metabolism th - lms.ipb.ac.id · 5/3/2017 materi ajar fisiologi veteriner ii (metabolisme) 59 lipid...
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METABOLISM
DIVISION OF PHYSIOLOGY
DEPARTMENT OF ANATOMY, PHYSIOLOGY ANDPHARMACOLOGY
FACULTY OF VETERINARY MEDICINE IPB
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References:
1. Cunningham’s Textbook of Veterinary Physiology 5th edition; Elsevier, pp 342-358
2. Clinical Anatomy and Physiology for Veterinary Technicians 3rd edition (Colville and Bassert), pp 417-444
3. Dee Unglaub Silverthorn Human Physiology An Integrated Approach, pp 739-765
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Foundation of nutrition and cell metabolism
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Metabolism
Metabolism
anabolism
catabolism
Metabolism: the sequence of reaction or succession of a chemical
processes that occur in the living organisms
Anabolism: synthesis of complex compounds from simple molecules,
example: the formation of glycogen from glucose
(glycogenesis); lipogenesis, protein synthesis,
Catabolism: breakdown of complex compounds into more simple
materials.for example: glycolysis, lipolysis, breakdown of
nutrients into CO2 + H2O + energy, etc
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Catabolism of food energy production
Essential for: - Maintaining body functions
- Digestion
- Metabolism
- Thermoregulation
- Physical activities
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Energy Transfer:
HS - Ko-A + as. Asetat asetil ko-A (reduced Ko-A)
- Energy produced by catabolism process is utilized for the formation of :
- Energy-rich phosphate compounds
ATP, hydrolized into ADP & AMP
Creatine phosphate
GTP (guanosine triphosphate)
CTP (cytidine triphosphate)
UTP (uridine triphosphate)
ITP (inosine triphosphate)
• Kelompok tio-ester : Koenzim-A (Ko-A)
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ATP and Energy Transfer Cells
In the cell, energy from the catabolism process will be transferred into ATP
• Hydrolysis ATP into ADP and P will release energy which is then used for cell activity
• ATP + H2O ADP + P + 7 kcal/mol
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First Law Thermodinamic :
Energy can not be formed nor destroyed, but
can be converted
Δ E = H + W
60 % 40 %
ATP
Total energy produced = The heat generated by the
body + work + energy stored
Δ E = released energy
H = heat
W = energy for work (transport,
mechanical and chemical
process)
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HEAT ENERGY 60%
Food molecules
(Carbohydrate,
Protein or Fat)
CO2 + H2O + NH3
Catabolism
CHEMICAL ENERGY 40%
ADP + P ATP
Energy used for cell functions: (1) Power and movement, (2) Membrane
Transport, (3) Molecule Synthesis
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Absorptive vs Post Absorptive
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Metabolic Pathway During Absorptive
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Metabolic Pathway During Post Absorptive
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Measured under the conditions:
- Resting
- Thermoneutral
- Post absorptive (12-14 hrs after meal)
Energy Balance
Balance between calory intake and & energy produced
If - catabolism of energy sources (endogenous)
If + energy will be stored and the individu will gain
weight
Basal Metabolic Rate (BMR)
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• The amount of energy / heat produced per unit time
• Energy is stored in the form of rich-energy
compounds (ATP, GTP, ADP, etc.)
