GASTROINTESTINAL

SYSTEM
Digestion and Absorption of Nutrients
Rondang R. Soegianto
2016

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Introduction

Functions of the GI Tract

Digestion
Secretion
Motility
Absorption

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Digestion:

Physical process: Chewing, GI contraction

Chemical process: Digestive enzymes

Source of digestive enzymes:

Exocrine glands - Salivary glands
Pancreas
Gallbladder
Liver
Also cells and glands in mucosa 3
Secretion:

During digestion, large volumes of fluid

secreted into lumen of GI tract from
exocrine glands and epithelial cells of
intestinal lumen.

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Motility

Secretions and luminal contents move from

mouth to anus by motility =
coordinated contraction of smooth muscle

Absorption

Products of digestion taken into the body

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Dietary Carbohydrate
A. Polysaccharide:
Plant carbohydrate:

- Cellulose, present in diet but no digestive

enzyme (cellulase)
- Amylum consists of :
Amylose (20%) α-1,4 links
Amylopectin (80%) α-1,4 and α-1,6 links
for branching

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Animal starch
- Glycogen
- Similar to Amylopectin with more branches

STARCH and GLYCOGEN are polymers of

glucose

Only one glucose residue has reducing

group on C1

Other glucose residues are non-reducing

ends
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B. Disaccharides

Sucrose: Fruc + Gluc

Lactose: Gluk + Galac
Maltose: Gluk + Gluc

C. Monosaccharides:
Gluc, Fruc, Galac
Reducing sugars with reducing group
on C1 or C2

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CLINICAL NOTE

Urinary sugar:
Glucosuria in DM

Fructosuria
Galactosuria Other metabolic disorder

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1.2 Carbohydrate Digestion
Glycoside hydrolysis  Monosach  Intestinal mucosa

Digestive Enzymes:
- Salivary α-amylase
pH opt ~ 7.0
- Pancreatic α- amylase

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Salivary amylase stopped
by acidity of stomach
Pancreatic amylase undergoes
buffering action of
Pancreatic juice and Bile in
Small intestine
Continues digestion of starch and
glycogen in food
Products: Oligosaccharides and
disaccharide (maltose)
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- Brush border carbohydrases are:

Sucrase-α-dextrinase, glucoamylase, lactase

In intestinal epithelial cells

Alpha-dextrinase specific for α-1,6-linkages in

amylopectin and glycogen

Products: Gluc, Fruc, Galac

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CLINICAL NOTE

Lactose Intolerance
Lactase hydrolyses β-1,4- links in lactose
Lactase deficiency causes: cramping, pain, etc
Watery diarrhea due to osmotic load by
unhydrolyzed disaccharide

Colonic bacteria produce metabolites of lactose 

Increase osmotic load, acids and gases

No more lactose in diet  No more problems

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1.3 Carbohydrate Absorption
Transport mechanisms by membrane carriers
Fruc: GLUT5, facilitated diffusion
Gluc + Galac : SGLT1, sodium dependent
symport
One gluc + 2 Na+ bind to SGLT1

Na+ for conformational change of

SGLT1 to bind gluc

Inside cell: sodium released

÷ Decreased affinity of SGLT1 for gluc
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Hence: Gluc released
 Na,K-ATPase transports Na+
to lateral intercellular space

against electrochemical gradient with

free ATP

Since ATP not directly involved, this is a

Secondary active transport

From mucosal cell into intercellular space:

Gluc, Fruc and Galac transported by GLUT2
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CLINICAL NOTE
Cholera and Dysentery
Practical use of cotransport
Administration of NaCl and glucose
orally
to cholera and dysentery patients
depleted of
Na+ due to diarrhea.
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2.1 Dietary Fat

Hydrophobic molecules

Major D F : Triacylglycerols =

Esters of an alcohol (glycerol) and FA

In nature: 3 different FA in molecule structure

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Fatty Acids:

Saturated : Palmitate, Stearate

Monounsaturated: Oleate

Polyunsaturated: Linoleate, Linolenate

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2.2 Fat Digestion

a.Salivary and lingual lipases

For TAG with short to

medium FA (cow’s milk)

Product: 2-monoacylglycerols

Help emulsify other fat in the diet

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b. In small intestine bile salts emulsify fats.
(Bile contains bile salts, lecithin, cholesterol)
Pancreatic lipase and co-lipase
secreted from pancreas

Lipase cannot penetrate layer of bile salts.

Colipase is needed to bind both to lipase
and bile salts at surface of fat droplets.

