PRASETYASTUTI
BIOCHEMISTRY DEPARTMENT
1)
PROSES PENCERNAAN DI CAVITAS ORAL
2)
3)
PROSES PENCERNAAN STOMACH
PROSES PENCERNAAN DI INTESTINE
Saliva
 Disekresi oleh glandula salivary
 Terdiri dari ± 99.5% air
 Mengandung mucin (glycoprotein) acts as
lubricant for
a) Mastication and
b) swallowing
 a vehicle for the excretion of certain drugs
(ethanol and morphine)
ion inorganic (K,Ca, HCO3, SCN, dan Iodine, Ig
(IgA)
 pH ± 6.8
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a -amylase Saliva
Menghidrolisis pati dan glikogen menjadi
maltosa dan oligosakarida dengan memutus
ikatan a (1->4) glycosidic
In active pada pH ≤ 4
lipase Lingual
Disekresi oleh glandula Ebner’s pada
permukaan dorsal tongue
30% TG diet di cerna di stomach oleh lipase
lambung dan lipase lingual menghasilkan asam
lemak dan 1,2-diacylglycerols.
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Pada bayi prematur (lipase pankreas tidak
disekresi dalam jumlah cukup
Pada anak defisiensi lipase pankreas
congenital, ½ TG dapat dicerna dan diabsorbsi.
Gastric juice: sekresi gastric
 jernih, cairan kuning pucat 0.2-0.5% HCL
 pH ± 1.0
 97-99% air
 Mucin dan garam inorganic
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HCL
a)
 Mendenaturasi protein dan membunuh
bacteria
b)
sel parietal merupakan sumber HCL
c)
Proses sama dengan “the chloride shift” (sel
darah merah, mekanisme renal tubular
sekresi H+)
Mekanisme sekresi asam lambung
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Kadar ion H dalam sekresi sel parietal 3 juta X lebih
tinggi dibanding dalam darah
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HC1 160 mM (ekivalen pH 0.8).
Klorida disekresi melawan gradien konsentrasi dan
gradien elektrik -- kemampuan sel parietal
mensekresi asam tergantung pada transport aktif
Pepsin
 Is
produced in the chief cell as zymogen,
pepsinogen
 Activated to pepsin by H+ and by pepsin itself
(autocatalysis)
 Endopeptidase( hydrolyzes peptide bonds
within the main polipeptude structur)
Rennin (chimosin, Rennet)
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Penting dalam proses pencernaan pada bayi (
mencegah mengalirnya susu dari lambung)
Tidak terdapat pada lambung orang dewasa
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Casein
Rennin, Ca
paracasein
Lipase
 Lambung
mensekresi lipase
 Lipase Lingual dan gastric mengawali
pencernaan lipid dengan menghidrolisa TG
yang mengandung asam lemak tidak jenuh
rantai pendek dan rantai sedang, umumnya
rantai panjang membentuk FFA dan 1,2diacylglycerols
 pH optimum 3.0 – 6.0
 Rusak pada pH rendah
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Chyme (isi stomach) - duodenum
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Sekresi pankreas dan biliari yang alkalin
menetralkan chyme yang asam sehingga pH ke
arah alkalin ---- ensim pankreas dan juice
intestinal aktif -- menghambat kerja pepsin
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Sekresi pankreas = saliva kandungan air,
beberapa protein dan senyawa organik dan
inorganiknya.
pH sekresi pankreas ≥ 7.5 – 8.0.
Disekresi sebagai zymogen
Aktivasi trypsinogen oleh enterokinase
(enteropeptidase) di sekresi oleh mukosa
intestinal .
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Menghidrolisis ikatan peptida lisin dalam
zimogen, melepas polipeptida kecil ---
tripsin aktif
sekali trypsin terbentuk , mengkatifkan
trypsinogen ---- > trypsin
kimotripsinogen -- kimotrypsin
proelastase -- elastase dan
procarboxypeptidase, --- carboxypeptidase
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karboksipeptidase
exopeptidase
Menghidrolisis ikatan peptida terminal
karboksil , membebaskan asam amino
Amylase
Menghidrolisis amilum dan glikogen menjadi
maltosa, maltotriosa (3 residu α-glucosa
diikat dengan ikatan α 1-4) dan a mixture of
branched (1---6) oligosaccharides (α- limit
dextrins), non branched oligosaccharides, and
some glucose
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Lipase
Menghidrolisis ikatan ester primer TG
Bekerja pada antar muka minyak dan air yang
mengemulsikan tetes lemak yang terbentuk
melalui agitasi mekanik dalam usus dengan
adanya produk aktivitas lipase gastrik dan
lipase lingual, garam empedu, kolipase,
fosfolipid dan phospholipase A2.
