IAS16

Question 1

metabolism significance

Answer 1

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

Question 2

catabolism relation w/ anabolism

Answer 2

catabolism breaks down large substances into small substances; anabolism creates large substances from small substances
catabolism converges, anabolism diverges
catabolism supplies energy for anabolism

Question 3

FA, glucose, AA metabolism convergent point

Answer 3

acetyl coA -> TCAC -> electron funneling in ETC to generate ATP

Question 4

TCAC intermediates anabolism

Answer 4

siphoned out for biosynthesis:
OAA -> carbs through PEP carboxykinase & GNG
citrate -> lipids
OAA, malate & ketoglutarate -> AA / proteins

Question 5

TCAC intermediates anabolism effect

Answer 5

less intermediates running TCAC, incomplete -> lower rate of ATP production

Question 6

replenishment of TCAC intermediates

Answer 6

anaplerotic Rx
pyruvate -> (malic enzyme) malate
pyruvate -> (pyruvate carboxylase) OAA
PEP -> (PEPK) OAA

Question 7

regulation of metabolism: why

Answer 7

simul. formation & degradation of organic products is a waste -> cat / ana are reciprocally regulated i.e. active pathway supresses other

Question 8

regulation of metabolism methods

Answer 8

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

Question 9

metabolic homeostasis

Answer 9

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

Question 10

metabolic homeostasis controlled by

Answer 10

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

Question 11

glucose importance

Answer 11

most cells use glucose preferably or solely for ATP generation & production of precursors of other pathways

Question 12

blood glucose level regulated by

Answer 12

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

Question 13

insulin function

Answer 13

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

Question 14

glucagon function

Answer 14

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

Question 15

epinephrine & cortisol function

Answer 15

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

Question 16

energy source for muscle contraction

Answer 16

low demand: blood glucose, FA, KB aerobically
high demand: glycogen anaerobically (forms lactate)
phosphocreatine -> creatine in heavy burst of activity

Question 17

ATP function in brain & significance

Answer 17

provide energy & maintain electric potential of neurons (power Na+/K+ ATPase pump)
hence in fasting, restoration of BGL for brain usage is 1st priority

Question 18

liver in prolonged fasting state

Answer 18

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

Question 19

diabetes types, causes & development

Answer 19

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

Question 20

diabetes general & type I symptoms

Answer 20

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