digestion & absorption of carbohydrate
DESCRIPTION
DIGESTION & ABSORPTION OF CARBOHYDRATETRANSCRIPT
CONTENTS
DIGESTION OF CARBOHYDRAT
EABSORPTION
OF CARBOHYDRAT
ECLINICAL
SIGNIFICANCE
DR SAKINA MBBS,M.D
Biological Importance
large molecules
small molecules
small molecules
Food
Digestion
Absorption
vitamins, minerals, monosaccharides and free amino acids
BLOOD
Digestion and absorption of carbohydrates
Carbohydrates present in the diet
Polysaccharides
Disaccharides
Monosaccharides
StarchGlycogen
LactoseMaltoseSucrose
GlucoseFructosePentose
In GIT, all complex carbohydrates are converted to simpler monosaccharide form which is the absorbable form.
Details of digestion of carbohydrates
2 Types of enzymes are important for the digestion of carbohydrates
Amylases Disaccharidases
Salivary Amylase
Pancreatic Amylase
convert polysaccharides to disaccharides
Convert disaccharides to monosaccharides which are finally absorbedMaltase
Sucrase-Isomaltase
Lactase
Trehalase
Digestion in
mouth
Digestion in stoma
ch
Digestion in
small intestine
DIGESTION OF CARBOHYDRATES
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.
Digestion in the Mouth
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
Glucose,Maltose and Maltotriose.
(Smaller molecules)
Drawback
Shorter duration of food in mouth.
Thus it is incomplete digestion of starch or glycogen in the mouth
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.
Sucrose Fructose + Glucose
HCl
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.
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).
Reaction catalyzed by pancreatic amylase
Starch/Glycogen
Maltose/ Isomaltose +Dextrins and
oligosaccharides
Pancreatic Amylase
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.
The different disaccharidases are :
1) Maltase,2) Sucrase-Isomaltase (a bifunctional enzyme
catalyzing hydrolysis of sucrose and isomaltose)
3) Lactase
Reactions catalyzed by Disaccharidases
Maltose Glucose + Glucose
Sucrose Isomaltose 3Glucose + fructose
Lactose Glucose + Galactose
Maltase
Sucrase Isomaltase
Lactase
Clinical significance of Digestion
Lactose intolerance is the inability to digest lactose due to the deficiency of Lactase enzyme.
Causes
CongenitalAcquired during lifetime
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.
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.
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.
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.
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
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.
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.
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.
Absorption of carbohydrates
3 mechanisms
Passive diffusion
Facilitated diffusion/Carrier mediated
Active transport
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.
Glucose transporters
Glucose transporters
Na+ dependent transporter
Na+ independent transporter
2 types
SGLT GLUT
Also called Also called
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.
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
Intestinal Epithelial Cell
Absorption of Glucose
Glucose
Glucose
Glucose
GLUT-5
Intestinal Lumen Na+
Na+
Na+ K+
K+
Na+-dependent transporter (SGLT)
GLUT-2
Portal Capillary Blood
ATP
Na+–K+ ATPase
ADP + Pi
secondary active transportfacilitated transport
Absorption of Glucose
Galactose
GLUT-5
Na+
Na+
Na+ K+
K+
Na+-dependent transporter (SGLT)
GLUT-2
ATP
Na+–K+ ATPase
ADP + Pi
Galactose
Galactose
Fructose
Fructose
Fructose
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.
Vitamin B6,B12, pantothenic acid, folic acid are required for absorption of glucose.
With advancing age, rate of absorption declines.
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.
THANK YOU