Glycolysis&TCA_Cycle.csv

oxidation to pyruvate through glycolysis; oxidation to ribose 5-phosphate through the pentose phosphate pathway; storage in the form of glycogen (animals) or starch or sucrose (plants)

around 5 mM (4 - 8 mM)

unregulated glucose transporter; widespread; high-affinity (Km = 1 mM); present in blood & cornea & placenta & brain & transformed (cancerous) cells

unregulated glucose transporter; found in liver and beta cells of pancreas; low-affinity (Km = 1 mM); allows glucose to enter liver quickly when blood glucose is high and allows glucose to exit the liver after gluconeogenesis when blood glucose is low

unregulated glucose transporter; found in neurons; high-affinity (Km = 1 mM); insulin-dependent

surface expression of this transporter is dependent on insulin; normally sequestered in microvesicles in the cytosol; found in skeletal muscle & adipose tissue & the heart; moderate affinity (Km = 5 mM)

converts fructose-6-phosphate to fructose 1 6-bisphosphate; requires 1 molecule of ATP; is the committed step of glycolysis

enzyme that converts glucose to glucose-6-phosphate; reaction requires ATP; reaction is irreversible and results in trapping of glucose molecule in cell

converts 1 3-bisphosphoglycerate to 3-phosphoglycerate; requires 1 molecule of ATP

converts PEP into pyruvate; produces ATP

inhibit conversion of G3P to 1 3 bisphosphoglycerate

inhibits step between intermediary of G3P -> 1 3 bisphosphoglycerate

transfer reducing equivalents from NADH in the cytosol across the mitochondrial membrane -> regeneration of NAD+; important shuttles include glycerol phosphate shuttle (NADH -> FADH2 in mitochondria) and malate-aspartate shuttle (NADH -> NADH in mitochondria)

negative feedback inhibition by G6P (competitive inhibition)

highly regulated; inhibited by ATP & citrate & H+ - allosteric regulation; also inhibited by glucagon

inhibited by ATP and alanine

glucokinase = only in liver; not inhibited by product; is positively regulated by glucose or insulin; is low affinity & high capacity while hexokinase is high affinity & low capacity

major controller of fructose 2 6 bisphosphate; secreted from pancreas; slows glycolysis by binding to receptors that activate adenylyl cyclase -> cAMP activation -> decreased F 2 6 BP

in liver - both epinephrine and glucagon increase adenylyl cyclase -> cAMP activation -> PKA -> phosphorylation of PFK-2 (deactivates) -> down-regulation of fructose 2 6 bisphosphate -> decreased rate of glycolysis; in heart - same pathway but opposite results - phosphorylation activates PFK-2 -> up-regulation of fructose 2 6 bisphosphate

opposes actions of glucagon in liver; affects metabolism of glucose by stimulating cAMP phosphodiesterase -> conversion of cAMP to AMP -> prevents down-regulation of glycolysis; can also indirectly upregulate fructose 2 6 bisphosphate through PFK-2

aerobic oxidation; anaerobic homolactic fermentation; anaerobic alcoholic fermentation

overall: pyruvate + fatty acids + amino acids -> acetyl coA + NADH + H+ + CO2; step 1 - pyruvate decarboxylated by E1 segment of PDH; acetyl -> enzyme-bound cofactor linked to TPP (CO2 released); step 2 - acetyl transferred to E2 cofactor (lipoic acid); step 3 - acetyl -> coenzyme A -> acetyl coA; 2 electrons transferred to E3 -> NADH

arsenic affects E2 unit of pyruvate dehydrogenase

TPP = vitamin B1 derivative; FAD = vitamin B2/riboflavin derivative; NAD = niacin derivative; B-complex insufficiency -> cannot make acetyl coA from pyruvate -> problems with energy metabolism

regulated by allosteric inhibition and competitive inhibition of end-products; acetyl coA & NADH can activate kinase that deactivates PDH (surplus of products -> PDH inactivation); substrates of reaction have opposite effect - deactivate kinase that deactivates PDH; upregulation of small ions -> activation of PDH

energetically favorable; regulation occurs via end products

fluorcitrate -> aconitase; malonate -> succinate dehydrogenase; arsenite -> alpha-ketoglutinate dehydrogenase