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Presented by :

Osama Sharafeddin

MBBS U of K

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Introduction :

There is no or little absorption in the stomach

; except for short & medium chain F.A andEthanol .

Small intestine is the main absorptive organ ;

90% .

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The contents change gradually from fluid to

semisolid state due to absorption of water

which starts in small intestine & continue incolon.

Amino acid &Carbohydrates are water

soluble; they are transported in the hepaticportal system.

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Products of digestion are : monosaccharides

;chiefly hexoses (Glucose , fructose, Galactose )

and pentoses (ribose) . Some oligo and disaccharides are hydrolysed

to monosaccharides in the mucosal surface ofsmall intestinal epithelium , by pancreatic

amylase &disaccharidases .

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Two main mechanisms of absorption :

1-facilitative transport ; with the gradient

2- active transport ; against the gradient .

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Glucose and other hexoses could be

transported by facilitative transporters

GLUTs ; mainly GLUT5 in the intestine ,GLUT2also participate in release of hexoses

into the capillaries. Fructose uses GLUT5 ,

but more slowly than glucose and galactose .

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Via the SGLT1 transporter ,Glucose is actively

transported against gradient ,coupled with

Sodium ; the former against the gradient andthe latter with the gradient .

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the energy required for this process is

obtained from ATP hydrolysis linked to a

pump that expels Sodium in exchange forPotassium .

This transporter is inhibited by Oubain , acardiac glycoside; and Phlorhizin in the renal

tubules.

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As an adaptive mechanism for increased

Carbohydrates in the diet , there is an

increase in the number of transporters in thebrush border .

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1- Lactose intolerance

may be attributable to lactase deficiency,

which is a rate limiting enzyme for Lactoseabsorption .

It should not be confused with milk

intolerance ; a sensitivity condition to milkprotein , usually -lactoglobulin .

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a- Inherited Lactase deficiency : rare ;

symptoms appear after birth ; management

by feeding lactose free diet , yoghurt feeding, Calcium supplementation and energy.

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b- Primary low lactase deficiency: relatively

common particularly among non whites;

gradual decrease of lactase action due todecreased expression .(failure of translation) .

c- Secondary low lactase activity : aconsequence of intestinal disease s: Tropical

sprue , kwashiorkor ,colitis, G.E, after surgeryof peptic ulcer .

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2-Sucrase deficiency :

both sucrase and isomaltase are deficient ;they coexist as a complex enzyme ;

symptoms appear from early childhood .

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3- Disacchariduria :

due to disaccharidase deficiency; more than300 mg of disaccharides appear in urine ; also

occur in patients with intestinal damage .

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4- monosaccharide malabsorption :

a- Mutation in SGLT1: slow glucose andgalactose absorption ; normal fructoseabsorption .

b- Fructose Sorbitol malabsorption .

Symptoms : diarrhea , flatulence , abdominalcramps .

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Products of protein digestion are absorbed as

individual amino acids .

Some dipeptides are hydrolyzed in theintestinal brush border .

A.A absorption is an energy dependentprocess; including carriers depending on a

mechanism similar to SGLT1 (coupled toNa+).

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Some carriers are specialized in Neutral a.a ;

others in Phe & Met ; and a special carrier for

Imino acids Pro & Hyp.

Na+ independent carriers include :

Neutral and lipophilic a.a carriers e.g Phe ,Leu

Cationic a.a e.g Lys .

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Large intestinal bacteria can form toxic

amines from amino acids by decarboxylation;

known as Ptomaines , some examples ofptomaines are:

Cadaverine LysAgmatine Arg

Tyramine TyrPutrescine Orn

Histamine His

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There is some evidence that some

protein fragments larger than amino

acids are absorbed in some conditions ;the situation which can lead to an

antigenic reaction .

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An example for the above theory is non

tropical sprue ; a disease characterized

by circulating antibodies to wheatgluten or its fractions , the harmful

molecule is a six or seven amino acid

particle .

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Thanks!