Energy storage Flashcards
Describe the major energy stores in a 70kg man.
- TAG
- 15kg
- 600,000kJ
- 15kg
- Glycogen
- 0.4kg
- 4,000kJ
- 0.4kg
- Muscle protein
- 6kg
- 100,000kJ
- 6kg
Describe the structure of glycogen
- polymer of chains of glucose residues
- chains originate from dimer of glycogenin
- residues linked by α-1,4 glycosidic bonds, with α-1,6 glycosidic bonds forming at branch points every 8-10 residues
- chains originate from dimer of glycogenin
• Describe the reactions involved in glycogen synthesis
- glucose + ATP → G6P + ADP
- hexokinase (glucokinase in liver) - ACTIVE
- G6P ↔G1P
- phosphoglucomutase
- G1P + UTP + H2O → UDP-glucose + Pi
- G1P uridylyltransferase - ACTIVE
- Glycogen (n residues) + UDP glucose → Glycogen (n+1 residues) + UDP
- glycogen synthase for α-1,4 glycosidic bonds
- branching enzyme for α-1,6 glycosidic bonds
• Describe the reactions involved in glycogen breakdown
- Glycogen (n residues) + Pi → G1P + Glycogen (n-1 residues)
- glycogen phosphorylase or de-branching enzyme
- G1P ↔G6P
- phosphoglucomutase
Glycogenolysis vs glycogenesis
- not simply reverse
- different enzymes allow for simultaneous inhibition of one pathway, and stimulation of another
• Identify the functions of muscle glycogen.
can only be use by muscle for energy production
- G6P fed into glycolysis
- lacks glucose-6-phosphatase
- glucagon has no effect
- AMP is allosteric activator of glycogen phosphorylase
- not in liver form of enzyme
Identify the function of liver glycogen
- released by liver into blood for use in other tissues
- G6P converted to glucose
- exported to blood
- buffers blood pH
- exported to blood
Glycogen synthase
rate limiting of glycogen synthesis
Glycogen phosphorylase
rate limiting of glycogen degradation
Regulation of liver glycogen metabolism
- Glucagon, adrenaline
- decrease glycogen synthase activity
- increase glycogen phosphorylase activity
- Insulin
- increase glycogen synthase activity
- decrease glycogen phosphorylase activity
Enzyme mechanism of action with glucagon, adrenaline and insulin
- glucagon, adrenaline
- phosphorylation
- insulin
- de-phosphorylation
• Explain the clinical consequences of glycogen storage diseases.
liver and/or muscle affected
- excess glycogen storage = tissue damage
- diminished stores = hypoglycaemia & poor exercise tolerance
Glycogen storage disease examples
- von Gierke’s disease: glucose-6-phosphatase deficiency
- McArdle: muscle glycogen phosphorylase deficiency
• Explain why glucose is produced from non-carbohydrate sources.
- gluconeogenesis requires after ~ 8-10hrs fasting
- maintain plasma glucose ~ 5mmol/L
- mostly occurs in liver and lesser extent in kidney cortex
• Explain how glucose is produced from non-carbohydrate
- pyruvate, lactate & glycerol → glucose
- essential & non essential amino acids
- whose metabolism involves pyruvate/intermediates of TCA
- mostly alanine
- whose metabolism involves pyruvate/intermediates of TCA
Why can acetyl coA not be converted to glucose.
- reaction catalysed by PDH is irreversible
- some carbon lost as CO2
What are the key enzymes & reactions in gluconeogenesis
- glucose-6-phosphatase
- g6p→glucose
- fructose-1,6-bisphosphatase
- f1,6bp→f6p
- phosphoenolpyruvate carboxykinase (PEPCK)
- oxaloacetate → phosphoenolpyruvate (intermediate of glycolysis)
- pyruvate carboxylase
- pyruvate→oxaloacetate
(all have -ve ∆G)
Regulation of gluconeogenesis.
- Glucagon, cortisol
- PEPCK: increased enzyme amount
- Fructose-1,6-bisphosphatase: increased enzyme amount & activity
- stimulates gluconeogenesis
- Insulin
- vice versa
- inhibits gluconeogenesis
- vice versa
Describe the Cori cycle.
- lactate produced in muscle/RBC in anaerobic glycolysis
- trafficked to liver, lactate → glucose (gluconeogenesis)
- glucose exit liver + returned to muscle
Explain why triacylglycerols can be used as efficient energy storage molecules in adipose tissue.
energy content per gram is twice that of carbs/protein
Adipocytes
- large lipid droplet of mainly TAG & cholesterol ester
- cytoplasm & organelles pushed to edge
- increase in size fourfold on weight gain before dividing to increase total number
- division is irreversible
• Describe how dietary triacylglycerols are processed for storage.
- TAG → fatty acids + glycerol
- pancreatic lipase
- Absorbed into intestinal epithelial cells
- Re-synthesised into TAG & packaged into chylomicron
- Drain into lymphatic system then enters circulation
- Storage
- TAG stored in adipose
• Describe how dietary triacylglycerols are processed for utilisation.
- Chylomicrons in circulation enter tissues
- Fatty acid oxidation to produce energy
- not cells lacking mitochondria e.g. RBC or brain
-> fatty acid don’t easily pass through blood-brain barrier
- not cells lacking mitochondria e.g. RBC or brain
• Describe how fatty acid degradation differs from fatty acid
synthesis.
Degradation
- cycle of reactions that remove C2 as acetyl coA
- occurs in mitochondria (separate enzymes)
- oxidative - produce NADH & FAD2H
- requires little ATP
- intermediates linked to coA
- regulated indirectly by fatty acid availability in mitochondria
- glucagon & adrenaline stimulate
- insulin inhibit
Synthesis
- cycle of reactions that add C2 as malonyl coA (consumes acetyl coA
- occurs in cytoplasm (multi-enzyme complex)
- reductive - requires NADPH
- requires lots of ATP
- intermediates linked to fatty acid synthase by carrier protein
- regulated directly by acetyl-coA carboxylase activity
- glucagon & adrenaline inhibit
- insulin stimulates
