integration of metabolism Flashcards
(21 cards)
outline metabolic features of the brain
requires continuous glucose supply
cannot use fatty acids
ketone bodies can partially substitute for glucose
hypoglycaemia causes faintness and coma
hyperglycaemia can cause irreversible damage
20% of resting metabolic rate
outline metabolic features of the skeletal muscles
ATP requirements vary due to activity
light contraction- requirements met by oxidative phosphorylation
vigorous contraction- O2 becomes limiting
glycogen breakdown and lactate formation
outline metabolic features of the heart
must beat constantly designed for complete aerobic metabolism the heart uses TCA cycle substrates loss of O2 causes cell death(myocardial infarction) 10% of resting metabolic rate
outline metabolic features of the liver
can interconvert nutrient types
glucose storage as glycogen
lipoprotein metabolism
20% of metabolic rate
what can be used to make nucleotides
glucose-6-phosphate and backbones of TCA intermediates
this also generates the bulk of NADPH needed for anabolic pathways
outline aerobic exercise in terms of muscles and liver
contractions increase ATP demand contractions increase glucose transport muscle glycolysis increases(adrenalin) gluconeogenesis increases(adrenalin) fatty acids increase(adrenalin)
how is the increased glucose demand met for muscles in exercise?
increase in number of glucose transporters
what to the requirements of muscle actomyosin ATPase balance with?
cations
what is the role of adrenalin in exercise?
increases gluconeogenesis by liver
increases release of fatty acids from adipocytes
outline anaerobic exercise in terms of muscles and liver
ATP demand cannot be matched by O2 delivery
transport cannot keep up with demand for glucose
muscle glycogen breakdown increases
lactate increases
liver uses lactate to form glucose(recovery)
how and why are NAD+ levels replenished
to maintain glycolysis. pyruvate is taken up by liver and converted to lactate by lactate dehydrogenase(LDH)
how are these pathways controlled
product inhibition
signalling molecules like hormones
compare the isoforms of hexokinase in liver(Hk IV) and muscle(Hk I)
Hk I(muscle) high glucose affinity (Km 0.1mM) highly sensitive to G-6-P inhibition Hk IV(liver) low glucose affinity (Km 4mM) less sensitive to G-6-P inhibition
where is glucose 6-phosphatase present?
liver but not muscle (it catalyses the reverse of hexokinase)
when is insulin secreted and what does it do?
when glucose levels rise
stimulates uptake and use of glucose and storage as glycogen and fat
when is glucagon produced and what does it do?
when glucose levels fall
stimulates production of glucose by gluconeogenesis and breakdown of glycogen and fat
what does adrenalin do ?
strong and fast metabolic effects to mobilise glucose for ‘fight or flight’
what do glucocorticoids do?
steroid hormones that increase synthesis of metabolic enzymes concerned with glucose availability
what is type I diabetes mellitus?
failure to secrete enough insulin(beta-cell dysfunction)
what is type II diabetes mellitus?
failure to respond appropriately to insulin(insulin resistance)
outline the complications of diabetes
hyperglycaemia with progressive tissue damage(retina, kidney, peripheral nerves etc)
increase in plasma fatty acids and lipoprotein levels with possible cardiovascular complications
increase in ketone bodies with the risk of acidosis
hypoglycaemia with consequent coma if insulin dosage is imperfectly controlled