1.

Carbohydrate Metabolism
Consists of :
glycolysis
oxidative decarboxylation
cycle of citric acid
oxidative phosphorylation
 Glycolisis
• Also called Embden-Meyerhof metabolic
pathway.
• Is the pathway of oxidation of glucose into
pyruvate + energy (ATP) + NADH.
• Glycolysis takes place in the cytosol.
• Glycolysis is the path of energy sources
especially for ripe red blood cells that no
longer have mitochondria.
• Phase requires energy
In this phase, the glucose molecule is rearranged, and 2
phosphate groups are bound to this glucose. The
phosphate group then creates an unstable 'modification'
sugar (fructose-1,6-bisphosphate), allowing the 'modified'
sugar to be split into two and forming a glyceraldehyde-3-
phospate sugar. Since the phosphate used in this step
comes from ATP (adenosine triphosphate), then 2 ATP
molecules are used. This phase is often called the
'investment' phase of energy, because it uses energy
(ATP) to run the process.
• Phase releases energy
In this phase, each glyceraldehyde-3-phosphate sugar is converted to
pyruvate, through several reactions. This reaction makes 2 ATP
molecules and 1 molecule NADH. Because this phase occurs twice,
then this process makes 3 ATP and 2 NADH overall.
The catalyst that triggers raction on Glycolysis is done by its own
enzyme, one of which is the phosphofurctokinase enzyme, which
catalyzes the formation of a sugar phosphate molecule (fructose-1,6-
bisphospate). This phosphofructokinase accelerates or retards the
process of glycolysis in response to the cell's need for energy.
In essence, Glycolysis converts glucose molecules (6 carbon) into
pyruvate molecules (3 carbon). The net product of this process is 2 ATP
molecules (4 ATP produced using 2 ATPs) and 2 NADH molecules.
Glycolysis settings - Inhibited by Glucose-6-phosphate.

Phosphofructokinase
Hexokinase This enzyme limits / regulates the
Catalyze all hexoses. glycolytic pathway rate.
There is almost in all cells, except the liver Enabled by increased AMP in the cytosol.
and Categorize only glucose alone. AMP increases because ATP is hydrolysed
It is in liver cells only. by a reaction that requires energy.
Influenced by;
fasting, diet, insulin, diabetes mellitus Pyruvate Kinase
Pyruvate Kinase is arranged in the liver.
Glucokinase This enzyme converts the excess glucose
Not inhibited by Glucose-6-phosphate. into pyruvate, subsequently metabolized
pancreatic-β cells. into acetyl-CoA in order to be stored as
Not influenced by; fatty acids for long-term energy reserves.
fasting, diet, insulin, diabetes mellitus
Clean Glycolytic Aerob Results
Glukosa + 2NAD+ + 2Pi + 2 ADP

