IAS16 Flashcards
metabolism significance
Secure useful substances (for synthesis of biomolecules OR energy generation in form of ATP)
Get rid of harmful substances
Keep substances in safe level in blood
catabolism relation w/ anabolism
catabolism breaks down large substances into small substances; anabolism creates large substances from small substances
catabolism converges, anabolism diverges
catabolism supplies energy for anabolism
FA, glucose, AA metabolism convergent point
acetyl coA -> TCAC -> electron funneling in ETC to generate ATP
TCAC intermediates anabolism
siphoned out for biosynthesis:
OAA -> carbs through PEP carboxykinase & GNG
citrate -> lipids
OAA, malate & ketoglutarate -> AA / proteins
TCAC intermediates anabolism effect
less intermediates running TCAC, incomplete -> lower rate of ATP production
replenishment of TCAC intermediates
anaplerotic Rx
pyruvate -> (malic enzyme) malate
pyruvate -> (pyruvate carboxylase) OAA
PEP -> (PEPK) OAA
regulation of metabolism: why
simul. formation & degradation of organic products is a waste -> cat / ana are reciprocally regulated i.e. active pathway supresses other
regulation of metabolism methods
diff. enzymes used for cat & ana to control rate of Rx with same starting & end points, often enzymes at start & end controlled -> dir. of Rx also controlled
cat & ana in diff. compartments -> enzymes, intermediates & reg. factor conc. all controlled
cellular level: flux of metabolites in pathway, role & metabolism of enzymes, negative feedback, transport of intermediates across organelle membrane
organism level: flux of metabolites from organ to organ, regulation by growth factors & hormones
metabolic homeostasis
to ensure enough blood circulation of fuel for ATP generation (const. flow of fuel)
balance btn: rate of intake, rate of oxidation of fuel, rate of fuel storage in excess, rate of mobilization from storage, rate of de novo synthesis
–> control of balance in substrate availability & need
metabolic homeostasis controlled by
blood concentration of metabolite affect rate of uptake or storage
hormones signal directly phy cond. of body & nutrient supply demand
nerve impulse from CNS directly influence metabolism
glucose importance
most cells use glucose preferably or solely for ATP generation & production of precursors of other pathways
blood glucose level regulated by
insulin & glucagon, blood levels change continuously depending on BGL, regulates carb, AA & lipid metabolism based on body needs: excess stored, appropriate fuel mobilized in demand
epinephrine & cortisol
insulin function
anabolism hormone
increase fuel uptake:
- glucose uptake into glycogen storage in liver
- TAG production in adipocyte
- AA uptake & protein synthesis by muscle
inhibit mobilization of fuels from stores e.g. TAG, protein & glycogen
transport glucose to muscle & liver cells to promote oxidation of glucose (as fuel) for ATP production
glucagon function
glucagon: insulin counterregulatory hormone, maintain fuel availability in absence of dietary glucose
- promote FA mobilization from adipocytes to generate ATP
- promote gluconeogenesis from AA, glycerol & lactate
- promote liver conversion from stored glycogen to glucose
no effect on muscles storage for sudden needs
epinephrine & cortisol function
blood levels mediated by CNS, insulin counter regulatory hormones, fuel mobilization in acute stress
epinephrine: promote FA mobilization from adipocyte, promote glucose production in liver
cortisol: promote FA mobilization from adipocyte, promote AA mobilization from muscles, promote gluconeogenesis
energy source for muscle contraction
low demand: blood glucose, FA, KB aerobically
high demand: glycogen anaerobically (forms lactate)
phosphocreatine -> creatine in heavy burst of activity
ATP function in brain & significance
provide energy & maintain electric potential of neurons (power Na+/K+ ATPase pump)
hence in fasting, restoration of BGL for brain usage is 1st priority
liver in prolonged fasting state
liver is major glucose source for brain
protein degradation into AA in muscle -> AA TA/DA in liver -> C portion enters TCAC & leaves imme. as OAA -> pyruvate -> glucose via GNG -> blood for brain usage
high rate of FA breakdown via beta oxidation -> acetyl coA forms; OAA siphoned out for GNG -> less OAA in TCAC to accept acetyl-coA -> accu. in liver, stimulates KB production -> [KB] in blood inc. for brain
effect: KB acidic -> blood pH drops -> ketoacidosis
diabetes types, causes & development
I: insufficient insulin production, autoimmune destruction of beta cells, develops early in life
II: insulin resistance (cells do not properly respond to insulin), associated w/ obesity, develops later in life
diabetes general & type I symptoms
blood sugar level elevated; body tries to dilute blood glucose -> extreme urination & thirst
I: no glucose production -> body thinks to be in prolonged fasting state -> ketoacidosis forms
dramatic weight loss
acetoacetate breakdown yields acetone –> acetone breath