• The unit of energy/heat measurement: kilocalori (K)
Definition : the amount of heat required for
increasing the temperature of 1 gr of water as much
as 1oC
Metabolic Rate
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- Energy measurement:
o Direct Calorimetry (equipped with climate chamber
bomb calorimeter )
o Undirect Calorimeter
- O2 consumption
- CO2 production}RQ (Respiratory Quotient): CO2 prod/ O2 cons
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Nutrient Respiratory Quotient
Carbohydrates 1
Proteins 0.8 - 0.9
Ketones (eucaloric) 0.73
Ketones (hypocaloric) 0.66
Triolein (Fat) 0.7
Oleic Acid (Fat) 0.71
Tripalmitin (Fat) 0.7
Malic acid 1.33
Tartaric acid 1.6
Oxalic acid 4.0
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Bomb calorimeter
http://image.wistatutor.com/content/feed/tvcs/image1_27.jpg
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Measurement of Metabolic Rate with Heat Production
Correlation
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Measurement of Metabolic Rate with Oksigen Consumption
Correlation
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Factors influenced metabolic rate:
- Muscular activities
- Food ingesti
- Environment temperature
- Height, weight and body surface area
- Sex
- Age
- Emotional state
- Body temperature
- Blood thyroid level
- Blood Epinephrine/norepinephrine level
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Control of Food Intake
“Satiety signals” receptor hungry
satiety
Involved plasma glucose level & hormone which regulate organic
compound metabolism (carbohydrate and fat)
Hormone that regulate metabolism :
- Insulin
- Glukagon
- GH
- Glucocortikoid
- Epinephrine
- Tyroxine no effect
Glucose
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Source of carbohydrate
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Absorptive Phase: Carbohydrate
Insulin stimulant: gastric inhibitory peptide
Storage of glucose by the liver glicogen and TG
Glucose glicogen
Glucose fatty acid via glycolysis 2 pyruvate acids acetil co-A Krebs cycle + oxaloacetate citrate to cytosol fatty acid
Glucose fatty acid (irreversible)
Krebs Cycle or Citric Acid Cycle (CAC) – also known as the Tricarboxylic Acid (TCA) cycle
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1. Aerobic catabolism through the glycolytic pathway would produce pyruvic acid and enter the Krebs cycle
In aerobic condition 38 molecules of ATP
produced, which 34 are from
oxidative phosphorylation, 2 ATP from
glycolysis and 2 ATP from the Krebs cycle
In anaerobic condition 2 molecules of ATP
produced
40% of energy from glucose under aerobic
conditions is transferred to ATP and the
remainder for heat production
Carbohydrate Catabolism
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GLYCOLYSIS
The group of phosphate is moved from metabolic phosphorylation to ADP. Substratephosphorylation generally occurs in the glycolytic pathway in which the enzyme involved is in the cytosol
Glucose + 2ADP + 2Pi
2 lactic acid + 2 ATP + 2 H20
Carbohydrates are the materials that can only be entered into the glycolytic pathway:
- Aerobic ATP and pyruvic acid
- Anaerobic ATP and lactic acid
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Glycolysis
Utilyzes
2 ATP
Produces: 4 ATP
Glycolysis produces:
• (4 - 2) = 2 ATP
• 2 pyruvic acid
• 2 NADH
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Anaerobic Glycolysis
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Cellular Respiration
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Krebs Cycle
Krebs Cycle
produces :
• 1 ATP
• 3 NADH
• 1 FADH2
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Biological oxidation
- Oxidation: reaction of compounds + O2 (loss of H +, e-)
- >< Reduction
- Oxidation is catalyzed by catalytic enzyme
Oxidative phosphorylation
- The formation of ATP through a process of oxidation by flavoproteins and cytochrome enzymes
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Oxidative phosphorylation
Reactions involving two H atoms combined with oxygen to form water
Occurs in the inner membrane of the mitochondria as the forming enzyme is in the mitochondria
H+ is obtained from catabolism of food and transferred to the mitochondria as coenym-2H
Coenzym-2H + ½ O2
Coenzym + H2O + 52 kcal/mol
The main source of ATP
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Oxydative Phosphorilation
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• Carbohydrates are stored in the form of
glycogen mainly in the liver and
skeletal muscle
• Glucose can be synthesized from the
amino acid, pyruvic acid and glycerol.
• Lactic acid can not be synthesized into
glucose except in the liver.