2Piruvat + 2NADH + 4H+ + 2ATP + 2H2O

Net Result Anaerobic Glycolysis
Glukosa + 2 ADP + 2 Pi

2 lactate + 2 ATP
 2. Citrate Acid Cycle
The citric acid cycle, or the tricarboxylic acid cycle, or the
Krebs cycle is the controlling center in cellular respiration.
This cycle occurs after Glycolysis and uses acetyl
coenzyme A (CoA), made from pyruvate oxidation, as its
starting material. (Read: Krebs Cycle)
The first stage of this cycle is, acetyl CoA joins the
oxaloacetate receptor molecule (4 carbon) to form a
citrate (6 carbon) molecule. Then, this citrate molecule
releases its carbon 2 in the form of carbon dioxide and
produces the NADH molecule. Enzymes that catalyze
these reactions are key in regulating the citric acid cycle,
accelerating or slowing down the reaction based on cell
energy requirements. (Read: Tripsin Enzyme Function)
Furthermore, the remaining 4 carbon molecules undergo
additional reactions, first making the ATP molecule, then
reducing the FAD (Flavin adenine dinucleotide) carrier to
FADH2, and finally producing NADH again. The set of
these reactions results in the return of the initial
molecule, oxaloacetate, in order for this cycle to be
repeated.
Overall, one cycle of citric acid cycle releases 2 molecules
of carbon dioxide and produces 3 NADH, 1 FADH2, and 1
ATP. Because of Glycolysis, there are 2 pyruvates
produced, then the citric acid cycle occurs twice for every
glucose molecule.
 3. Phosphate Path Pentosa
The pentose phosphate pathway or pentose phosphate pathway is a
metabolic pathway that runs parallel to Glycolysis. If the products of
Glycolysis are reprocessed through cellular respiration to produce energy,
there is also an alternative branch of Glycolysis to produce sugars that make
up DNA and RNA. The path called the Pentosa Phosphate Path is unique
because there is no energy in the form of ATP that is produced and used in
this pathway. (Read: Role of DNA and RNA in Protein Synthesis)
Just like any other process in cellular respiration, the molecules passing
through the pentose phosphate line are mostly made of carbon. An easy way
to understand this path is to follow its carbon.
The breakdown of glucose in Glycolysis produces the 6-carbon molecule
needed in the process of the pentose phosphate pathway. In the first step of
glycolysis, glucose is altered by the phosphate group to produce glucose-6-
phosphate. These pentose phosphate paths may use 6-phosphate glucose
molecules produced by Glycolysis or other methods.
Phosphate Path Pentosa is divided into 2 phases,
namely the oxidative phase and non oxidative
phase. The word 'oxidative' comes from the
word 'oxidation', oxidation is the breakdown of
molecules when the molecule loses at least one
electron.
• Oxidative phase
In this phase, 2 NADP + molecules are reduced to NADH, utilizing
energy from the conversion of glucose-phosphate to ribulose-5-
phosphate. The overall reactions to this process are:
Glucose-6-phosphate + 2 NADP + + H2O -> Ribulose 5-phosphate + 2
NADPH + 2 H + + CO2.
• Non-oxidative phase
this non-oxidative phase is reversible (reversible). This allows different
molecules to enter the pentose phosphate path in different areas of
the non-oxidative phase and can be transformed to the first molecule
of the non-oxidative phase (ribulose-5-phosphate). Ribulose-5-
phosphate is a precursor of the sugars that make up DNA and RNA,
and also the product of the oxidative phase. (Read: Differences of DNA
and RNA)
 4. OXIDATIVE FOUNDATION
OXIDATIVE FOUNDATION
Oxidative phosphorylation is an electron-
transferred process of NADH and FADH2 produced
by glycolysis, fatty acid oxidation and citric acid
cycle. The mechanism of action that occurs in the
mitochondria. Each NADH or FADH2 will transfer
two electrons into a protein complex and each
electron passing through the protein complex will
release two protons into the 'inner membrane' of
the mitondria. The transferred proton is derived
from the mitochondrial matrix.
GLYCOGENESIS AND GLYCOGENOLISIS
IN THE HEART AND
MUSCLE
• Glycogen Function Muscles:
Source Glycolysis in the muscles themselves
• Glycogen Heart Function:
Consider Blood Glycos between meals
Fasting 12-18 Hours: Glycogen Heart runs out
2. Lipid Metabolism
Lipid metabolism
3. Protein Metabolism
• Protein tersusun atas sejumlah asam amino
yang membentuk suatu untaian (polimer)
dengan ikatan peptida
• protein juga memiliki gugus amina (NH2) dan
gugus karboksil (COOH)
 MACAM PROTEIN
• Berdasarkan banyaknya asam amino dapat
dibedakan menjadi:
– Peptide: 2 – 10 asam amino
– Polipeptide: 10 – 100 asam amino
– Protein: > 100 asam amino

• Beberapa jenis protein antara lain:

