FORM & FUNCTION (CHO:Glucose) Flashcards
ATP
-energy currency
-when it hydrolyzes, energy is released
-drives reactions that has a positive change of energy
reactions that have a positive change of energy
-active transport/pumping of ions to maintain osmotic balance
-muscle contraction (myosin & actin)
-synthesis of macromolecules and other biomolecules
ways to generate ATP
- CHO
-glycolysis
-55-75% - Lipids
-beta oxidation
-15-30% - Proteins
-deamination
-10-15%
*all form Acetyl Co-A which will go into the TCA cycle
carbohydrate
-sugar
-carbon hydrate (6C with water)
-mono-, di-, and poly-saccharides
-stored as polysaccharides (glycogen)
glucose regulation
major form of mammalian fuel
1. Energy (ATP)
2. Storage (glycogen)
3. Storage (fat)
normal glucose in blood
-5mmol/L
-excess glucose must be transported and processed in tissues
hyperglycemia
-high blood glucose
Ex. diabetic: can’t take up glucose into tissues
hypoglycemia
-low blood glucose
Ex. starvation
glucose transporters (GLUT)
-class of proteins that allow glucose to passively transport into tissues
-most are unidirectional
GLUT2
-transports glucose in AND out of liver
-insulin insensitive
GLUT4
-transports glucose into heart, skeletal muscles and fat
-insulin sensitive
>when insulin is high=increase GLUT4=increase transport of glucose into cells
skeletal muscle and fat
-major glucose depository
>where the body stores excess glucose
glucose trapping
-glucose phosphorylation traps the molecules as charged phosphate group prevents diffusion out of cell
-liver uses glucokinase
-muscles use hexokinase
glucokinase and hexokinase
-same catalytic activity
-different regulatory properties
*forms glucose 6-phosphate
glucose 6-phosphate
-used for glycolysis and glycogen
insulin (brief)
-high glucose caues high insulin
*goal is to move excess glucose out of blood and into tissues to avoid hyperglycemia
liver insulin
-stimulates glucokinase to increae glucose trapping inside the cell
muscle insulin
-stimulate GLUT4 to increase glucose uptake inside the cell
glycolysis phases
- preparatory
- pay off
preparatory phase
-spend ATP to make ATP
-hexokinase: traps glucose
-phosphofructokinase (PFK)
PFK
-controls rate of glycolysis
-allosterically regulated by ATP level
*rate limiting step
-committed step (irreversible) *fructose 1,6-biphosphate destined to complete glycolysis
PFK allosterically regulated
-high ATP inhibits enzyme (negative feedback, inhibits glycolysis)
-high AMP: reverse ATP inhibition (favours glycolysis)
pay off phase
-4ATP molecules: substrate level phosphorylation
-2 NADH: shuttled to the ETC
-2 pyruvate molecules: enters the TCA
*anaerobic so far
clinical relevance
-deficiency in muscle PFK: rare mutation in dogs
Ex. glycogen storage disease type 7
glycogen storage disease type 7
-glycolysis slows down at step 3 (PFK)
-impairs glucose conversion to ATP
-PFK activity in muscle: 1-4% (exercise intolerant)
-PFK activity in RBC: 6-22% (hemolytic crisis: death of RBC)
-reported in spaniel breeds
2 pyruvate from pay off phase
- Aerobic condition: Acetyl-CoA
- Anaerobic condition: lactate
Lactate
-caused when rate of glycolysis is greater than TCA cycle (ex. intense exercise)
*primary role is to regenerate NAD+ (required for payoff phase)
-pyruvate is converted to lactate by dehydrogenase
*net ATP is still 2
lactic acid
-weak acid
-pKa=3.8
-favours reation to lactate + H+
prolonged anaerobic glycolysis
-can cause metabolic acidosis
-anion gap increased from a decrease in HCO3-
glycolysis in RBC
- Can only use anaerobic glycolysis
- Contains an alternate pathway
-2,3-biphosphoglycerate (2,3-BPG), is formed (regulateds Hb-O2 interaction)
-up to 15% of glucose in RBC can pass through this shunt
2,3-BPG function
-binding to Hb allosterically to regulate O2 affinity
-binding promotes oxygen dissociation=release oxygen to needy tissues
*decrease Hb-O2 saturation=improves re-oxygenation
-pH dependent