Carbohydrate metabolism
(continued)
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Cell Membrane
Blood
Glucose
Uridine diphosphate
glucose
Glycogen
Glucose-1-P
Glucose-6-P
Glycolysis
glucokinase/hexokinase
Glucose
phosphatase
phosphorylase
Glycogenesis and Glycogenolisis
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Synthesis of glucose to glycogen
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Glucose phosphorylation is irreversible
except in the liver cells, renal tubular
epithelial cells, and intestinal epithelial
cells because of the presence of glucose
phosphatase enzyme
Oxidation of 1 gram of glucose molecule
produces energy as much as 686.000
calories
Formation of 1 gram of ATP molecule needs
12.000 calories breakdown of glucose
produces 38 mol ATP
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Breakingdown of glycogen into glucose:
glycogenolysis
Activation of phosphorylation is stimulated by
epinephrine and glucagonAMP cyclic
The release of energy from glucose glycolysis
(produces two molecules of pyruvic acid)
38 molecules of ATP
The release of energy from glucose can be via
Glycolysis pathway (Embden Meyerhof)
Pentose phosphate pathway
(Phosphogluconate)
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GLYCOGENESIS- From glucose- From lactic acid, glycerol, pyruvic acid,
and some deaminated amino acids glucose glycogen
GLYCOGENOLYSIS- Phosphorylation phosphorylase enzyme- Activated by epinephrine and glucagon AMP cyclic
GLYCOLYSIS- Releasing of energy from glucose molecule
GLUCONEOGENESIS- Occurs in the liver, and some in the kidney
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Regulation of energy release from glycogenolysis glycolysis
1. Inhibition to the enzyme phosphofructokinase by ATP inhibits theformation of fructose 1,6-phosphatase
2. Inhibits by citrate ions3. The mechanism of the ATP-ADP-AMP
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LIPID : - Triglyceride (neutral fat) - Phospholipid- Cholesterol
Triglyceride (TG) : long chain fatty acids + glycerol
- Stearate acid (C 18, saturated) - Oleic acid (C16, unsaturated) - Palmitic acid (C16, saturated)
LIPID
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Saturated Fatty Acid
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Unsaturated Fattyu Acid
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LIPID
Triglyceride source of energy
PhospholipidCholesterol } Cell Membrane
Triglyceride as energy 146 mol ATP
The amount of ATP formed from 1 gr of lipid is 2,5 times of ATP formed from 1 gr of carbohydrate
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Digestion of TG fatty acid + glycerol
chylomicron (small droplet of TG), apoB
enter the limph vessel
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Hydrolysis of chylomicrons by LPL (lipoprotein lipase) in the adipose tissues and the liver fatty acid and glycerolthen synthesis of TG again in theliver and adipose cells
When it is needed for energyTG from adipose tissue or fat deposit is
transported to other tissues in the form of free fatty acids or non-esterified fatty acid bound to albumin
Controls: - Glucose levels in adipose cells -
glycerophosphate hydrolysis of TG- Hormones that increase hydrolysis of TG
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LIPOPROTEIN
Composition : TG, cholesterol, phospholipidand protein
It is syntesized in the liver Function : lipid transport in the blood Types :
- VLDL TG, cholesterol and phospholipid are moderate
- IDL TG , cholesterol and phospholipid >>
- LDL no TG, cholesterol , phospholipid is moderate
- HDL protein , cholesterol and phospholipid <<
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Lipid Metabolism Lipid is particularly stored in the adipose tissue
- The fatty acids are broken down in the mitochondria and enter the Krebs cycle
- Fatty acid binds to glycerophosphate to form triacylglycerol
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TG for energy production :- Hydrolisis of TG fatty acid and dan glycerol- Transport to the tissues oxiidation- Glycerol glycerol 3-phosphat enter the glycolytic pathway
Stages: Transports of fatty acid into the mitochondria
carnitine carrier Beta oxidation conversion of fatty acid into acetyl CoA Oxidation of acetyl-CoA in the Krebs cycle Final result is 146 molecules of ATP
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Lypolysis
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Lypolysis
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Keton Bodies:- Acetoacetic acid (keto acid)- -hydroxybutyric acid- Acetone