– Glikoprotein: gabungan glukose dengan protein
– Lipoprotein: gabungan lipid dan protein
• ASAM AMINO
Asam amino esensial adalah golongan asam
amino yang harus tersedia dalam diet karena
tidak dapat disintesis oleh tubuh, sedangkan
asam amino non-esensial adalah golongan
asam amino yang dapat disintesis oleh tubuh
(dalam hati).
 FUNGSI PROTEIN :
• Pembentukan jaringan baru seperti: rambut,
kuku.
• Mengganti jaringan yang rusak seperti:
pengelupasan mukosa usus.
• Mengganti asam amino yang hilang misalnya
lewat urin.
• Mensintesis asam amino nonesensial dengan
menggabungkan asam keto melalui proses
transaminasi oleh hati.
• Mensintesis molekul fungsional seperti;
hormon, enzim dsb.
Metabolisme protein Meliputi:
• Degradasi protein (makanan dan protein
intraseluler) mjd asam amino
• Oksidasi asam amino
• Biosintesis asam amino
• Biosintesis protein
 DEGRADASI PROTEIN
≈ PENCERNAAN PROTEIN
• Degradasi protein dr makanan  asam amino :
terjadi di saluran pencernaan
• Protein diabsorpsi di usus halus dalam bentuk
asam amino → masuk darah
• Dalam darah asam amino disebar keseluruh sel
untuk disimpan
• Didalam sel asam amino disimpan dalam bentuk
protein (dengan menggunakan enzim)
• Hati merupakan jaringan utama untuk
menyimpan dan mengolah protein
 PROTEIN

Stimulate mukosa lambung

 hormone gastrin

Stimulate sekresi HCl oleh

sel parietal & pepsinogen
oleh chief cell

pH rendah  antiseptic

& protein mengalami degradasi 

mudah dipecah oleh enzim2

pepsinogen  pepsin oleh aktifitas

USUS HALUS
pepsin sendiri

 diputus 42 aa pd N terminal
Masuknya as. Amino : stimulate sekresi Pepsin menghidrolisis iktn peptide
hormone cholecystokinin pd N terminal dkt Tyr, Phe and Trp
Lambung
Kondisi asam
 sekresi Pankreas
Kondisi pH  Zymogen hormone
mjd aktif: sekretin Sekresi
bikarbonat
Tripsinogen Trypsin, Menetralisir pH
(oleh enteropeptidase) ±7
Sekresi bbrp enzim: trypsinogen,
Trypsin activate 
chymotrypsinogen,
chymotrypsin, procarboxypeptidase
carboxypeptidase
Secret aminopeptidase Asam Amino
Bebas
 ASAM AMINO
• Asam amino yang berasal dari makanan (diet)
dan dari pemecahan protein tubuh selanjut
dibawa oleh sirkulasi darah ke dalam amino
acid pool (gudang penimbunan asam amino)
yaitu darah dan cairan jaringan (interseluler).
• Asam amino selanjutnya digunakan untuk:
biosintesis protein tubuh, mengganti jaringan
yang rusak, dan jika diperlukan dapat diubah
menjadi sumber energi.
• Kira-kira 75% asam amino digunakan untuk
sintesis protein.
• Asam-asam amino juga menyediakan
kebutuhan nitrogen untuk:
– Struktur basa nitrogen DNA dan RNA
– Heme dan struktur lain yang serupa seperti
mioglobin, hemoglobin, sitokrom, enzim dll.
– Asetilkolin dan neurotransmitter lainnya.
– Hormon dan fosfolipid
 Jalur metabolik utama asam amino
I. pertama, produksi asam amino dari
pembongkaran protein tubuh, digesti protein
diet serta sintesis asam amino di hati.
II. pengambilan nitrogen dari asam amino.
III. katabolisme asam amino menjadi energi
melalui siklus asam serta siklus urea sebagai
proses pengolahan hasil sampingan
pemecahan asam amino.
IV. sintesis protein dari asam-asam amino.
Jalur-jalur metabolik utama asam amino
 Katabolisme asam amino
• Asam-asam amino tidak dapat disimpan oleh
tubuh. Jika jumlah asam amino berlebihan
atau terjadi kekurangan sumber energi lain
(karbohidrat dan protein), tubuh akan
menggunakan asam amino sebagai sumber
energi.
• Tidak seperti karbohidrat dan lipid, asam
amino memerlukan pelepasan gugus amin.
• Gugus amin ini kemudian dibuang karena
bersifat toksik bagi tubuh
• Jika jumlah protein terus meningkat → protein
sel dipecah jadi asam amino untuk dijadikan
energi atau disimpan dalam bentuk lemak
• Katabolisme asam amino terjadi di hati
dengan proses:
1. deaminasi atau
2. transaminasi
 Transaminasi
• Adalah proses perubahan asam amino
menjadi jenis asam amino lain.
• Proses transaminasi didahului oleh perubahan
asam amino menjadi bentuk asam keto,
secara skematik digambarkan sebagai berikut:

