Integration of metabolism
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The document summarizes metabolism during fed and fasted states. During feeding, carbohydrates, fats, and proteins from food are absorbed and stored or used for energy in the liver, adipose tissue, muscle, and brain. The liver converts nutrients to glycogen, triglycerides, or sends to other tissues. In fasting, glycogen stores are used for glucose followed by gluconeogenesis and lipolysis while ketone bodies and fatty acids provide energy and preserve proteins.
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Integration of metabolism
- 2. STARVE FEED CYCLE • Use of metabolic fuel for storage and energy production • During absorptive stage – Storage • During post absorptive stage/starvation – Used as fuel Food intake CO2 + H2O + Urea Storage Metabolism Absorptive stage Post absorptive stage
- 3. METABOLIC CROSSROADS Carbohydrates Glucose-6-phosphate Fats Fatty acids Cholesterol Acetyl CoA Pyruvate Amino acids Proteins Glycerol
- 4. FED STATE CARBOHYDRATE METABOLISM: LIVER Glucose from GUT Uptake to liver via GLUT - 2 Phosphorylation by glucokinase Glucose – 6 – phosphate formation Glycogen synthesis PPP pathway NADPH generation Facilitates FA synthesis Activation of PDH complex Acetyl CoA *
- 5. FED STATE LIPID METABOLISM: LIVER Chylomicron remnants Glycerol Pyruvate Fatty acids * Glycolysis Glycerol Acetyl CoA TAG VLDLTo adipose tissue
- 6. FED STATE PROTEIN METABOLISM: LIVER Amino acids from GUT Acetyl CoA TCA cycle Pyruvate Protein synthesis To replenish the proteins, that have been used during postabsorptive state BCAAs are transferred to muscle
- 7. FED STATE CARBOHYDRATE METABOLISM: ADIPOSE Glucose from GUT Influx of Glucose to adipocytes via GLUT-4 Phosphorylation by glucokinase Glucose – 6 – phosphate formation Activation of PDH complex PPP pathway NADPH generation Acetyl CoA Facilitates FA synthesis Glycerol
- 8. FED STATE LIPID METABOLISM: ADIPOSE Chlylomicrons (From GUT) VLDL (From Liver) Lipoprotein lipase Fatty acid Acetyl CoA TAG Chylomicron remnants Stored in Adipocytes
- 9. FED STATE CARBOHYDRATE METABOLISM: MUSCLE Glucose from GUT Uptake to muscle via GLUT - 4 Phosphorylation by hexokinase Glucose – 6 – phosphate formation Glycogen synthesisActivation of PDH complex Acetyl CoA TCA cycle and energy generation
- 10. FED STATE PROTEIN METABOLISM: MUSCLE Amino acids from GUT BCAAs are transferred to muscle Transfer to muscle for protein synthesis Energy production and protein synthesis
- 11. FED STATE METABOLISM: BRAIN Glucose from GUT Uptake to brain via GLUT - 1 Glucose – 6 - phosphate Pyruvate Acetyl CoA TCA cycle
- 12. • Allosterically regulated: 1. PFK-1 2. Fructose 1,6 bisphosphatase (Gluconeogenesis) • Covalent modification: 1. Glycogen synthase 2. PFK-2 domain 3. Pyruvate Kinase 4. Acetyl CoA carboxylase 5. HSL 6. Glycogen phosphorylase (Glycogenolysis) • Induction and repression: 1. Acetyl CoA carboxylase 2. Fatty acid synthase 3. Phosphoenolpyruvate carboxykinase (Gluconeogenesis)
- 13. Fasting: Voluntary refusal to take food Starvation: Forceful deprivation of food
- 14. Stages of fasting Stage Duration Sources of glucose Early From 10-12 hours after meals, upto 2 days Hepatic glycogenolysis, gluconeogenesis Intermediate 2 days to 24 days Gluconeogenesis, fatty acid oxidation and ketone bodies Advanced Beyond 24 days FA oxidation and ketone bodies
- 15. Starve-feed switch • Blood insulin : glucagon ratio is the switch • In fed state the ratio is 0.5 • After overnight fasting, the ratio is 0.15 • High ratio promotes glycogenesis, glycolysis • Low ratio promotes glycogenolysis, neoglucogenesis
- 18. PROLONGED STARVATION - GLUCONEOGENESIS Gluconeogenesis Glycerol Propionyl CoA Amino acids
- 19. PROLONGED STARVATION - LIPOLYSIS Starvation Acetyl CoA Carboxylase HSL Malonyl CoA CPT-1 Fatty acyl CoA Acetyl CoA Pyruvate Oxaloacetate Neoglucogenesis TAG Glycerol
- 20. PROLONGED STARVATION – KETOGENESIS Acetyl CoA Ketone bodies Oxaloacetate for TCA ATP generation from FA
- 21. PROLONGED STARVATION – PROTEOLYSIS Muscle protein Pyruvate, oxaloacetate ketoglutarate Neoglucogenesis Alanine, aspartate, glutamate Glutamine
- 22. METABOLISM IN LIVER DURING FASTING Glycogen Glucose – 6 – PO4 Glucose To blood Pyruvate Acetyl CoA Ketone bodies Amino Acids, lactate Fatty acids
- 23. How ketone bodies helps in preserving essential proteins?
- 24. METABOLISM IN ADIPOCYTE DURING FASTING TAG Fatty acids Glycerol To tissue as energy source To liver for gluconeogenesis Acetyl CoA Energy production
- 25. Adipose tissue and muscle cannot utilize glucose formed from neoglucogenesis during fasting. Why?
- 26. METABOLISM IN MUSCLE DURING FASTING Fatty acids Ketone bodies Acetyl CoA Acetyl CoA TCA cycleAmino acids Gluconeogenic precur.
- 27. Insulin : Glucagon, Epinephrine Adenylate cyclase cAMP Active protein kinase Enzyme phosphorylation Glycolysis Lipogenesis Chol. synthesis Protein synthesis Gluconeogenesis Fatty acid oxidation
- 28. Work ATP use ATP AMP Active AMP kinase Enzyme phosphorylation Glycogenolysis FA oxidation Glycolysis Lipogenesis Cholesterol synthesis Protein synthesis
Editor's Notes
- Fed state – NO gluconeogenesis, as acetyl CoA is being used for FA synthesis
- FA synthesis from acetyl CoA is promoted by increased citrate from TCA cycle, and increase formation of malonyl CoA, which ultimately inhibit CPT-1 of FA oxidation Glycerol kinase is present in liver
- Transaminases for BCAA is present only in muscles
- Blood glucose level in fed state is 100-110 mg% Blood glucose after overnight fasting is 70 mg%
- Main purposes of lipolysis: Provides ATP for body function Provides glucose for vital need of body
- NADH from oxidation of FA pushes acetyl CoA to ketogenesis Liver lacks thiophorase, that’s why cant use ketone bodies
- Because no insulin
- Initially FA and ketone bodies, after 3 weeks, only FA oxidation, which produces Acetyl CoA, which inhibits PDH and spares pyruvate for gluconeogenesis Muscle cannot sense glucagon level. Only sense fall of insulin and sustained glucocorticoids