increase in the condition of hunger, diabetes
If ketosis
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Formation of TG from Carbohydrate Irreversible Started with glycolysisConversion of glucose to acetyl-coACitrate is transported into cytosol Needs insulin
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Protein
Amino acid is the final product of protein digestion
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MATT HILL PVMethionin Arginin Tryptophan Treonine Histidin
Isoleusin Lysin Leusin Phenylalanin Valine
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Protein Metabolism
Anabolisme protein synthesis
Catabolism
Amin group will be eliminated from the amino acids and will form a keto acid which can then be catabolized to generate energy that is then transferred to the ATP or can be synthesized into fatty acids
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General Protein metabolism pathway
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Amin group will be eliminated from the amino acid by way of:
Oxidation deamination, which would produceammonia. Ammonia formed is then converted into urea in the liver and excreted through the kidneys
Transamination, in which the amine group will be transferred to the keto acids and to form new amino acids
Protein Catabolism
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Deamination dan Transamination
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Protein Catabolism
- Free amino acid is stored in the form of cellular protein, and will undergo catabolism in most tissues, especially in the intestinal
mucosa, liver, skeletal muscle, kidney and brain.
- Lysin and Leusin form non-gluconeogenic intermediate products
- Protein catabolism process will particularly release amine group α-keto acids oxidation CO2
ATP formation
Glucose and lipid synthesis
- Cellular protein amino acid by enzyme: intracellularlysosome
- Exception: protein in the nucleic chromosome structural protein (collagen and contractile protein)
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In the liver, amino acids undergo deamination process released of amine group and the formation of keto-analog enter carbohydrate metabolism pathway
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- Released NH3 is converted to ureum and excreted (in mammals)
- In the reptile and birds NH3 is converted to uric acid
- In the aquatic species N waste is excreted in the form of ammonium ion
Oxidation and deamination of amino acid
- Deamination products : -keto acidenter siklus Krebs oxidation energy
Ureum formation by the liver- Deamination ammonia (NH3) ureum
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Formation and excretion of urea is a main waste product of N from protein catabolism
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Protein Metabolism in the Liver
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The main metabolic fuel components:
• Glucose (stored in the form of glycogen, in the liver and muscle)
• Amino acid (stored in the form of muscle protein)
• Fatty acid (3 fatty acids+1 glycerol in ester bond, stored in the form of TG in the adipose tissue)
• Keton bodies: acetone, acetoacetic acid,
-hydroxybutiric acid (from the fatty acid)
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Functional State in the Regulation of Metabolism
1. Absorptive stage: Stage where the nutrients from the digestive tract enterthe bloodstream
2. Post-absorptive stage: stage where the digestive tract is of nutrients so that the energy is taken from the storage
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NUTRIENT REQUIREMENT AT THE STAGE OF ABSORPTION
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In the absorption phase, liver takes up the glucose and converts it into glycogen and TG
Transport of fatty acid out side the cell as Very Low Density Lipoprotein (VLDL)
Circulation of amino acid in the blood is regulated by the liver
The fate of amino acid in the liver:
1. Is utilized for protein synthesis
2. Is converted into the form of analog carbohydrate and enter the Krebs cycle
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Influence of diet on insulin and glucagon
Insulin Glucagon
Carbohydrate + -
Protein + +
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Nutrients Requirement in
Post-absorptive Stage
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Post-absorptive Phase
• Glucagon, Insulin ↓
• Hormone-sensitive lipase (HSL) release of fatty acid from the adipose tissue
