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