Energy storage Flashcards
name some cells with an absolute requirement for glucose as main source of energy.
- RBC
- Neutrophils
- innermost cells of kidney medulla
- lens of eye (as blood disrupts vessels)
name some consequences of hypoglycaemia.
- confusion
- weakness, nausea
- muscle cramps
- brain damage and death
what is the body’s response for the issue of keeping stable blood glucose levels?
- store of glucose known as glycogen.
where is glycogen stored in the body?
- muscle as intra and intermyofibrillar glycogen.
- liver as granules in hepatocytes.
describe the structure of glycogen.
- glucose polymer, with many glucose residues.
- a 1-6 glycosidic bonds join the branches every 8-10 residues and a 1-4 glycosidic bonds join the chains.
- branched structure originating from primer core dimer protein glycogenin that converts glucose to glycogen.
how is glycogen stores utilised in liver?
- G6P converted to glucose and exported to blood.
- liver glycogen is a buffer of blood glucose levels.
how is glycogen utilised in muscle?
- muscle lacks Glucose-6-phosphotase to convert G6- into glucose so enters glycolysis.
what is the rate limiting enzyme for glycogenesis?
- glycogen synthase
what is the rate limiting enzyme for glucogenolysis?
- glycogen phosphorylase
what happens to the two pathways at high levels of glucagon/adrenaline?
- glycogenesis decreases and increases.
* muscle cells do not have glucagon receptors so unaffected by high glucagon levels.
what happens to the two pathways at high levels of insulin?
- glycogenesis increases and glycogenolysis decreases.
why do glycogen storage diseases arise?
- inborn errors of metabolism, inherited.
- deficiency or dysfunction of enzymes of glycogen.
- excess glycogen storage leads to tissue damage.
- diminished stores lead to hypoglycaemia and poor exercise tolerance.
what are some examples of glycogen diseases?
DEFICIENCY NOT LACK
- von gierkes disease : G6-phosphatase deficiency
- mcardle disease : muscle glycogen phosphorylase deficiency.
why is it necessary for gluconeogenesis to take place?
- beyond 8h, liver glycogen starts to deplete so alternative source needed.
what are the precursors of gluconeogenesis?
- lactate : from anaerobic in cori cycle
- glycerol : adipose breakdowns triglycerides
- amino acids : mainly alanine
what are the key enzymes in gluconeogenesis? and what are the main control sites of pathway?
- phosphoenolpyruvate carbocykinase (PEPCK)
- oxaloacetate to glycolysis pathway intermediate.
- fructose 1-6, bisphosphatase
- as phosphofructokinase irreversible.
- glucose-6-phosphatase
- hexokinase irreversible.
PEPCK and fructose 1-6, bisphosphatase control sites.
when is gluconeogenesis regulated?
- starvation
- prolonged exercise
- stress
- stimulated by glucagon and cortisol.
- inhibited by insulin.
how are lipids stored?
- glycerol and fatty acids stored as triacylglycerols.
- TAG hydrophobic so stored an anhydrous adipose.
- utilised in exercise, starvation, stress and pregnancy.
- storage and mobilisation under hormone control.
describe structure of adipose/
- large lipid drops filled with TAG or cholesterol with organelles pushed to side.
- 30 billion fat cells - 15kg.
What is lipogenesis?
- fatty acid synthesis mainly in liver, carbon from pyruvate.
what is the key regulatory enzyme in lipogenesis?
- acetyl-CoA carboxylase which is increased in activity by insulin and citrate allosterically, and decreased by glucagon and adrenaline and AMP allosterically.
compare B-oxidation and FA synthesis.
- remove C2 vs add C2
- in mitochondria vs in cytoplasm
- oxidative vs reductive
- insulin inhibits vs insulin stimulates