Products:
2-monoacylglycerols + FA from C1 and C3
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Schematic structure and function of bile salts
(Sherwood Fig 16-18 Page 621) 26
Schematic representation of a micelle
(Sherwood Fig 16-19 Page 622) 27
c. Formation of bile salts micelles
Bile salts and lecithin aggregate to form
small clusters, micelles (<< emulsion)
Micelles contain: TAG, Monoacylglycerols,
FA, Fat soluble vitamin
Emlsn, micll: neg, solubl prot sticking outside

Cholesteryl esters in diet are hydrolyzed by

cholesterylester hydrolase
Unesterified cholesterol and chol. esters
taken up in hydrophobic core of bile salt
micelles  chylomicrons
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e. Phospholipids in diet hydrolyzed by
pancreatic phospholipase A2

Removes fatty acid at C2

Product:
Lysophospholipid, a powerful detergent

FA and phospholipid incorporated into

micelles  chylomicron

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f. Digestion and Absorption of TAG

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g. Absorption of dietary lipids
FA and 2-MAG packaged into micelles
= micro droplets emulsified by bile salts.
and lecithin
Also included in micelles: Cholesterol
Fat soluble
vitamins
Micelles  Microvilli

Short and medium FA (C4 – C12) do not

need bile salts for absorption.
Enter portal blood directly. 31
CLINICAL NOTE

Steatorrhea: lipid malabsorption 

increased lipid (including vit’s A, D, E, K
and essential FA) in feces caused by
disturbed lipid digestion and/or absorption

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h. Secretion of lipids from enterocytes

Newly synthesized TAG and cholesteryl

esters are very
hydrophobic  aggregate in aqueous
environment (blood)

Must form chylomicrons then released

from enterocytes into lymphatic vessels.
Chyle = milky lymph
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i. Chylomicron formation

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j. Enterohepatic circulation of bile salts

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k. Bile acids are synthesized from cholesterol

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CLINICAL NOTE

Cholestyramine = anion exchange resin

Binds bile acids ≠ Reabsorption

Used therapeutically along with

HMG-CoA reductase Inhibitors in
hypercholesterolemia

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3.1 Digestion of Protein

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Activation of gastric and pancreatic zymogens

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Gastric juice:
Chief cells: pepsinogen
Parietal cells: HCl

Pancreatic Enzymes
a. Proteolytic enzymes
b. Pancreatic amylase
c. Pancreatic lipase
(the only enzyme important in fat digestion)

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Endopeptidase - pepsin, trypsin

Exopeptidase
- carboxypeptidase (pancreas)
aminopeptidase
int’nal mucosa
dipeptidase

Product: Free amino acids

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Absorption of amino acids
Utilize Na-dependent transport proteins

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Protein turnover

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Nitrogen Balance
Intake vs Output (losses thru faeces, skin,
urea and ammonia in urine)

I > O Growth, recuperation

I < O Malnutrition, burns
I ~ O Balanced healthy adults

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Gastrointestinal hormones

Gastrin: pyloric glands and proximal

duodenum
Stimulates acid and pepsinogen secretion in
stomach

Gastrin secretion stimulated by protein

meals and vagus nerve.

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Secretin: upper intestine

Stimulates water and bicarbonate secretion by

pancreas to neutralize acidification by acid
chyme.

Cholecystokinin: duodenum and proximal

jejunum
Stimulates pancreatic enzymes.
Hormone secretion increased by fats,
peptides, amino acids in lumen of small
intestine.
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 Intestinal Putrefaction
and Fermentation
• Most ingested food absorbed from
intestine.
• Residue  large intestine  absorbtion
of water  contents become more solid
• Bacterial activity occurs  fermentation
and putrefaction
• Production of gases: CO2, CH4, H2, N2, H2S

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 Decarboxylation of AA
• Production of toxic amines caused by
bacterial decarboxylation: ptomaine
• Lysine  cadaverine
Arginine  Agmatine
Tyrosine  Tyramine
Ornithine  Putrescine
Histidine  Histamine
Many amines = vasopressors (x Histamine)
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 Other products of putrefaction
• Tryptophan   Indole, Skatole
Responsible for odor of feces
• S amino acids such as cysteine  
mercaptans: CH3CH3SH ethyl mercaptan,
CH3SH methyl merc. as well as H 2S
• Bacterial NH3 absorbed and removed in liver (
urea). Liver disease  ammonia intoxication 
hepatic coma (neomycin as
• antibacterial drug)

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REFERENCES
1. Medical Biochemistry, A.C. Brownie, J.C.
Kernohan
ELSEVIER, 2005
2. Lippincott’s Illustrated Reviews: Biochemistry
P.C. Champe, R.A. Harvey, D.R. Ferrier
Lippincott Williams & Wilkins 2005
3. Basic Medical Biochemistry. A Clinical Approach
D.B. Marks, A.D. Marks, C.M. Smith
Williams & Wilkins 1996
4.Harper’s Illustrated Biochemistry 27th ed. 2006
5.Human Physiology, L. Sherwood, 2004.
6. Harper’s Review of Biochemistry, 18 ed., 1981
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