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Metabolic interrelationship in well fed state ط       Metabolic integration during well fed state ط      Inter-organ  relationship ط      Hormonal balance: Insulin/glucagon ratio                                           N L3  537-45  ;  D4   528-29. Metabolic Interrelation.

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slide1

Metabolic interrelationship in well fed state

ط      Metabolic integration during well fed state

ط     Inter-organ  relationship

ط     Hormonal balance: Insulin/glucagon ratio

                                          N L3  537-45  ;  D4   528-29

slide2

Metabolic Interrelation

  • Well-Fed State fig13.2 D4 (Mixed Fuels)
  • Early-Fasting State fig13.3 D4(3-4 hr post-absorptive period)
  • Fasting Statefig13.4 D4 (early / Intermediate / prolonged starvation)
  • Re-fed State fig13.6 D4
slide3

Metabolic Interrelation

1. Well-Fed State fig13.2 D4 (Mixed Fuels)

- In well-fed state the diet supplies the energy requirement (Glc, AA, fat)

- increase INS : Glg ratio (Glc, AA, fat)

slide4

Metabolic Interrelation

  • 1. Well-Fed State fig13.2 D4 (Mixed Fuels)
  • * Carbohydrate (diet) => Glc (liver) activated by INS =>
  • a) produce NADPH
  • b) stored as Glycogen
  • c) Oxidized to Pyruvate =>
    • · anaerobically produce Lactate
    • · complete oxidation (aerobically) through TCA cycle => CO2 + H2O
    • · converted to fat (G3P => glycerol) and stored in AT or muscle
    • - no cori cycle
    • Glc (liver) => other tissues activated by INS
  • d) Brain/Testis (main source): CO2 + H2O
  • e) RBCs/Adrenal Medulla (only source): Pyruvate/Lactate
  • f)  Adipose tissue: fat
  • g) Muscle: Glycogen / CO2 + H2O
slide5

Metabolic Interrelation

  • 1. Well-Fed State fig13.2 D4 (Mixed Fuels)
  • * Protein (diet) => AA (liver) activated by INS =>
  • a) usually AA pass liver (↑Km Enzs, except tRNA Enz during growth) to all tissues and activated by INS =>
    • ·  synthesize protein
    • ·  enters the carbon skeleton & oxidized completely => CO2 + H2O
  • b) if concentration of dietary AA is high it does not pass the liver
    • ·  synthesize protein
    • ·  enters the carbon skeleton & oxidized completely => CO2 + H2O
    • ·  produce urea
    • ·  converted to fat =>transported by VLDL, stored in AT & muscle
slide6

Metabolic Interrelation

1. Well-Fed State fig13.2 D4 (Mixed Fuels)

* Fat (diet) => Chylomicron (lymph) =>

a) reaches Adipose tissue

·         Stored as TG

b)  reaches muscle

·         Stored TG

·         Oxidized to CO2 + H2O

slide7

Metabolic Interrelation

  • 2. Early-Fasting State fig13.3 D4(3-4 hr post-absorptive period)
    • - In early fasting, hepatic glycogenolysis is an important source of bld glc
    • Fat & prt reduce gastric emptying fig13.3 D4, fig14.1 NL3
  • * Glycogen (liver) activated by Glg => Glc (gluconeogenesis) => other tissues
  • a) Muslce: alanine cycle
  • b) RBCs: cori cycle
  • c) Brain: CO2 + H2O
    • - End stage: bld glc and ins are low
    • - no protein synthesis
slide8

Metabolic response to starvation

ط     Stages of starvation and hormonal balance

ط     Post absorptive period : Duration and characters

ط     Early starvation : Duration and  fuel  utilization

ط     Intermediate starvation : Duration and fuel utilization, glucose alanine and fatty acid cycle

ط     Prolonged starvation : characters and causes of death after prolonged starvation

ط     Refeeding after prolonged starvation

ط     Integration of carbohydrates, Lipid and protein metabolism during starvation

ط     Regulatory role of ketone Bodies and T3 in starvation

                                          N L3 545-9;  D4   529 -34 

slide9

Metabolic Interrelation

  • 3. Fasting Statefig13.4 D4 (early/intermediate/prolonged starvation)
  • In fasting state, gluconeogenesis is required from AAs & glycerol
  • A. Fasting State (early starvation)
  • · Early stage: most tissues utilize glc fig13.4 D4, fig14.2, Table14.1 NL3
  • · Then: only brain & anaerobic tissues
  • · This will increase FA oxid in muscle & other tissues (e.g. kidneys)
  • · Up to 24 hours
slide10

Metabolic Interrelation

  • 3. Fasting Statefig13.4 D4 (early/intermediate/prolonged starvation)
  • A. Fasting State (early starvation)
  • * Glucose (liver) =>Cori cycle
    • a) Lactate (RBCs) =>
    • b) Glucose (liver) =>
    • c) Lactate (RBCs) =>
    • d)Glucose (liver) =>
slide11

