DIGESTION AND

ABSORPTION

DIGESTION 1
 INTRODUCTION
 DIGESTION IN THE MOUTH
 DIGESTION IN THE STOMACH
 DIGESTION IN THE INTESTINE
 PANCREATIC SECRETION
 INTESTINAL SECRETION
 ABSORPTION
 PUTREFACTION & FERMENTATION BY
BACTERIA IN THE LARGE INTESTINE
 CLINICAL ASPECT

DIGESTION 2
Foodstuff :
• Water
• Carbohydrate
• Lipid
• Vitamins
• Minerals

Undernutrition  impaired growth

defective immune systems
Reduced work capacity

- Excessive food  obesity, CVD, Cancer

- Deficiency  ill health

Most foodstuffs : unavailable absorbed

broken down  digestive process
DIGESTION 3
 HORMON
HORMON
BRAIN
MOUTH PAROTID
SALIVARY GLAN
FOOD
SUBLINGUAL
AND TRACHEA
SUBMANDIBULAR
SALIVARY GLANDS VOLUNTARY

INVOLUNTARY

LIVER
STOMACH
GALLBLADDER

PANCREAS

SMALL INTESTINE

LARGE INTESTINE

RECTUM ANUS
DIGESTION 5
⇛CARBOHYDRATE DIGESTION

Polysaccharides  oligo di  Mono  absorp

Blood glucose by carbohydrate test

Glycemic index :
Blood glucose by eq amount glucose

Fructose & alcohol sugar, sucrose  less absorbed 

glycemic index <<

⊞ Mouth : Saliva by salivary glands

⋙ lubricant for mastication & swallowing
⋙ vehicle for excretion : ethanol, morphine
iorganic ions, IgA
⋙ pH  6.8
DIGESTION 6
Physics
Chewing : divides food  surface area >> 
attacked enzyme >>

Chemist : (enzymes)
⋙ lingual lipase (produodenal)
⋙ amylase : Hydrolysis starch & glycogen
 maltose (disaccharides)
attach -(14) glycosidic bond
inactive at pH  4,0

DIGESTION 7
DIGESTION IN STOMACH

Gastric secretion :
 gastric juice (97 – 99% water)
 clear, pale yellow
 0.2 – 0.5 % HCl
 pH  1.0
 digestive enzymes : pepsin, rennin, lipase

DIGESTION 8
PARIETAL CELL :

- H+ (chloride shift)
- active process (H+-K+-ATPase)
- intrinsic factor (facilitate absorption
vitamin B12) from ileum

⇛ HCl  proteins denatured

⇛ low pH  destroying microorganisms

DIGESTION 9
DIGESTION 10
CHIEF CELLS :

1. PEPSINOGEN

- initiates protein digestion

- activated by H+, pepsin itself (autocatalysis)
- splits protein  polypeptides
(proteoses & pepton)
- endopeptidase
- specific for aromatic amino acids (Tyr)
dicarboxylic amino acids (Glu)

DIGESTION 11
2. RENNIN (absent in adult)
Rennin

Casein (milk) + calcium paracasein

Pepsin
Proteosa & pepton

3. LIPASE : produodenal
- low pH inactive, after feeding active
- pH optimum : 3.0 – 6.0
- hydrolyze lipid (short, medium &
unsaturated long fatty acids (exp. milk)
DIGESTION 12
DIGESTION 13
DIGESTION 14
DIGESTION 15
DIGESTION IN THE INTESTINE

Stomach content (chyme) :

- neutralized by alkaline (pancreatic & biliary)
- pepsin inactive

BILE : from liver  gallblader  duodenum

1. Emulsification
2. Neutralization
3. Excretion : bile acid & cholesterol, drugs, toxins,
bile pigments & inorganic (Cu, Zn, Hg)
DIGESTION 16
 PANCREATIC SECRETION
pH : alkaline (7.5 – 8.0 or higher)

 Enzymes :
1. Trypsin : basic amino acid
Activated : enteropeptidase/enterokinase, trypsin

2. Chymotrypsin : uncharged amino acid

(aromatic amino acid)
3. Elastase : broad specificity

Secreted : zymogen, activated by trypsin

endopeptidase
DIGESTION 17
DIGESTION 18
4. Exopeptidase :carboxypeptidase  AA

5. Amylase

6. Lipase : primary ester link

7. colipase

8. phospholipase A2

9. Cholesteryl ester hydrolase

10. Rnase, Dnase

DIGESTION 19
 Intestinal Intestinal Lymphatic
lumen epithelium vessels

Pancreatic lipase

TAG 1,2 DAG 2-MAG TAG

pancreatic 72%
lipase 2-MAG Chylo
Synthetase micron
FA Acyl-CoA TAG
ATP, CoA
isomerase
FA
1-MAG 6%
1-MAG Glycerol Glycerol
FA -3-P

