreatic
Amylase
Maltose/ Isomaltose
+
Dextrins and
oligosaccharides
Digestion in Small Intestine
Note:
• Main digestion takes place in the small
intestine by pancreatic amylase
• Digestion is completed by pancreatic amylase
because food stays for a longer time in the
intestine.
What are Disaccharidases?
• They are present in the brush border epithelium of
intestinal mucosal cells where the resultant
monosaccharides and others arising from the diet
are absorbed.
Lactase
• Lactose Glucose + Galactose
Clinical significance of Digestion
• Lactose intolerance is the inability to digest
lactose due to the deficiency of Lactase
enzyme.
• Causes
Primary Secondary
Congenital Lactose intolerance
• It is a congenital disorder
• There is complete absence or deficiency of
lactase enzyme.
• The child develops intolerance to lactose
immediately after birth.
• It is diagnosed in early infancy.
• Milk feed precipitates symptoms.
Baby with Lactose Intolerance
Primary Lactase deficiency
3 mechanisms
Na+
2 types Na+ independent
dependent transporter
transporter
Also called Also called
SGLT GLUT
Na+ dependent transporter
• Type of co-transport
• 2 binding sites on the transporter, one for Na+ and other
for glucose.
• Na + binding is important because after Na +
binding, conformational changes occurs so that glucose
can bind.
• Na + is transported across cell membrane, down the
concentration gradient and glucose goes against a
concentration gradient.
• ATP is spent at the level of Na-K ATPase pump to expel
Na out.
• Both glucose and galactose are absorbed by a sodium-
dependent process.
• They are carried by the same transport protein (SGLT
Figure- Showing the co transport of Glucose, mediated by SGLT-
1/2. SGLT-1 are present on the intestinal cells while SGLT-2
are present on the proximal renal tubular cells.
3 reasons for expulsion of sodium
1) Na + is osmotically active, causes osmotic
flow to cells, leading to osmolysis.
2) Na + concentration has to be kept minimal to
maintain the downward gradient.
3) Na + is inhibitory to many enzyme actions.
Energy released is
Solvent Downward captured for transport of
gradient of glucose against a conc.
drag Na+ Gradient.
releases
absorption energy
Na expelled
This type of
out through
absorption
Na-K
is called
ATPase
solvent drag
pump.
Energy is
consumed
at the level
of ATP
Water 3 sodium
carries are expelled
dissolved out and 2 K
glucose with are
it internalised
The Na removed
to paracellular
spaces exerts
osmotic pressure
that causes flow of
water to
intracellular
spaces
Clinical significance
• In deficiency of SGLT- 1, glucose is left
unabsorbed and is excreted in feces.
Galactose is also malabsorbed.
• In deficiency of SGLT- 2, the filtered glucose is
not reabsorbed back, it is lost in urine, causing
glycosuria.
• Solvent drag is not the main mechanism of
glucose absorption but is important after a
carbohydrate rich diet.
• Absorption of galactose is faster than glucose.
• In kidney, reabsorption of filtered glucose
takes place by a similar mechanism, i.e, it is
also a co-transport with Na. The transporter is
SGLT- 2.
• In intestine, it is SGLT- 1.
Na+ independent transporters
• Used for facilitated transport.
• These transporters are numbered from 1 to
14 GLUT.
• In the intestine, GLUT 2 are present towards
the serosal surface of intestinal epithelial
cells and GLUT 5 are present towards the
luminal surface.
Location of GLUT 2 and GLUT 5 in intestine
Diagram showing absorption of
monosaccharides
Purpose of GLUT 5 and GLUT 2