metabolic interrelationship in well fed state ط metabolic integration during well fed...
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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. - PowerPoint PPT PresentationTRANSCRIPT
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
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
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)
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
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
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
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
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
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
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) =>
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
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
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
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
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
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
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
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
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
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
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