UCI SOM Thompson
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| Fructokinase is found where | liver
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| Fructose metabolism pathway | fructose (fructokinase) fructose-1-P (aldolase b) dihydroxyacetone-P + glyceraldehyde (triose kinase) glyceraldehyde-3-P
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| Fructokinase deficiency | benign
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| Aldolase b defficiency | hereditary, liver damage and failure, death, hypoglycemic; Pi is sequestered as fructose-1-P; treat by removing fructose
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| Fructose synthesis occurs where | liver, seminal vesicles, ovaries
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| Fructose synthesis pathway | glucose, sorbitol, fructose
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| Lactose synthesis pathway | glucose1P, UDP-glucose, UDP-galactose, lactose
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| Galactose degradation pathway | galactose (galactokinase) galactose1P (galactose1P uridylytransferase)glucose1P
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| Galactokinase deficiency | galactose in blood and urine, cataracts
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| Uridyl transferase deficiency | galactose in blood and urine, cataracts, dysfunction of liver, kidney, spleen, intestine, and brain, DEATH
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| UDP glucose is used in what | glycogen, proteoglycans, lactose synthesis
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| Proteoglycans | core protein attached to many long, linear chains of glycosaminoglycans
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| Glycoproteins | proteins that contain short chains of oligosaccharides that are usually branched
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| Hurler’s syndrome | mucopolysaccharide disease with corneal clouding
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| Hunter’s syndrome | mucopolysaccharide disease with no corneal clouding, x-linked
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| Location of fatty acid synthesis | liver, fat cells
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| Location of gluconeogensis | liver, kidney
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| Location of heme synthesis | bone marrow
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| Location of PPP | liver, fat cells, adrenal cortex, mammary gland
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| Location of amino acid synthesis and breakdown | liver
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| Location of urea synthesis | liver
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| Location of cholesterol synthesis | liver
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| Location of steroid hormone synthesis | adrenal cortex, gonads
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| Enantiomers | mirror images
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| Do we have D or L sugars | D sugars
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| Epimer | sugars that differ only in one hydroxyl group position
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| Amylose/amylopectin | starch
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| Carbohydrate digestive enzymes in intestine | isomaltase, glucoamylase, lactase, sucrase
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| How do most cells get glucose past the membrane | facilitated diffusion
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| Glut1 and Glut3 | basal transporters for the brain; high affinity, low Km
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| Glut 2 | glucose transporter in intestine, liver, and kidney
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| Glut 4 | glucose transporter in adipose and muscle tissue; regulated by insulin
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| Glut 5 | transports fructose
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| SGLT1 | glucose (or galactose) and sodium transporter into enterocyte cells
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| Lactose intolerance is cause by | inability to make lactase
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| Difference between glucokinase and hexokinase | glucokinase is only in the liver, has a high Km and a high Vm, and is not inhibited by glucose6P
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| Why phosphorylate glucose | 1)net negative charge traps molecule in cell 2)conserves energy 3)commits the cell to use the glucose
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| Glucose to pyruvate structure names, no enzymes | glucose, glucose6P, fructose6P, fructose16bP, glyceraldehyde3P, dihydroxyacetoneP, 13bisphosphoglycerate, 3Pglycerate, 2Pglycerate, phosphenolpyruvate, pyruvate
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| Glucose to pyruvate enzymes | hexokinase (glucokinase), phosphoglucose isomerase, phosphofructokinase 1, aldolase, triose phosphate isomerase, glyceraldehyde3PDH, phosphoglycerate kinase, phosphoglycero mutase, enolase, pyruvate kinase
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| Regulated steps in glycolysis (enzyme names) | hexokinase, PFK1, pyruvate kinase
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| what is 2,3BPG used for | lowers Hb’s affinity for O2
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| hexokinase regulation | -G6P, +insulin
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| PFK1 regulation | +F26BP, +AMP, -ATP, -citrate
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| Pyruvate kinase regulation | -alanine, +F16BP, (in liver, -phosphorylation from cAMP)
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| Pyruvate to lactate biproduct | NADH goes to NAD+
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| What kind of Fatty acids feed into glycolysis | only odd number FA through succinyl CoA
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| Is inactive pyruvate kinase phosphorylated or not | inactive pyruvate kinase is phosphorylated
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| Pyruvate DH: number of subunits and enzymes; cofactors and regulation | 2 subunits, 3 enzymes, 5 cofactors (NAD, FAD, CoA, lipoic acid, TPP), -acetyl CoA, -NADH
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| Congenital lactic acidosis | pyruvate DH not working; bypass with ketogenic diet
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| TCA cycle (enzymes included) | acetyl CoA with Oxaloacetate (citrate synthase) citrate (aconitase) isocitrate (isocitrate DH) alpha ketoglutarate (alpha ketoglutarate DH) succinyl CoA (succinate thiokinase) succinate (succinate DH) fumarate (fumurase) malate (malate DH) oxaloacetate
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| NADH in TCA comes from what rxns | isocitrate DH, alpha ketoglutarate DH, malate DH
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| FADH in TCA comes from what rxn | succinate DH
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| GTP in TCA comes from what rxn | succinate thiokinase
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| CO2 in TCA leaves from what rxn | isocitrate DH, alpha ketoglutarate DH
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| Alpha ketoglutarate cofactors | FAD, NAD, TPP, lipoic acid, CoA
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| Regulated TCA steps | citrate synthase, isocitrate DH, alpha ketoglutarate DH
