metabolic interrelationship in well fed state ط metabolic integration during well fed state ط...
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Metabolic interrelationship in well fed state Metabolic integration during well fed state طInter-organ relationship طHormonal balance: Insulin/glucagon ratio ط N L3 537-45 ; D4 528-29
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Metabolic Interrelation
1. Well-Fed State fig13.2 D4 (Mixed Fuels)2. Early-Fasting State fig13.3 D4 (3-4 hr post-absorptive
period)3. Fasting State fig13.4 D4 (early / Intermediate /
prolonged starvation)4. Re-fed State fig13.6 D4
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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)
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Metabolic Interrelation
1. Well-Fed State fig13.2 D4 (Mixed Fuels)* Carbohydrate (diet) => Glc (liver) activated by INS =>a) produce NADPHb) stored as Glycogenc) 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 cycleGlc (liver) => other tissues activated by INS
d) Brain/Testis (main source): CO2 + H2Oe) RBCs/Adrenal Medulla (only source): Pyruvate/Lactatef) Adipose tissue: fatg) Muscle: Glycogen / CO2 + H2O
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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
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Metabolic Interrelation
1. Well-Fed State fig13.2 D4 (Mixed Fuels)* Fat (diet) => Chylomicron (lymph) =>a) reaches Adipose tissue· Stored as TGb) reaches muscle· Stored TG· Oxidized to CO2 + H2O
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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 tissuesa) Muslce: alanine cycleb) RBCs: cori cyclec) Brain: CO2 + H2O
- End stage: bld glc and ins are low- no protein synthesis
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Metabolic response to starvationStages of starvation and hormonal balance طPost absorptive period : Duration and characters طEarly starvation : Duration and fuel utilization طIntermediate starvation : Duration and fuel utilization, glucose alanine and fatty acid cycle طProlonged starvation : characters and causes of death after prolonged starvation طRefeeding after prolonged starvation طIntegration of carbohydrates, Lipid and protein metabolism during starvation طRegulatory role of ketone Bodies and T3 in starvation ط N L3 545-9; D4 529 -34
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Metabolic Interrelation
3. Fasting State fig13.4 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
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Metabolic Interrelation
3. Fasting State fig13.4 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) =>
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Metabolic Interrelation
3. Fasting State fig13.4 D4 (early/intermediate/prolonged starvation)
A. Fasting State (early starvation)* Protein => AA activated by Glucagona) 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
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Metabolic Interrelation
3. Fasting State fig13.4 D4 (early/intermediate/prolonged starvation)
A. Fasting State (early starvation)* Fat (Adipose tissue) => Hydrolyzed to Glycerol + Fatty Acidsa) 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 + H2Ob) Fatty Acids reaches muscle· Oxidized to CO2 + H2O
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Metabolic Interrelation
3. Fasting State fig13.4 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
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Metabolic Interrelation
3. Fasting State fig13.4 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
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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
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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
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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
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Metabolic Interrelation
A. Early Re-feeding After Fasting* Carbohydrate (diet) => Glc (liver) activated by INS =>a) Glc reach brain => oxidized to CO2 + H2Ob) Glc reaches Adipose tissue => converted to fat (G3P => glycerol) and storedc) Glc reaches muscle => stored as Glycogend) Glc reaches RBCs => Lactate
· Lactate reaches liver => glc stored as glycogen
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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
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Metabolic Interrelation
A. Early Re-feeding After Fasting* Fat (diet) => Chylomicron (lymph) =>a) reaches Adipose tissue
· Stored as TGb) reaches muscle
· Stored TG· Oxidized to CO2 + H2O
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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