Integration of metabolism Flashcards
What can the brain not use as a metabolic fuel source
fatty acids
where is the body’s main carb store
liver
what is glucose stored as
glycogen
what method of respiration does skeletal muscle do in light contraction
ox phos
why can’t skeletal muscle do ox phos in vigorous exercise
ATP consummation faster than supplied, limited by O2 and glucose/fatty acid
what does muscle do in vigorous exercise
break down glycogen
what happens in anaerobic respiration
pyruvate to lactate which enters liver
What fuel can the brain use
ketone bodies and glucose
hypoglycaemia causes…
fainting and coma
hyperglycaemia causes..
irreversible change
How is heart designed for aerobic respiration
many mt
what fuel does the heart use
TCA substrates: fatty acid and ketone bodies
loss of O2 to heart causes
MI
metabolic processes that take place in liver
glycolysis, gluconeogenesis, transamination, lipoprotein metabolism
how much of body’s metabolic rate does liver do
20%
what happens to excess glucose - 6- phosphate
turns to glycogen - liver and muscle
what happens to aexcees acetyl CoA
turns to fatty acid
in fasting what happens to acetyl CoA
ketone body production
how can pyruvate and TCA intermediates make AA
backbones form nucleotides
how does glucose-6-phosphate contribute to the production of NADPH
make nucleotides via pentose phosphate pathway
at what glucose conc will the body become hypoglycaemic
3mM
How does the body avoid hypoglycaemia
breakdown glycogen, release fatty acids, convert acetyl CoA to ketone bodies
how long does it take for glycogen stores to be depleted
12-18 hours
purpose of gluconeogenesis
produce glucose from non-carb sources (pyruvate)
when is gluconeogenesis important
starvation
why is gluconeogenesis not a reversal of glycolysis
different enzymes - irreversible reactions
where does gluconeogenesis occur
liver
what does gluconeogenesis need and why
ATP source, make reactions energetically favourable
which precursors enter gluconeogenesis
lactate, aa, glycerol
How can lactate regenerate pyruvate
Cori cycle - LDH
Where do AA come from for gluconeogenesis
diet/breakdown of muscle
What does triglyceride hydrolysis do?
yield fatty acid and glycerol - glycerol backbone generate DHAP
which enzymes catalyse the irreversible reactions in glycolysis
hexokinase, phosphofructokinase, pyruvate kinase
enzymes in gluconeogenesis
pyruvate carboxylase (p - oxyloacetate) phospoenolpyruvate carboxykinase (o-phospoenolpyruvate) Fructose 1,6 bisphosphatase(fructose 1,6 bp - f 6 p)
glucose 6 phophotase (g-6-p - glucose)
where does pyruvate decarboxylase act
mt
waste product of deamination
urea
What are the glycogenic AA skeletons
Pyruvate, alpha - ketoglutarate, succinyl CoA, fumarate, oxaloacetate
what are the ketogenic aa skeletons
acetyl CoA, acetoacetyl CoA
What are glucogenic AA
skeleton give ris to glucose by gluconeogenesis
what are ketogenic AA
used to synthesis fatty acid and ketone bodies
How is the increased demand for glucose met?
increase in the number of glucose transporters on membrane of muscle cells
what does adrenaline do
increase glycolysis and gluconeogenesis rate, increase release of fatty acids
why is pyruvate converted to lactate in anaerobic respiration
restore NAD+ levels
Which reactions are the best to control to control metabolic pathways
irreversible steps
How can you control metabolic pathways
product inhibition, signalling molecules
Km hexokinase 1 (muscle)
o.1mM
effect of low Km
active at low glucose conc
What inhibits hexokinase 1
glucose-6-phosphate
Km of hexokinase 1V (liver)
4mM
effect of high Km
less sensitive to blood glucose conc
sensitivity of hexokinase 1V to glucose-6-phosphate
low
where is glucose-6-phosphotase found
liver
What do glucocorticoids do
increase synthesis of met enzymes concerned with glucose availability
where are adrenaline and glucocorticoids secreted from
adrenal glands
insulin effects:
increased glucose uptake, liver and muscle, triglyceride synthesis, increased use of metabolic intermediates (stimulatory effect on synthesis and growth)
to stop glucose levels dropping…
glucagon secreted, gluconeogenesis, fatty acid breakdown as a substrate for ATP production.
what happens after prolonged fasting
glucagon/insulin ratio increases hydolysise fatty acids TCA intemediates break down protein break down ketone bodies from fatty acids and aa
overall effect of diabetes
metabolism controlled as if in starvation
what causes acidosis
increase in ketone bodies
How does diabetes cause cardiovascular problems
increased fatty acids and lipoprotein levels
effect of glucagon
stimulate gluconeogenesis
risk of relative excess of glucagon compared to insulin
high heptic output of glucose - hyperglycaemia