Glycolysis
Glycerol DIGESTION
Glycerol
20

22%
INTESTINAL CELL SECRETION

1. Aminopeptidase : exopeptidase
2. Dipeptidase
3. Disaccharidase, oligosaccharidase, maltase
4. Sucrase-isomaltase complex : 16 bond
5. lactase
6. Trehalase
7. Phosphatase
8. Polynucleotidases : nucleic acid  nucleotides
9. Nucleosidases : nucleosides  free nitrogen base

+pentose phosphate
10. Phospholipase : phospholipids  glycerol, fatty
acid, phosphoric acid & bases 21
DIGESTION
PRODUCT OF DIGESTION

- Carbohydrate : monosaccharides
- Proteins : Amino acid
- TAG : fatty acids, glycerol, monoacylglycerols
- Nucleic acid : nucleobases, nucleosides,
pentoses

- Polysaccharides, lignin (dietary fiber) :

can’t be digested by mammalian enzymes 
as bulk residues
DIGESTION 22
ABSORPTION

- Stomach (short & medium chain fatty

acids, ethanol)
- Small intestine :  90% foodstuffs & water
- Large intestine : other water

DIGESTION 23
TRANSPORT : 2 PATHWAYS

1. Hepatic portal system :

directly to the liver : water-soluble nutrients
2. Lymphatic vessels :
to bloodstream : lipid-soluble nutrients

 ABSORPTION OF MONOSACCHARIDES

- jejunum  portal venous system

hexose : glucose, fructose, mannose, galactose
pentose : ribose
DIGESTION 24
DIGESTION 25
DIGESTION 26
GLUCOSE ABSORPTION

1. SODIUM-DEPENDENT GLUCOSE TRANSPORTER

(SLTG-1) :
- bind glucose & Na+ at separate sites
- need free energy
- inhibited by ouabain & phlorhizin

2. CARRIER-MEDIATED DIFFUSION

DIGESTION 27
LIPID ABSORPTION

2-MAG, fatty acid, 1-MAG(<<) 

leave oil phase  diffuse into micelles
(bile salts, phosphatidyl-choline, cholesterol)
 soluble  intestinal epithelium

In intestinal wall :

- 1-MAG  glycerol & FFA (by lypase)

- 2-MAG  + fatty acid  Lipid
- Short & medium-chain absorbed  hydrolyzed
- Free glycerol  portal vein  reutilization
- Long fatty acids  absorbed  reform lipid
DIGESTION 28
◈ PROTEIN ABSORPTION

 Almost completely digested  absorbed

 portal blood
 L-isomer : active transport
 Inhibit by 2,4-dinitrophenol

PUTREFACTION & FERMENTATION

 Digestion residue  large intestine 

water absorbed
 Fermentation & putrefaction)  gases
(CO2, CH4, H2, N2, H2S, acetic, lactic, propionic
& butyric acids) DIGESTION 29
Ammonia from N substrates  portal 
removed from the blood  liver

Liver disease : {ammonia} in the peripheral

blood   toxic

- Oral drug neomycin  antibacterial 

{ammonia} from intestine 

- High protein diets in liver disease &

gastrointestinal hemorrhage patients 
ammonia intoxication
DIGESTION 30
BENEFICIAL OF BACTERIA IN INTESTINE

Intestinal flora  25% feces dry weight certain

vitamins synthesized by bacteria (vitamin K, biotin)

 CLINICAL ASPECTS

Limited solubility cholesterol  gallstones

Free cholesterol + phospholipid (phosphatidylcholine)

+ bile salt (Redinger-Small triangle)  micelle

cholesterol supersaturated/precipitated) 
crystals  stone
DIGESTION 31
DEFECTS ENZYMES CARBOHYDRATE DIGESTION

1. Lactose intolerance (deficiency of lactase)

 abdominal cramps, diarrhea & flatulence
 accumulation lactose  fermentation irritation

3 types :
a. inherited lactase deficiency : intolerance birth
b. Secondary low-lactase activity
c. Primary low-lactase activity : gradual decline activity

2. Sucrase deficiency

3. Disaccariduria (disaccaridase deficiencies)

4. Monosaccaride malabsorption
DIGESTION 32