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.

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