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Kimotripsin
spesifik untuk ikatan peptida yang mengandung
residu asam amino yang tidak bermuatan
Elastase
Menghidrolisis ikatan yang berdekatan dengan
residu asam amino kecil (glisin, alanin dan serin)
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Cholesteryl ester hydrolase
Mengkatalisis hydrolysis cholesteryl esters -
diabsorbsi dari intestine dalam bentuk bebas tidak
teresterifikasi
Ribonuclease (Rnase) and deoxyribonuclease (Dnase)
Phospholipase A2
Menghidrolisis ikatan ester pada posisi 2
glycerophospholipids yang berasal dari biliary dan
diet dietary origins to formembentuk
lysophospholipid
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Bile
Diproduksi oleh liver diantara waktu makan
Berperan penting dalam pencernaan
gallbladder menyimpan bile
Sifat-sifat bile
1. emulsification -- menurunkan tegangan permukaan
2. Neutralization menetralkan kimus yang asam yang
berasal dari lambung
3. excretion -- wahana asam empedu dan ekskresi
cholesterol, obat2, toksin, pigmen
empedu, macam2 substansi inorganik
( Cu, Zn, Hg)
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Juice intestinal di sekresi oleh glandula
Brunner dan Lieberkuhn
- Aminopeptidase
: exopeptidase menghidrolisis ikatan peptida
didekat amino terminal asam amino dari
polypeptide dan oligopeptida dan dipeptidase
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- disaccharidases and oligosaccharidases
- Maltase ( maltose -- 2 mol glucose)
- Sucrase [ sukrosa --glukosa + fruktosa]
- Lactase ( lactose - galactose + glucose
- Trehalase : hydrolysing trehalosa
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- Phosphatase: menghilangkan phosphate dari fosfat
organik
Polynucleotidases
Mengubah asam nukleat -- nucleotida
Nucleosidases
Mengkatalisis fosforilasi nukleosida - basa nitrogen
+ pentose phosphate
Phospholipase
Phospholipids - glycerol, fatty acids, phosphoric
acid, bases ( choline)
Secretion Enzyme
Substrate
Action
Saliva
Ptyalin
Starch
Hydrolysis
to form
dextrins
Gastric
juice
Pepsin
Protein
Gastric
lipase
Fats
Hydrolysis
of peptide
bonds
Hydrolysis
into free
fatty acids
Final
Product
Secretion
Enzyme
Substrate Action
Pancreatic
exocrine
secretion
Lipase
Fat
Final
Product
Hydrolysis to Fatty
monoacids
glycerides
Cholesterol Cholesterol
esterase
Hydrolysis to Cholesesters of
terol
cholesterol
and fatty
acids
alphaAmylase
Hydrolysis
Starch,
dextrins
Dextrin,
maltose
Secretion Enzyme
Substrate Action
Pancreatic
exocrine
secretion
Protein
Hydrolysis Polypeptides
Chymotrypsin Protein
Hydrolysis Polypeptides
Carboxypeptidase
Hydrolysis Amino acids
Trypsin
Polypeptides
Final
Product
Ribonuclease Ribonu-cleic Hydrolysis Monoacids
nucleotides
Elastase
Fibrous
protein
Hydrolysis Amino acids
Secretion
Enzyme
Substrate Action
Brush border CarboxyPolypepenzymes
peptidase; tides
aminopeptidase;
dipeptidase
Hydrolysis
Final
Product
Amino
acids
Enterokinase
Trypsino-gen Activates
to trypsin
Polypeptidases
and
peptides
Sucrase
Sucrose
Glucose,
fructose
Hydrolysis
Secretion Enzyme
Substrate
Action
Brush
border
enzymes
Isomaltase
Dextrin
Final
Product
Hydrolysis Glucose
Maltase
Maltose
Hydrolysis Glucose
Lactase
Lactose
Hydrolysis Glucose,
galactose
Nucleotidases
Nucleic acid
Hydrolysis Nucleotides
Nucleosidases Nucleosidases Hydrolysis Purine and
and
pyrimidine
phosphorylase
bases
A
Lactose intolerance
Lactase activity is rate-limiting for lactose
absorption
The syndrome should not be confused with
intolerance to milk
Sign and symptoms
Cramps, diarrhea, flatulence
(accumulation of undigested lactose, osmotically
active  hold water- fermentative action on
the sugar of the intestinal bacteria - produce
gases )
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Lactase deficiency: the small intestine produces low
levels of lactase and cannot digest much lactose.
Lactose malabsorption. Lactase deficiency may cause
lactose malabsorption. In lactose malabsorption,
undigested lactose passes to the colon. The colon,
part of the large intestine, absorbs water from stool
and changes it from a liquid to a solid form. In the
colon, bacteria break down undigested lactose and
create fluid and gas. Not all people with lactase
deficiency and lactose malabsorption have digestive
symptoms.
Lactase deficiency and lactose malabsorption may lead to lactose
intolerance
1. Inherited lactase deficiency
 Relatively rare
 Symptoms develop very soon after birth
 - The feeding of lactose-free diet –>
disappearance of the symptoms
 - consumtion of live culture yogurt ( provides
active β–galactosidase , Ca and energy to
replase milk
2. Secondary low-lactase activity
 Digestion of lactose is limited even in normal
humans, intolerance to milk is not uncommon
as a consequence of intestinal diseases.
