This document provides information about the digestion and absorption of carbohydrates and their clinical significance. It discusses how carbohydrates are digested by amylases in the mouth, stomach, and small intestine. Disaccharides are further broken down by disaccharidases in the small intestine. The monosaccharides glucose, fructose, and galactose are then absorbed into the bloodstream, primarily through sodium-dependent and sodium-independent glucose transporters. Clinical conditions like lactose intolerance result from deficiencies in disaccharidases like lactase. Overall, the document outlines the multi-step process of carbohydrate digestion and absorption and its implications for health.

1. Student’s Corner
Selected for publication
Biochemistry For Medics
www.namrata.co

2. Topic:
Digestion and Absorption
of carbohydrates with
clinical significance.
Presented by : THOSADU RAMDU Pooja.
Roll no. : 102.

3. CONTENTS
Digestion of
carbohydrates
Absorption of
carbohydrates
Clinical significance

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

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

6. Digestion in
mouth
Digestion in
stomach
Digestion
in small
intestine

7. 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.

8. 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.

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

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

11. 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

12. 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.

13. 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).

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

15. 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.

16. 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

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

18. 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

19. 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.

20. Baby with Lactose Intolerance

21. 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.

22. Adult with lactose intolerance

23. Secondary lactase deficiency
• It may develop in a person with a healthy small intestine during
episodes of acute illness.
• This occurs because of mucosal damage or from medications
resulting from certain gastrointestinal diseases, including
exposure to intestinal parasites such as Giardia lamblia.
• In such cases the production of lactase may be permanently
disrupted.
• A very common cause of temporary lactose intolerance is
gastroenteritis, particularly when the gastroenteritis is caused
by rotavirus.
• Another form of temporary lactose intolerance is lactose
overload in infants. Secondary lactase deficiency also results
from injury to the small intestine that occurs with celiac
disease, Crohn’s disease, or chemotherapy.
• This type of lactase deficiency can occur at any age but is more
common in infancy.

24. Intestinal parasite Rotavirus
(Giardia lamblia)

25. Clinical manifestations
• In the form of abdominal
cramps, distensions, diarrhea, constipation, flatulenc
e 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.

26. • 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

27. 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.

28. • 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.

29. Management of lactose intolerance
• Avoidance of dairy products.
• Although the body’s ability to produce lactase
cannot be changed, the symptoms of lactose
intolerance can be managed with dietary changes.
• Most people with lactose intolerance can tolerate
some amount of lactose in their diet. Gradually
introducing small amounts of milk or milk products
may help some people adapt to them with fewer
symptoms.
• Partly digested dairy products can also be given.

30. • Lactose-free, lactose-reduced milk,
Soy milk and other products may be
recommended.
• Lactase enzyme drops or tablets(Yeast tablets)
can also be consumed.
• Getting enough calcium is important for people
with lactose intolerance when the intake of milk
and milk products is limited.
• A balanced diet that provides an adequate
amount of nutrients—including calcium
and vitamin D—and minimizes discomfort is to
be planned for the patients of lactose
intolerance.

31. 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.

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

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

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

35. 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

36. 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.

37. 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.

38. 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

39. 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.

40. • 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.

41. 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.

42. Location of GLUT 2 and GLUT 5 in intestine

43. Diagram showing absorption of
monosaccharides

44. Purpose of GLUT 5 and GLUT 2
>Mainly responsible for pouring all the
> For the transportation of
absorbed glucose into blood.
fructose.(least affinity for glucose).
>GLUT 2 transporter transports all
>Fructose is mainly transported by
absorbed glucose to blood. It is down a
facilitated diffusion.
concentration gradient.
>By GLUT 5, fructose moves down the
>Transporter is present but there is no
gradient and the process is faster than
energy expenditure.
passive diffusion.
>Pentoses are absorbed by passive
>Energy is not consumed.
diffusion which is a very slow process.

45. 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.

46. • Vitamin B6,B12, pantothenic acid, folic acid are
required for absorption of glucose.
• With advancing age, rate of absorption declines.
• Note: Insulin has no role in the absorption of
monosaccharide like glucose.

47. Uptake of glucose in peripheral cells
• Mechanism: facilitated diffusion.
• There are 7 important glucose transporter for
uptake of glucose into special cells.
• They have been numbered from 1 to 7 (GLUT
1 to GLUT 7).
• They are biologically important.

48. Tissue specific Tissue distribution Functions Clinical significance
glucose transporter
GLUT-1 Present in almost all Na-independent Cancer cells express
(great affinity for cells with an high level of GLUT-1,
glucose) abundance in RBC. so they can
internalize more of
glucose, which is
used as a source of
energy for rapidly
dividing cells.
GLUT-2 Present in intestine, Releases insulin by Diabetes Mellitus.
(low affinity for liver and pancreas. movement of glucose
glucose, it can into β-cells of
transport only when pancreas.
there is glucose load (Acts as a sensor for
in the body) the release of insulin
by pancreas.)
Promotes uptake of
glucose in liver cells,
lowering down blood
glucose.

49. GLUT 3 Brain cells, all other Cancer cells express
cells of body high level of GLUT-
3, so they can
internalize more of
glucose, which is
used as a source of
energy for rapidly
dividing cells
GLUT 4 Adipose tissue, The only
skeletal muscles, transporters which
cardiac muscles are under the
influence of insulin.
Insulin promotes
uptake of glucose in
the tissues by
mobilizing the
transporters to the
cell surface
whenever there is
high glucose
concentration in the
blood.

50. GLUT 5 Intestine at the Mainly for the
(least affinity for luminal surface, transport of fructose
glucose) testicles, seminal
vesicles
GLUT 6 Non-functional
transporter product of
a pseudogene.
No role in absorption
of glucose in
peripheral cells.
GLUT 7 Surface of Transportation of
endoplasmic glucose across the
reticulum membrane of
endoplasmic
reticulum.
SGLT 1 Kidney, intestine For the absorption of In cases where SGLT 1
glucose. is deficient, glucose is
left unabsorbed and is
excreted in faeces.
SGLT 2 Kidney For the re-absorption If deficient, filtered
of glucose. glucose is not re-
absorbed and is lost in
urine.

51. References
• www.namrata.co- Biochemistry for medics
• Lecture notes
• Sciencephotolibrary

52. Thank you for
your attention
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