Metabolism/Glycolysis Review (57/58) Flashcards
Liver: fuel preference
fatty acids, glucose, amino acids
Skeletal muscle: fuel preference (at rest)
fatty acids
Skeletal muscle: fuel preference (exertion)
glucose
Heart muscle: fuel preference
fatty acids
Brain: fuel preference (fed state)
glucose
Brain: fuel preference (starvation)
ketone bodies/glucose
Carbs: kcal/g (dry)
4
Protein: kcal/g (dry)
4
Fat: kcal/g (dry)
9
Threshold for hypoglycemia, fasting conditions
60 mg / 100 mL
Insulin promotes what, in relation to glucose?
Glycogenesis (glucose → glycogen)
Glycolysis (glucose → lactate (into CAC))
Fed states
Glucagon / epinephrine promote what, in relation to glucose?
Glycogenolysis (glycogen → glucose)
Gluconeogenesis (lactate → glucose)
Fasting states
Hexokinase location in tissue
Present in all cell types
Inhibitor of hexokinase
Glucose-6-phosphate (G6P); feedback inhibition
Levels of hexokinase
Constant, non-inducible
Is hexokinase saturated at low glucose concentrations
Yes
Glucokinase location in tissue
Liver and pancreas
Inhibitor of glucokinase
Fructose-6P; translocates glucokinase to the nucleus (inactive)
Active/inactive locations of glucokinase
Nucleus: inactive
Cytosol: active
Up-regulator of GK activity?
Glucose (promotes translocation to nucleus)
Chronic hyperglycemia level
110+ mg / 100 mL (leads to insulin resistance and beta cell dysfunction)
Glucose utilization of brain, per day
120 g glucose / day
Glucose utilization of muscle tissue, per day
40 g glucose / day
Glycolysis end product (anaerobic)
Lactate
Glycolysis end product (aerobic)
CAC (pyruvate (in mitochondria) → acetyl CoA → lactate)
Stages of glycolysis
Priming stage (ATP investment) Splitting stage (fructose 1,6 bisphosphate can be converted to 2 molecules, further generating pyruvate) Oxidoreduction - phosphorylation stage (ATP earnings; happens twice because of splitting stage)
NAD+ conversion to NADH happens at which stage of glycolysis
Immediately after splitting stage
What does the NAD+ conversion to NADH catalyze?
Conversion of glyceraldehyde 3-phosphate to 1,3-bisphosphoglycerate
Participates in NAD+ conversion to NADH
Dehydrogenase
Key, irreversible enzymes for glycolysis/gluconeogenesis
Hexokinase/glucokinase
PFK-1
Pyruvate kinase
Levels of glucokinase
Inducible; synthesis is increased by insulin
Glucokinase affinity (Km)
Low; not saturated at physiological glucose concentrations
Pyruvate carboxylase genetic deficiency
Increased levels of alanine, lactate, and pyruvate
PDH genetic deficiency
Increased circulatory levels of pyruvate and lactate
NAD+ must be regenerated to maintain __________
Glycolytic flux
Functions as coenzyme in oxidation reaction
Anaerobic respiration replenishment of NAD+
Lactate dehydrogenase
Reduction reaction, leading to lactate or EtOH production
Aerobic respiration replenishment of NAD+
Metabolite shuttle system (NADH cannot pass mitochondrial membrane)
Two types of NAD+ shuttles for regeneration
Malate-asparate shuttle
Glycerol-phosphate shuttle
Function of pyruvate dehydrogenase (PDH)
Catalyzes conversion of pyruvate and CoASH (coenzyme A) to AcCoA (acetyl CoA)
Vitamin cofactors required to activate PDH
Thiamine (B1): PDH-E1 and Thiamine PPi
Riboflavin (B2): Dihydrolipoyl dehydrogenase E3 and FAD
Niacin (B3): Dihydrolipoyl dehydrogenase E3 and FAD
Pantothenate (B5): Dihydrolipoyl transacetylase E2 and lipoate CoA
Lactate dehydrogenase A deficiency (LDHA)
Insufficient levels of lactate dehydrogenase leads to lower levels of NAD+, limiting flux through the glyceraldehyde-3-P dehydrogenase reaction
Glycolysis net gain (ATP)
2 ATP, 2 pyruvate
Lactate formation is favored in _________
anaerobic conditions
Low levels of NADH leads to ________
Decreased lactate formation
Galactosemia is caused by a deficiency in one of these two enzymes
Galactokinase
Galactose 1-phosphate uridyltransferase (classic, most common, most severe)
Deficiency in aldolase B
Hereditary fructose intolerance