integration of metabolism Flashcards

(31 cards)

1
Q

describe metabolism pathways?

A

pathways and cycles and reactions occur in integrated manner to fulfil cell requiement

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2
Q

what is unique about brain metabolism ?

A

Require glucose

and can use keton bodies under CERTAIN CONDITIONS

SOLELY GLUCOSE AND KETON BODIES

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3
Q

Unique metabolism of muscles?

A

Use glucose

Fatty acids

Ketone bodies

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4
Q

metabolism of liver?

A

Provide fuel to brain and muscles

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5
Q

metabolism of adipose tissue?

A

Provide fuel

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6
Q

RBCs?

A

ONLY GLUCOSE cuz theres no mitochondria

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7
Q

what are 2 types of metabolism ?

A

Anabolism –> BUILDING

Catabolism —> Breaking down to produce energy

Anabolism reactions will happen in other places than catabolic reaction

if they occur at the same place = wont occur at the same time /phase

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8
Q

what regulates metabolism?

A

Enzyme levels –> ALLOSTERIC INERACTION and covalent modification and transcription ( like phosphorylation for example)

Compartmentalization —> like how glycolysis in cytosols and TCA in mito

Specialization of organs

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9
Q

what are central themes of metabolism ?

A

ATP

Reducing molecules ( NADH, FADH, NADPH )

Biomolecules

Biosynthetic and degradation pathways are distinct

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10
Q

describe ATP?

A

Universal energy carrier

Atp is generated by oxidation of metabolic fuels —> Glucose , fatty acids or AA

substrative phosphorylation where molecules with higher energy levels are able to phosphrylate ADP into ATP

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11
Q

describe reducing molecules?

A

Redox agent for reductive biosynthesis

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12
Q

describe biomolecules ?

A

Constructed from a small set of building blocks

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13
Q

what are 3 metabolic key crossroads ?

A

Glucose 6 phosphate

Pyruvate

Acetyl- COA

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14
Q

what are key junctions between Glucose 6 phosphate 6 pathways?

A

When glucose is transported into cells it rapidly become GLUCOSE 6 P

1- G6P can become pyruvate ( most common and main )

2- G6P can be converted to G1P and become glycogen ( in liver)

3- Converted to ribose 5 phosphate by the pentose phosphate pathways

4- Glucose 6 phosphate can e generated from glycogen stores or by gluconeogenesis

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15
Q

junctions between pathways of PYUVATE ?

A

Pyruvate is generated from :

1- G6P by glycolysis

Pyruvate is REDUCED into LACTATE under ANEROBIC CONDITION

Lactate produced must be subsequently oxidized back into pyruvate

2- Pyruvate is also TRANSAMINATED to form alanine
- Several AA are gedraded into pyruvate

3- Pyruvate maybe CARBOXYLATED to form Oxaloacetate in the matrix of the mitochondria —> FIRST STEP OF GLUCONEOGENSIS

4- OXIDATION of pyruvate into Acetyl COA by pyruvate dehydrogenases complex ( for citric acid cycle )–IRREVERSIBLE–> this is between Carbohydrate and fatty acid metabolism

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16
Q

what are the junctions between pathways Acetyl Coa pathways?

A

Acetyl Coa is generated from :

1- Oxidation decarboxylation of PYRUVATE

2-from B oxidation of fatty acids

3- Acetyl Coa is produced from degradation of KETOGENIC AA

4- Acetyl Coa may be completely OXIDIZED into CO2 via the citric acid cycle

5- Converted to HMG COA —> cholesterol or ketone bodies

6- Acetyl Coa may be exported into cytosol and converted to FATTY ACIDS

17
Q

what are 2 types of AA?

A

Ketogenic –> converted to acetyl Coa directly

Glucogenic –> Converted to pyruvate which then to Acetyl Coa

18
Q

what is the metabolic profile of brain?

A

Glucose is fuel for the brain

Consumes 120 g/day of glucose

60-70% of utilization of glucose

DURING STARVATION = KETONE BODIES

19
Q

describe metabolic prolife of muscles?

A

Major fuels —>

WELL FED = GLUCOSE

Fasting/starvation = FATTY ACIDS, KETONE BODIES ( while brain and RBC will use glucose )

Storage of glycogen –> 3/4 of all glycogen

Highly affected by physical activity

Glycogen in the muscle is degraded into glucose 1-P –> Glucose 6 P –> Glycolysis –> Energy

Glycogen in the muscle is not intended to provide blood glucose cuz of LACK of enzyme GLUCOSE 6 PHOSPHATE ( BUT LIVER CAN DONATE GLUCOSE TO BLOOD cuz it has the enzyme )

Glucose is for burst activity —> Produce lactate ( anerobic )

20
Q

what is the source of ATP in burst activity ?

