DIGESTION & ABSORPTION OF CARBOHYDRATE

1. CONTENTS
DIGESTION OF
CARBOHYDRATE
ABSORPTION OF
CARBOHYDRATE
CLINICAL
SIGNIFICANCE
DR SAKINA MBBS,M.D

2. Biological Importance
Food
large molecules small molecules
Digestion
small molecules
Absorption
vitamins,
minerals,
monosaccharides
and
free amino acids
BLOOD

3. Carbohydrates present in the
diet
Polysaccharides
Disaccharides Monosaccharides
Starch
Glycogen
Lactose
Maltose
Sucrose
Glucose
Fructose
Pentose
In GIT, all complex carbohydrates are
converted to simpler monosaccharide
form which is the absorbable form.

4. Details of digestion of carbohydrates
2 Types of enzymes are important for the digestion
of carbohydrates
Amylases Disaccharidases
convert polysaccharides to
disaccharides
Salivary
Amylase
Pancreatic
Amylase
Convert disaccharides to
monosaccharides which
are finally absorbed
Maltase
Sucrase-Isomaltase
Lactase
Trehalase

5. Digestion
in mouth
Digestion
in stomach
Digestion
in small
intestine

6. 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.

7. 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.

8. Starch, Glycogen and dextrins
(Large polysaccharide molecules)
α- Amylase
Glucose,Maltose and Maltotriose.
(Smaller molecules)

9. Drawback
 Shorter duration of food in mouth.
 Thus it is incomplete digestion of starch or glycogen
in the mouth

10. Digestion in the Stomach
 There is no enzyme to break the glycosidic bonds in
gastric juice.
 However, HCl present in the stomach causes
hydrolysis of sucrose to fructose and glucose.
HCl
Sucrose Fructose + Glucose

11. Digestion in Duodenum
 Food bolus reaches the duodenum from the stomach
where it meets the pancreatic juice.
 Pancreatic juice contains a carbohydrate splitting
enzyme,
pancreatic amylase
(amylopsin) similar
to salivary amylase.

12. Action of pancreatic amylase
 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).

13. Reaction catalyzed by pancreatic amylase
Starch/Glycogen
Pancreatic
Amylase
Maltose/ Isomaltose
+
Dextrins and
oligosaccharides

14. 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.

15. 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.
 The different disaccharidases are :
1) Maltase,
2) Sucrase-Isomaltase (a bifunctional enzyme catalyzing
hydrolysis of sucrose and isomaltose)
3) Lactase

16. Reactions catalyzed by Disaccharidases
Maltase
 Maltose Glucose + Glucose
Sucrase Isomaltase
 Sucrose Isomaltose 3Glucose + fructose
Lactase
 Lactose Glucose + Galactose

17. Clinical significance of Digestion
 Lactose intolerance is the inability to
digest lactose due to the deficiency of
Lactase enzyme.
 Causes
Congenital Acquired during lifetime
Primary Secondary

18. 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.

19. Primary Lactase deficiency
 Primary lactase deficiency develops over time
 There is no congenital absence of lactase but the
deficiency is precipitated during adulthood.
 The gene for lactose is normally expressed upto RNA
level but it is not translated to form enzyme.
 It is very common in Asian population.
 There is intolerance to milk + dairy products.

20. Secondary lactase deficiency
 It may develop in a person with a healthy small intestine
during episodes of acute illness.
 occurs because of mucosal damage or from medications
resulting from certain gastrointestinal diseases,
 common cause of temporary lactose intolerance is
gastroenteritis, particularly when the gastroenteritis is
caused by rotavirus.
 Secondary lactase deficiency also results from injury to
the small intestine that occurs with celiac disease,
Crohn’s disease, or chemotherapy.

21. Clinical manifestations
 In the form of abdominal cramps, distensions, diarrhea, constipation,
flatulence upon ingestion of milk or dairy products
Biochemical basis
 Undigested lactose in
intestinal lumen is
acted upon by bacteria
and is converted to
CO2 , H2 , 2 carbon
compounds and 3 carbon
compounds or it may
remain undigested.