 Tropical and non tropical sprue
 Kwashiorkor
 Colitis
 Gastroenteritis
 After surgery for peptic ulcer
3. primary low-lactase activity
 Gradual decline in activity of lactase
 Not due to lack of lactase mRNA
B. Sucrase Deficiency
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An inherited deficiency sucrase and isomaltase (
sucrase and isomaltase occur together as a complex
enzyme)
C. Disacchariduria
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An increase excretion of disaccharides
≥ 300 mg disaccharide excreted in the urine
D. Monosaccharide Malabsorption
Congenital condition due to a single mutation in
which glucose and galactose are absorbed only
slowly defect in the Na glucose
cotransporter carrier mechanism (SGLT1)
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Fructose is not absorbed via this transporter
- absorbtion of fructose is normal
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CHYLURIA :
chylomicrons are present in urine
The presence of an abnormal connection
between the urinary tract and the lymphatic
drainage system of the intestine
Feeding TG in place of dietary fat ---
disappearance of chyluria.
Colipase deficiency :
defect pancreatic lipase activity
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Lactase deficiency: the small intestine produces low
levels of lactase and cannot digest much lactose.
Lactose malabsorption. Lactase deficiency may cause
lactose malabsorption. In lactose malabsorption,
undigested lactose passes to the colon. The colon,
part of the large intestine, absorbs water from stool
and changes it from a liquid to a solid form. In the
colon, bacteria break down undigested lactose and
create fluid and gas. Not all people with lactase
deficiency and lactose malabsorption have digestive
symptoms.
Lactase deficiency and lactose malabsorption may lead to lactose
intolerance
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Primary lactase deficiency, (lactase non
persistence) is the most common type of
lactase deficiency. In people with this
condition, lactase production declines over
time. This decline often begins at about age
2; however, the decline may begin later.
Children who have lactase deficiency may not
experience symptoms of lactose intolerance
until late adolescence or adulthood.
Researchers have discovered that some
people inherit genes from their parents that
may cause a primary lactase deficiency.
 Secondary
lactase deficiency results from
injury to the small intestine. Infection,
diseases, or other problems may injure the
small intestine. Treating the underlying cause
usually improves the lactose tolerance
 Developmental
lactase deficiency may occur
in infants born prematurely. This condition
usually lasts for only a short time after they
are born.
 Congenital lactase deficiency is an extremely
rare disorder in which the small intestine
produces little or no lactase enzyme from
birth. Genes inherited from parents cause
this disorder.
JA, Assa’ad A, Burks AW, et al. Guidelines for the
diagnosis and management of food allergy in the United
States: report of the NIAID-sponsored expert panel. Journal of
Allergy and Clinical Immunology. 2010;126(6 suppl.):S1–S58.
2Suchy FJ, Brannon PM, Carpenter TO, et al. National
Institutes of Health Consensus Development Conference:
lactose intolerance and health. Annals of Internal Medicine.
2010;152(12):792–796.
 1Boyce
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1. Stomach and Intestine
Peptic ulcers
Peptic ulcer is a general term that refers to ulcers
occurring in the lower esophagus, the stomach, or
the duodenum (upper part of the small intestine).
What is the difference between a duodenal ulcer
and a gastric ulcer?
A duodenal ulcer is a break in the lining of the
upper part of the small intestine (the duodenum); a
gastric ulcer is a break in the lining of the stomach.
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2. Bile and the Biliary System
a. Gallstones (Cholelithiasis)
There are two major types of gallstones, which form
due to distinctly different pathogenetic mechanisms
1. Cholesterol Stones
About 90% of gallstones are of this type. These
stones can be almost pure cholesterol or mixtures of
cholesterol and substances such as mucin.
The key event leading to formation and progression
of cholesterol stones is precipitation of cholesterol in
bile. There are clearly important genetic
determinants for cholesterol stone formation. There
is also an important gender bias in development of
stones - the prevalence in adult females is two to
three times that seen in males and use of
contraceptive steroids is a risk factor for
development of gallstones.
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2. Pigment Stones
Roughly 10% of human gallstones are pigment stones
composed of large quantities of bile pigments, along
with lesser amounts of cholesterol and calcium salts.
The most important risk factor for development of
these stones is chronic hemolysis from almost any
cause - bilirubin is a major constituent of these
stones. Additionally, some forms of pigment stones
are associated with bacterial infections. Apparently,
some bacteria release deconjugate bilirubin, leading
to precipitation as calcium salts
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b. Jaundice
Jaundice, is yellowing of the skin, sclera (the white of the eyes)
and mucous membranes caused by increased levels of bilirubin in
the human body. Usually the concentration of bilirubin in the
blood must exceed 2-3mg/dL for the coloration to be easily
visible. Jaundice comes from the French word jaune, meaning
yellow