A

Phosphocreatine

21
Q

describe adipose tissue metabolic prolife ?

A

Triacylglycerols –> Stored in adipose tissue

Enormous reservoir of metabolic fuel

Synthesis of TAG needs glucose

Glucose lvl determines if FA are released into blood or not

Well fed —> High insulin –> activate synthesis of Triglycerides and thus FA synthesis

Glucose will get into glycolysis -> reach intermediate DHP –>Glycerol phosphate –> add to fatty acyl Coa = triacylglycerols to be stored

Fasting —> Glucagon –> ACTIVATE HSL = break down stored TAGS –> glycerol will be used for gluconeogenesis and FFA will be sued for energy and Acetyl Coa will be used for keton energies

22
Q

Describe metabolic prolife of kidney ?

A

Excretion of urine

Excretion of waste products

Blood plasma is filtered

Water and glucose REABSORBED

during starvation –> IMP SITE FOR GLUCONEOGENSIS

23
Q

Liver prolife in carbohydrate metabolism ?

A

Essential for providing fuel to brain ,muscles and other organs :

Glycogenolysis
Gluconeogenesis
Ketogenesis

Most compounds is absorbed from diet —> PASS THROUGH LIVER

Regulate metabolites in blood

Pentose phosphate pathway –> produces NADPH –> REDUCING AGENTS FOR CHOLESTEROL SYNTHESIS AND FATTY ACID

G6P –> liver glycogen or sent outside to blood or pyruvate

pyruvate –> Acetyl Coa

ACETYLCOA–> fatty acids

or Cholesterol or ketone bodies or TCA

24
Q

Liver prolife of FATTY ACIDS?

A

Synthesize :

Fatty acids

Lipoproteins

Cholesterol

Ketone bodies

TaGS

Fatty acids will converted to triglycerides and wont be stored here instead = exported as VLDL if this is disrupted = FATTY LIVER

Acetyl Coa –> Cholesterol = bile sites

or Acetyl Coa –> KETONE BODIES then to blood

or Acetyl Coa –> TCA cycle

25
liver prolife of AA?
Liver cells will: Synthesis proteins like albumin ( all plasma prorteins are from liver except immuno) AA are broken down in the liver by UREA CYCLE Gluconeogenesis --> Glucogenic AA will be converted to pyruvate (ALANINE ) We cant store AA so we convert them to pyruvate ESPECIALLY ALANINE
26
what is the function of insulin on metabolism ?
released in well fed state ( 2 hours of last meal )--> WILL START FED STATE : 1- Stimulate storage of fuels --> Synthesis of TAGs in adipose tissue and muscles 2- Accelerate uptake of blood glucose 3- Stimulates Glycogen synthesis in muscle and liver 4 Accelerate glycolysis in liver 5- Increase synthesis of fatty acids 6- Stimulates the synthesis of proteins 7- SUPPRES gluconeogenesis of liver
27
what is the function of glucagon in short starvation?
Main target organ is liver 1- Mobilizes Glycogen stores ( breakdown ) 2- Inhibit glycogen synthesis 3- Inhibit fatty acid synthesis 4- Stimulates gluconeogenesis in LIVER --> large amount of glucose in liver is released in blood stream to maintain the lvl 5- Promotes muscles + Liver use FATTY ACIDS as fuel when blood glucose lvl drop FATTY ACIS ARE NOT GLUCOGENIC SUBSTRATE it cannot be used in gluconeogenesis like Pyruvate , glycerol , lactate, AA, WHY? cuz fats will break down to ACETYL COA but ACETYL COA CANNOT BE CONVERTED BACK TO PYRUVATE so not useful
28
what is the first priority in prolonged starvation ?
Provide sufficient glucose to brain and other tissues thar are dependent on it
29
what is the second priority in prolonged starvation ?
PRESERVE PROTEIN by shifting from utilization of glucose to utilization of fatty acids + KETONE BODIES Mobilization of TAGS in adipose tissue + GLUCONEOGENESIS by liver ---> MUSCLE SHIFT FROM GLUCOSE TO FATTY ACID AS FUEL
30
what happens after 3 days of starvation ?
Liver form large amount of : Keton bodies will released to blood--> BRAIN and HEART uses them as fuel
31
what happens after several weeks of starvation ?
Ketone bodies are major fuel of brain After depletion of TAG stores ( glycerol will be used for gluconeogenesis and FFA for energy ) The proteins degradation is stimulated --> death due to loss of heart, liver and kidney function ( CUZ we get AA from protein for energy and AA --> PYRUVATE --> GLUCOSE ) Excessive triglyceride breakdown will cause keton bodies to slowly raise ( cuz end product is Acetyl Coa and can be used for ketone bodies ) and once it does it will make brain favor the use of keton bodies over glucose ( shifting utilization of glucose to fatty acids and ketone bodies )