• HSL is active because of insulin secretion is decrease in the phase of post-absorptive(Insulin stimulates dephosphorylation) and cathecolamine secretion
• Final product: Free fatty acid = Non Esterified Fatty Acid (NEFA)
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BCAA: Branch-Chain Amino Acid
(Valine, Leucine, Isoleucine)
Amino acid of muscle origin as a source of
glucose
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Source of blood glucose :
1. Glycogenolysis (glycogen breakdown)
2. Gluconeogenesis (synthesis of glucose from lipidand protein)
SOURCE OF ENERGY DURING LACK OF FOOD:
fatty acid, triglyseride and keton bodies
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In the state of satrving/ fasting
- Fast mobilization of the NEFAs to the liver
• Oxidation for energy production
• Esterification TG production
• Ketone bodies production
In the liver mitochondria + carnithineBut depending on the existence of : CPT 1 (carnitine palmitoyl transferase I) enzyme
Is inhibited by malonyl CoA
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Starvation:
1. Phase 1- Decreased of LMB- The source of glucose comes from liver
glycogen (depleted in a matter of hours)- Next energy sources: fat catabolism (fatty
acids and glycerol) and amino acids glucose
- Production of ketone bodies2. Phase 2
• After 1 – 2 weeks, brain and other tissues utilize glucose and ketone bodies
• The main source of energy comes from the lipid
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Starvation:
Phase 3• Protein as a energy source (the liver, plasma protein,
then protein in the GI tract, liver and the muscle)• Decreasing of the size and function of the organ• Decreasing of the plasma protein decreasing of the
oncotic pressure ascites
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RUMINANTS
• Supply of glucose is from the gluconeogenesis(propionate VFA succinate oxaloacetate Krebs cycle)
• Acetate and butiric acid acetil ko-A Krebscycle unable to form oxaloacetate or glucose
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Endocrine and Nerve System Regulation in the
Phase of Absorption and Post-absorption
1. Insulin
Is an amino acid and is secreted by the βcell of pancreas
High plasma glucose stimulates insulinsecretion
Insulin action:
1. Increases cell membrane ability to uptake glucose
2. Increases enzyme function
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Effect of Insulin on carbohydrate metabolism
Increases glucose uptake by the cells (T)
Stimulates glycolysis (E)
Stimulates glycogen synthesis (E)
Inhibits of glycogen catabolism (E)
Inhibits gluconeogenesis (E)
Resuts :
Decreasing of plasma glucose concentration, increasing glycogen storage
Increasing glucose uptake compared to the releasing of glucose from the liver
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Effect of Insulin on Lipid Metabolisme
Stimulates TG synthesis (E)
Inhibits TG catabolism (E)
Stimulates lipoprotein lipase in the endothelial cells (E)
Results :
Decreasing of plasma glycerol and free fatty acid concentration
Increasing of fat storage and decreasing of the utilization of fat for energy
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2. Glucagon
Is an amino acid and is secreted by the αcell of pancreas
Regulation of glucagon secretion:
1.Low of plasma glucose
2.High of plasma amino acid
3. Activation of sympathetic nerve and ephinephrine in the circulation
4.Inhibition of parasympathetic nerve
5.Other hormones (GH, cortisol etc)
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3. Epinephrine and sympathetic nerve to the
liver and adipose tissues
Plasma Glukosa
Adrenal medula
Sekresi Epinefrin
Plasma Epinefrin
Otot Rangka
Glikogenolisis
Asupan Glukosa
Plasma Glukosa, asam lemak, gliserol
Aktivitas saraf simpatis
menuju jaringan lemak dan
hati
Hati
Glikogenolisis
Glukoneogenesis
Jaringan lemak
Lipolisis
Reflex melalui reseptor
glukosa pada otak
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4. Cortisol
Efffect of cortisol on the metabolism:
1. Basal concentration of cortisol is a stimulant forgluconeogenesis and lypolysis in the phase of post-absorptive
2. The increase of cortisol concentration will cause:
a. Increasing of protein catabolism
b. Increasing of gluconeogenesis
c. Decreasing of glucose uptake by the cells
d. Increasing of TG breakdown
Results: Increasing plasma amino acid, glucose and free fatty acid
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5. Growth Hormone
Function:
1. Stimulates lypolysis in the adipose tissues
2. Increases gluconeogenesis by the liver
3. Decreasing glucose uptake by the tissues