Alanin + α-ketoglutarat ↔ piruvat + glutamate

 Deaminasi oksidatif

• adalah proses pemecahan (hidrolisis) asam

amino menjadi asam keto dan ammonia
(NH4+),
• Proses deaminasi kebanyakan terjadi di hati,
• Deaminasi menghasilkan 2 senyawa penting
yaitu senyawa nitrogen dan nonnitrogen.
1. Senyawa nonnitrogen yang mengandung
gugus C, H, dan O selanjutnya diubah
menjadi asetil Co-A untuk sumber energi
melalui jalur siklus Kreb’s atau disimpan
dalam bentuk glikogen.
2. Senyawa nitrogen dikeluarkan lewat urin
setelah diubah lebih dahulu menjadi ureum
 EKSKRESI NH3

• NH3 → tidak dapat diekskresi oleh ginjal

• NH3 harus dirubah dulu menjadi urea oleh
hati →agar dapat dibuang oleh ginjal → urin
• Jika hati ada kelainan (sakit) → proses
perubahan NH3 → urea terganggu →
penumpukan NH3 dalam darah → uremia
• NH3 bersifat racun → meracuni otak → coma
• Karena hati yang rusak → disebut Koma
hepatikum
 Pembentukan Asetil Koenzim A

• Setelah mengalami pelepasan gugus amin,

asam-asam amino dapat memasuki siklus
asam sitrat melalui jalur yang beraneka ragam.
• Asetil koenzim A merupakn senyawa
penghubung antara metabolisme asam amino
dengan siklus sitrat.
– Ada dua metabolic yang menuju kepada
pembentukan asetil koenzim A yaitu melalui asam
piruvat dan melalui asam asetoasetat
Gambar : kaitan antara asam amino dengan siklus asam sitrat
 Siklus Urea

• Gugus-gugus amin dilepaskan menjadi ion

amonium (NH4+) yang selanjutnya masuk ke
dalam siklus urea di hati. Dalam siklus ini
dihasilkan urea yang selanjutnya dibuang
melalui ginjal berupa urin.
• Proses yang terjadi di dalam siklus urea
 KREATIN DAN KREATININ
• Kreatin disintesa di hati dari: metionin, glisin dan
arginin
Dalam otot rangka difosforilasi membentuk
fosforilkreatin (simpanan energi)

istirahat
Kreatin + ATP ↔ Fosforilkreatin →
Kreatinin
gerak urine
• Kreatinin dalam urin berasal dari pemecahan
posfokreatin.
• Kreatinuria secara normal dapat terjadi pada
anak-anak, wanita selama mengandung dan
setelah melahirkan. Pada laki-laki sangat
jarang terjadi kecuali pada kondisi kerja yang
berlebihan. Kreatinuria pada laki-laki biasanya
terjadi akibat kelaparan, tirotoksikosis, DM
yang tidak terkontrol, dan kerusakan otot
(myopati).
 Biosintesis asam amino
• asam amino non esensial di buat utamanya di
liver
• Semua asam amino berasal dari senyawa
intermediet Glikolisis, siklus asam sitrat, dan
pentose phosphat pathway
AMINO ACIDS BIOSYNTHESIS
4. Relation of metabolism
 Organ specialization
• BRAIN : require a steady supply of glucose
from the blood
• HEART MUSCLE: Aerobic metabolism; fatty
acids, ketone bodies, glucose, pyruvate, and
lactat
• ADIPOSE TISUE : Store and release fatty acids
• LIVER : Central of metabolic, major function is
a glukosa buffer
• KIDNEY : filters wastes and maintains blood PH
 If you were hungry:
• Your liver : Glikogen degradation,
gluconeogenesis (from amino acid)
• Increase keton body synthesis in order to
brain energy
 If you were full:
• Your liver: increase glycogenesis, fatty acids
synthesis, and amino acid synthesis.
• Decrease gluconeogenesis
5. Metabolism of Purine &
Pyrimidine Nucleotides
• The three processes that contribute to purine
nucleotide biosynthesis are, in order of
decreasing importance.
• 1. Synthesis from amphibolic intermediates
(synthesis de novo).
• 2. Phosphoribosylation of purines.
• 3. Phosphorylation of purine nucleosides.
The more important mechanism involves
phosphoribosylation by
PRPP of a free purine (Pu) to form a
purine 5′-mononucleotide (Pu-RP).
Pu + PR-PP → Pu-RP + Ppi