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| TCA regulators | -ATP, -NADH, -Succinyl CoA, +ADP
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| Anapleurotic rxns | (fill up) replenish depleted cycle intermediates
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| Amphibolic cycle | eg TCA cycle; both degredation and biosynthesis processes occur
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| Other citrate uses | make fatty acids and cholesterol
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| Other alpha ketoglutarate uses | glutamate and glutamine
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| Other succinyl CoA uses | needs odd chain fatty acids, isoleucine, methionine, valine; used to make porphyrins
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| Other fumarate uses | needs aspartate, phenylalanine, tyrosine
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| Other malate uses | glucose formation
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| Other oxaloacetate uses | needs/makes amino acids; made from pyruvate and CO2
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| Glycerol-phosphate shuttle | dihydroxyacetone phosphate oxidizes NADH (cytoplasmic glycerol3PDH) glycerol3P reduces FAD (mitochondrial Glycerol3PDH) only 2 ATP’s
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| Malate-aspartate shuttle | 3ATP’s
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| Superoxide dismutase | conversts superoxide to hydrogen peroxide
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| Mutations in superoxide dismuatese leads to | LAS (lu Gherig’s disease)
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| Glutathione | used in turning hydrogen peroxide into water
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| Enzymes in converting hydrogen peroxide into water | glutathione peroxidase and glutathione reductase
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| NADPH | used to reduce glutathione
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| Goals of PPP | NADPH and nucleotide biosynthesis
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| Pathways that require NADPH | reduce glutathione, FA synthesis, FA chain elongation, cholesterol synthesis, neurotransmitter synthesis, nucleotide synthesis
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| PPP oxidative steps | glucose6P to ribulose5P givine off 2 NADPH and CO2
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| PPP first step enzyme | glucose 6PDH
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| Transketolase | rxns 5 and 7 in PPP; requires TPP; transfers 2 Carbons
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| Transaldolase | rxn 6 in PPP; transfers 3 carbons
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| Glucose6PDH deficiency | acute hemolytic anemia
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| Tissue dependent on glucose | Brain, RBC, kidney medulla, cornea of eye
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| % of guconeogenesis in liver and kidney | 90% liver 10% kidney
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| 3 purposes of gluconeogenesis | 1)production of blood sugar 2)maintain levels of TCA cycle intermediates 3) clears lactate
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| gluconeogenesis cycle | lactate (lactate DH) or alanine (transamination) to pyruvate (pyruvate carboxylase) oxaloacetate (PEP carboxykinase)… glyceraldehyde3P… (fructose 16Bisphosphotase)… (glucose6phosphotase)
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| formation of dihydroxyacetoneP in gluconeogenesis | glycerol (kinase) glycerol3P (glycerol 3PDH) dihydroxyacetoneP
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| is Acetyl CoA a precursor for gluconeogenesis | NO NO NO NO NO
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| required for pyruvate carboxylase | biotin, CO2, ATP
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| where is glucose6Pase found | liver and kidney
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| how many ATP equivalents are needed to make one glucose molecule through gluconeogensis | 6
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| regulation of pyruvate carboxylase | +acetyl CoA
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| regulation of PEP carboxykinase | +glucagon, +epinephrine, +glucocorticoids, -insulin
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| regulation of fructose1,6BPase | -F26BP, +ATP, +citrate, +glucagon
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| regulation of glucose6Pase | +glucagon
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| cori cycle | reconversion of lactate to glucose in liver
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| problem with too much ethanol on an empty stomach | makes lots of NADH which then moves NADH rxns towards lactate, glycerolBP, and malate. Also, lactate, alanine, and glycerol are not used for gluconeogenesis
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| effect of insulin in liver | -cAMP, -PKA, noP on PFK2/F26BPase, +PFK2/-F26BPase, +glycolysis
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| effect of glucagon/epinephrin in liver | +cAMP, +PKA, P on PFK2/F26BPase, -PFK2/+F26BPase, +gluconeogenesis
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| effect of epinephrine in muscle | +PKA, P on PFK2/F26BPase, +PFK2/-F26BPase, +glycolysis
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| effect of insulin in muscle | -PKA, no P on PFK2/F26BPase, -PFK2/+F26BPase, -glycolysis, glucose goes to glycogen
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| where in the cell is glycogen stored | cytoplasmic granules
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| 3 reasons for glycogen | 1)rapid mobilization 2)source of ATP even in absence of O2 3)maintain blood glucose levels
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| glycogenen | protein that starts it all off; adds up to 8 glucose molecules onto itself after which glycogen synthase takes over
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| glycogen degredation | glycogen phosphorylase uses an inorganic phosphate (not ATP) to make Glucose1P; debranching enzyme moves last 3 of 4
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| phosphoglucomutase | glucose1P to glucose6P
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| glycogen synthesis | glucose1P with UTP (UDP glucose pyrophosphorylase) UDP glucose with 2Pi; UDP glu can’t add until there are 8 glu molecules; UDP glucose (glycogen synthase) branching enzyme (must be 4 glc between each branch)
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| regulation of glycogen synthase | +G6P, -cAMP dep P
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| regulation of glycogen phosphorylase | -G6P, -ATP, +P of phosphorylase kinase, (-glucose (liver), + AMP (muscle))
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| regulation of phosphorylase kinase | +Ca2+, +cAMP dep P
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| glycogen regulation by epinephrine in liver or muscle | +cAMP, +PKA, P of phosphorylase kinase (active), P of phosphorylase (active), degredation of glycogen
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| glycogen storage diseases | most are recessive
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| glucose 6 phosphatase defficiency | increased amount of glycogen with normal structure; liver enlarged, failure to thrive, severe hypoglycemia, ketosis, hyperuricemia, hyperlipemia (give frequent high carb feedings)
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