Metabolic Interrelation

  • 3. Fasting Statefig13.4 D4 (early/intermediate/prolonged starvation)
  • A. Fasting State (early starvation)
  • * Protein => AA activated by Glucagon
  • a) Protein (Liver) => AA => Glucose
    • ·  Reach brain => Oxidized to CO2 + H2O
  • b) Protein (Muscle) => AA => Alanine / Glutamine
    • ·  Alanine reaches liver => gluconeogenesis to glucose + urea
      • - Glucose reach brain => Oxidized to CO2 + H2O
      • - Urea reaches kidney => excreted
    • · Glutamine reaches Gut => Alanine
      • - alanine reaches liver => gluconeogenesis to glucose + urea
        • * glucose to brain => oxidized to CO2 + H2O
        • * urea to kidneys => excretion
slide12

Metabolic Interrelation

3. Fasting Statefig13.4 D4 (early/intermediate/prolonged starvation)

A. Fasting State (early starvation)

* Fat (Adipose tissue) => Hydrolyzed to Glycerol + Fatty Acids

a)       Glycerol + Fatty Acids reach Liver

·         Glycerol => Glucose

- reaches brain => Oxidized to CO2 + H2O

·         Fatty Acids => Ketone bodies

- reaches brain => Oxidized to CO2 + H2O

- reaches muscle => Oxidized to CO2 + H2O

b)       Fatty Acids reaches muscle

·         Oxidized to CO2 + H2O

slide13

Metabolic Interrelation

3. Fasting Statefig13.4 D4 (early/intermediate/prolonged starvation)

B. Intermediate Starvation

· Early stage: high gluconeogenesis (lact, glycerol, G-AA) fig14.3, Table14.3 NL3

· Later stage: high KB

· 1-24 days

slide14

Metabolic Interrelation

3. Fasting Statefig13.4 D4 (early/intermediate/prolonged starvation)

C. Prolonged Starvation

· Low prt degrade – enz activity (AAs) fig14.4, Table14.4 NL3

· The rate of carb, lipid, prt metab reach steady state

· Constant high KB concentration

· Low N excretion

· Ends with Re-feeding or death

· Death is caused by pneumonia, low Ab, shock

slide15

Metabolic Interrelation

Role of KB

· 2-24 days: high KB is produced for brain, nervous tissue, kidney cortex, s.intest epithelial cells, heart

· Also decrease in glc utilization, FA oxid and prt degrad in other tissues

slide16

Metabolic Interrelation

  • Role of T3
  • · Thyroxine does not control metab rate
  • · Starve 2-3 days decrease basal metab rate (not thyroxine)
  • · The active for is triiodothyronine (T3)
  • · During starvation: decrease production of T3 from T4
    • Increase production of reverse-T3 from T4
  • · This is to control prt deg & energy expenditure
  • · Hypothyroid during starvation decrease prt breakdown and urea excretion and increase survival
slide17

Metabolic Interrelation

  • 4. Re-fed State fig13.6 D4 (after fasting / after starvation)
  • In early-refed state, fat is metabolized normally and normal glucose metabolism is slowly re-established
  • A. Early Re-feeding After Fasting
  • · Glc is the main fuel in breakfast fig13.6 D4, fig14.10 NL3
slide18

Metabolic Interrelation

  • A. Early Re-feeding After Fasting
  • * Carbohydrate (diet) => Glc (liver) activated by INS =>
  • a) Glc reach brain => oxidized to CO2 + H2O
  • b) Glc reaches Adipose tissue => converted to fat (G3P => glycerol) and stored
  • c) Glc reaches muscle => stored as Glycogen
  • d) Glc reaches RBCs => Lactate
    • ·  Lactate reaches liver => glc stored as glycogen
slide19

Metabolic Interrelation

  • A. Early Re-feeding After Fasting
  • * Protein (diet) => AA (liver) activated by INS =>
  • a) AA (liver) =>
    • ·  Stored as Glycogen + release Urea
    • ·  Protein Synthesis
  • b) AA reach all tissues =>
    • ·  synthesize protein
slide20

Metabolic Interrelation

  • A. Early Re-feeding After Fasting
  • * Fat (diet) => Chylomicron (lymph) =>
  • a) reaches Adipose tissue
    • ·  Stored as TG
  • b) reaches muscle
    • ·  Stored TG
    • ·  Oxidized to CO2 + H2O
slide21

Metabolic Interrelation

B. Re-feeding After Starvation

· Same as re-feeding after fasting plus high prt-AA metab

· 2 days: increase Glg, GH GC and deacrease INS lead to hogh FA, KB, Glc, AA

· 2-4 days; FA, Glc , KB ratio fig14.5 NL3