Biochemistry - Heck Flashcards
absorptive state
after a meal - immediate
blood glucose level increases
insulin released
glycogen synthesis
protein synthesis
triglyceride synthesis
brain and RBCs - insensitive to insulin
post-absorptive state
during fast - 12 hours or overnight
glucagon released
glycogenolysis in liver
AA uptake for gluconeogenesis
epinephrine released
- muscle - AA to blood
- adipose - FA to blood
liver
maintain blood glucose
synthesize ketones from acetyl CoA
adipose
take up FA and convert to TGs for long term storage
resting skeletal muscle
release AA to blood
active skeletal muscle
fast twitch - anaerobic glycolysis from glycogen
slow twitch - oxidative metabolism of glycogen
-after several hours - switch to lipolysis
muscle contraction
activates the TCA cycle
via:
increase in Ca
increase in ADP
decreased NADH/NAD ration
high intensity level of exercise
increased lactate dehydrogenase
- convert pyruvate to lactate
- with anaerobic metabolism
NADH dehydrogenase
in ETC complex 1
increases with high intensity exercise
anaerobic muscle metabolism
high intensity exercise
need for ATP - exceeds mito capacity for ox phos
lactate production - increased NADH/NAD ratio directs pyruvate into lactate
H production - decreased pH, causing pain and fatigue
-lactic acid dissociates to lactate and H
aerobic muscle metabolism
low intensity exercise
rate of ATP utilization is lower
increased CO2 - complete oxidation of glucose to CO2
TCA cycle
generates NADH and FADH2
-driving force for ETC
NAD and FAD
from ETC
increase activity of TCA cycle
myosin ATPase
stimulates ADP
-increases activity of isocitrate DH (rate limiting of TCA cycle)
isocitrate DH
produces NADH - driving ETC
buildup of NADH
inhibit TCA cycle
-inhibit alpha-KG DH and isocitrate DH
muscle contraction
increase Ca
stimulates - isocitrate DH and alpha-KG DH - increased TCA cycle activity
citrate
with buildup - unable to proceed through TCA cycle
inhibits acetyl CoA entering TCA cycle
aerobic metabolism supplements
probably no immediate benefit
rate limiting factor - O2 availability, not cycle intermediates
CoQ, succinate, riboflavin, niacin, pantothenate
exercise
increases skeletal m capacity and efficiency for fuel ox
over time:
- more TCA cycle enzymes
- more ETC components
- more mitochondria - size and productivity
also more vasodilatory and lymphatic drainage
major metabolic source in anorexic
fuel for skeletal muscle - is fatty acids
ketone bodies
made in liver
-fuel for brain and skeletal m
elevated ammonia in blood
liver failure
elevated ketones in blood
during starvation
from FA produced by liver
severe hypoglycemia
passing out
unresponsive
starvation
prolonged fasting 2 days
glucagon and epinephrine elevated
- muscle - FA
- brain - ketones and glucose
- RBCs - glucose
decrease in body temp, BP, and HR - so don’t burn much glucose
epinephrine
stimulates muscle glycogenolysis
glucagon
stimulate switch to lipolysis
skeletal muscle pain in anorexic
pH and lactic acid
- skeletal m - anaerobic metabolism
- this is because iron deficiency anemia - inhibit O2 delivery to tissue
- also - messes up ETC**
amenorrhea
body fat >22%
reduced LH and FSH production
death by starvation
40% ideal body weight lost
20-50% body protein lost
70-95% body fat stores lost
starvation
depletion of muscle glycogen
depletion of adipose TAGs
depletion of glucose from liver glycogen
vitamin deficiency
also seen in starvation
sx - fatigue, nausea, loss of appetite
riboflavin, niacin, thiamine, pantothenate
riboflavin
for FAD and FMN
-part of ETC
niacin
precursor to NAD+
thiamine
for alpha-KG DH
pantothenate
precursor to CoA
iron deficient anemia and ETC
non-heme iron proteins
function in electron transport
causes fatigue
metabolic sources of energy
glucose, AAs, FAs - to acetyl CoA
acetyl CoA to TCA cycle
glucagon
phosphorylation of rate-limiting enzymes
insulin
dephosphorylation of rate-limiting enzymes
insulin independent
brain and RBCs
RBC
utilize glucose anaerobically
released in postabsorptive state
glucagon and epinephrine
marked elevation of epinephrine and glucagon
starvation - prolonged fasting
liver fuel
glucose and AA - well fed
FA - fasting
skeletal m fuel
glucose well fed
FA, ketone - fasting
cardiac m fuel
FA - well fed
FA, ketone -fasting
synthesis of ketones
in liver
fast twitch fibers
anaerobic glycolysis
slow twitch fibers
oxidative
postnatal period
switch to beta-ox of FAs in cardiac muscle
citric acid cycle
oxidation of acetyl CoA to CO2
releases energy as NADH, FADH2, and GTP
isocitrate DH regulation
inhibited by NADH and ATP
stimulated by ADP
alpha-ketoglutarate DH regulation
requires thiamine, lipoic acid, CoA, FAD, and NAD
lack of thiamine slow oxidation of acetyl CoA
succinyl CoA synthetase
catalyzes phosphorylation of GDP to GTP
ATP synthase
F0 component - proton flow
F1 component - ATP synthase - phosphorylate ADP
cyanide poisoning
irreversible binding of cytochrome a/a3 in ETC
carbon monoxide
binds cytochrome a/a3 less tightly than cyanide
citrate
carries acetyl CoA to cytoplasm for FA synthesis
lesch nyhan disease
purine salvage enzyme deficiency
-hypoxanthine guanine phosphoribosyl pyrophosphate transferase - HPRT
CNS deteriration, mental retardation, spastic cerebral palsy, self mutilation
orotic aciduria with megaloblastic anemia
OMP synthase deficiency
purine salvage pathway enzyme
HGPRT
deficient - lesch nyhan