22.  CO2 and H2 causes Distensions and flatulence
 Lactose + 2C + 3C are osmotically active.
 They withdraw H2O from intestinal mucosal cell and
cause osmotic diarrhea or constipation because of
undigested bulk.
Abdominal distension Flatulence

23. Diagnosis
 Two tests are commonly used: -
 Hydrogen Breath Test
 The person drinks a lactose-loaded
beverage and then the breath is
analyzed at regular intervals to
measure the amount of hydrogen.
Normally, very little hydrogen is
detectable in the breath, but
undigested lactose produces high
levels of hydrogen. The test takes
about 2 to 3 hours.

24.  Stool Acidity Test
 The stool acidity test is used for infants
and young children to measure the
amount of acid in the stool. Undigested
lactose creates lactic acid and other short
chain fatty acids that can be detected in
a stool sample. Glucose may also be
present in the stool as a result of
undigested lactose.
 Besides these tests, urine shows- positive
test with Benedict’s test, since
lactose is a reducing sugar and a small
amount of lactose is absorbed in the
intestinal cell by pinocytosis and is
rapidly eliminated through kidneys in to
urine.(Lactosuria)
 Mucosal biopsy confirms the diagnosis.

25. Sucrase-Isomaltase deficiency
 These 2 enzymes are synthesized on a single polypeptide chain,hence ,
their deficiencies coexist.
 Signs and symptoms
 Same as that of lactose intolerance.
 Urine does not give +ve test with Benedict’s test because of sucrose(Non
reducing sugar).
 History confirms the diagnosis.
 Most confirmatory test is mucosal
biopsy.

26. Absorption of
carbohydrates
3 mechanisms
Passive
diffusion
Facilitated
diffusion/Carrier
mediated
Active
transport

27. Features Passive diffusion Facilitated
diffusion
Active transport
Concentration
gradient
Down the
concentration
gradient from high
to low.
Down the
concentration
gradient from high
to low.
Against a
concentration
gradient from low
to high
Energy
expenditure
none none Energy expenditure
is in the form of ATP
Carrier protein/
transporter
Not required required required
Speed Slowest mode Fast Fastest mode
Note: Glucose is a polar molecule. It
cannot pass through lipid bilayer of
cell.

28. Glucose transporters
Glucose transporters
Na+ dependent
transporter
Na+ independent
transporter
2 types
Also called Also
SGLT GLUT
called

29. Absorption of
Monosaccharides
The major monosaccharides
resulting from carbohydrate digestion are –
 D-glucose,
 D-galactose and
 D-fructose.
Absorption is
carrier mediated.
 Pentoses are absorbed by
simple diffusion.
 Monosaccharides are first transported
from the lumen to the small intestinal epithelial cells
and then into capillaries of portal venous system.

30. Absorption of Glucose
from the small intestinal lumen
by carrier mediated mechanism
involving transporter proteins
1) Na+-dependent transporter
by secondary active transport
and to a less extent by
2) Na+-independent transporter
by passive transport
into the intestinal epithelial cells

31. Absorption of Glucose
facilitated transport secondary active transport
Intestinal
Epithelial Cell
Glucose
Glucose
Glucose
GLUT-5
Intestinal Lumen
Na+
Na+-dependent transporter
(SGLT)
Na+ K+
Na+
K+
GLUT-2
Portal Capillary Blood
ATP
ADP + Pi
Na+–K+ ATPase

32. Absorption of Glucose
Galactose
GLUT-5
Na+
Na+-dependent transporter
(SGLT)
Na+ K+
Na+
K+
GLUT-2
ATP
ADP + Pi
Na+–K+ ATPase
Galactose
Fructose
Fructose
Galactose
Fructose

33. Factors affecting rate of absorption of
Monosaccharides
 The absorption is faster through intact mucosa.
The absorption is decreased if there is some
inflammation or injury to the mucosa.
 Thyroid hormones ↑ the rate of absorption of
glucose.
 Mineralocorticoid,i.e Aldosterone ↑ the rate of
absorption.

34.  Vitamin B6,B12, pantothenic acid, folic acid are
required for absorption of glucose.
With advancing age, rate of absorption declines.

35. 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.

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