A second salvage mechanism involves phosphoryl

transfer from ATP to a purine ribonucleoside (Pu-R):
Pu-R + ATP → PuR-P + ADP
Phosphorylation of the purine nucleotides,
catalyzed by adenosine kinase, converts adenosine
and deoxyadenosine to AMP and dAMP
The biosynthetic pathway for pyrimidine nucleotides.
6. Pengaturan glukosa darah
• The blood glucose are primarily regulated through the action
of hormones. In particular, the hormone insulin, direct the
flow of glucose from blood to heart, muscles, and the adipose
(storage of fats). It also encourages the improvement of
glycogen synthesis as energy needs are met (for example,
after eating).
•
• When blood glucose levels down (for example, a few hours
after eating), glucagon and epinephrine (also known as
adrenaline) take glucose from the fact that there is stored as
glycogen in the heart and muscle tissue. Low levels of insulin
in this situation also means that the entry of glucose into cells,
muscle and adipose, so that these cells turn to the use of fuel
non-karbohidrat.
• Hearts are the control of the main blood glucose levels,
with the ability to respond to the hormonal, which shows
blood glucose levels well be reduced or increased. One of
the function of the most important of the liver is to
produce glucose for the circulation.
•
• Levels of low blood glucose (hypoglycemia) can lead to
strong disruption of the function of the central nervous
system, which can manifest itself in the form of dizziness,
trouble talking, or even a loss of consciousness.
•
•
• Hiperglikemia (high blood sugar), which is
characteristic of diabetes mellitus, according to the
excess glucose by liver cells along with the other cells
to utilize glucose. Patients with diabetes mellitus
type 1 depends on external sources of insulin to their
survival because (in many cases) the autoimmune
they destroy the cells in the pancreas to secrete
insulin. Patients with diabetes mellitus type 2
diabetes may be more general have the production
of insulin is relatively low or resistance to the impact.
7. Metabolic Abnormalities
 1. Carbohydrate Metabolic
Abnormalities
• Galactosemia (high levels of galactose in the blood)
• Glycogenosis (Glycogen storage diseases)
• Hereditary fructose intolerance is a hereditary disease
in which the body can not use fructose because it does
not have the enzyme phosphofruktaldolase. As a
result, fructose-phosphatase, which results from the
breakdown of fructose accumulated in the body, blocks
the formation of glycogen and blocks the conversion of
glycogen into glucose as an energy source.
• Diabetes Mellitus (Hiperglycemia)
 2. Metabolic Abnormalities of Amino
Acids
• Phenylketonuria is a disease in which the patient can not metabolize
phenylalanine properly because the body does not have an enzyme that
oxidizes phenylalanine into tyrosine and can occur damage to the child's
brain.
• Alkaptonuria is a rare condition in which the urine secreted by a person
is dark when it comes into contact with air. this disease is declining.
• Prolinemia or Hyperprolinemia, is a condition that occurs when proline
amino acids are not well broken down by proline oxidase enzymes or
pyrroline-5-carboxylate dehydrogens, causing build up of proline in the
body.
• Maple syrup urine disease (MSUD) or Maple urinary syrup is a
congenital disorder in which the body is unable to properly process
certain protein building blocks (amino acids). This condition gets its
name from the distinctive sweet smell of infected baby's urine.
 3. Lipid Metabolic Abnormalities
• (Obesity) Occurrence of calories gained more
than the metabolized calories
(hypometabolism) Calories needed decreased,
so that weight gain, although fed is not
excessive.
• Hyperlipidemia: The accumulation of fat
occurs in blood vessel walls and it is called
arteriosclerosis.
 4. Purine and Pyrimidine Metabolic
Abnormalities
Purine
Hyperuricemia
Hyperuricemia
Xantin Urea / Xantin Litiasis

Pyrimidines
Hyperuricemia with overproduction of PPRP
Ornitine transcarbamoilase deficiency