Ackerman Lectures 1 and 2 Flashcards

1
Q

aldo-sugars

A

D-glyceraldehyde (3), erythrose (4), ribose (5), glucose (6), mannose (6), galactose (6)

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2
Q

keto-sugars

A

dihydroxyacetone (3), ribulose (5), xylulose (5), fructose (6)

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3
Q

linear to cyclic isoform

A

addition of alcohol C to carbonyl C

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4
Q

hemi-acetal anomeric carbon

A

glucose; C1

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5
Q

hemi-ketal anomeric carbon

A

fructose; C2

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6
Q

glucose and galactose difference

A

C4; OH down and up, respectively

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7
Q

sucrose

A

glucose + fructose

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8
Q

lactose

A

galactose + glucose

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9
Q

maltose

A

glucose + glucose

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10
Q

reducing sugars

A

glucose, galactose, fructose, maltose, lactose–NOT sucrose (b/c link is at both anomeric Cs)

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11
Q

starch and glycogen vs cellulose

A

alpha vs beta 1,4 linkages, respectively

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12
Q

GLUT-1

A

in RBC, brain, kidney; glucose uptake

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13
Q

GLUT-2

A

liver, panc b-cell, intestinal contraluminal memb; rapid uptake/rel of glucose, high capacity, low affin; essential to liver fxn

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14
Q

GLUT-3

A

brain, kidney; glucose uptake

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15
Q

GLUT-4

A

skel musc, heart, adipose; insulin-stim glucose uptake; E storage

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16
Q

GLUT-5

A

SI; fructose, glucose absorp

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17
Q

glycolytic stages

A

hexose; splitting; triose

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18
Q

hexose stage

A

glucose–>F16BP; 2 mol ATP consumed per glucose; hexokinase, p-hexose isomerase, PFK-1

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19
Q

splitting stage

A

cleave F16BP–>1 aldo and 1 keto-sugar; keto isomerized to aldo; aldolase, triose-P-isomerase

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20
Q

triose stage

A

3C aldo sugar–>3C acid (pyruvate); 2 ATP prod per 3C intermed via subst-level phos; GA3PDH, PG kinase, PG mutase, enolase, pyruvate kinase

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21
Q

hexokinase

A

Pi transfer from ATP to glucose; low Km; traps glc in cell; -4 kcal/mol

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22
Q

p-hexose isomerase

A

converts aldo sugar to keto form (G6P–>F6P); +0.5kcal/mol

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23
Q

PFK-1

A

P transfer from ATP to F6P; E from hydrol 2ATP conserved in F16BP; -3.4kcal/mol

24
Q

aldolase

A

splits F16BP into GA3P (ald) and DHAP (ket); fwd despite +5.7kcal/mol; pulled by exergonic rxns of triose

25
Q

triose-P-isomerase

A

inter-converts GA3P with DHAP; KEY STEP b/c only ald can proceed; w/o, no net ATP yield; +1.8kcal/mol

26
Q

GA3PDH

A

phos GA3P to 1,3BPG; includes oxid of ald to acid; NAD+ is e- acceptor here; +1.5kcal/mol

27
Q

phosphoglycerate kinase

A

P trans from C-1 of 1,3BPG to ADP to form ATP; leaves 3-PGA intermed; first anaerobic ATP synth step; -4.4 kcal/mol

28
Q

PGA mutase

A

reversible P position shift; +1.1 kcal/mol

29
Q

enolase

A

non-hydrol cleavage (lyase) splits out H2O to create high-E phosphoenol intermed; -0.8 kcal/mol

30
Q

pyruvate kinase

A

hydrol enol-P and transfers P to ADP–>ATP; leaves pyruvate; 2nd anaerobic ATP synth step; -7.5 kcal/mol

31
Q

for every glucose that enters…

A

steps 1-5 occur once (6-CHO to two 3-CHO); steps 6-10 occur twice (two 3-CHO to two Pyr)

32
Q

input

A

glc + 2ATP + 2NAD+ + 2Pi + 4ADP

33
Q

output

A

2 Pyr + 2ADP + 2NADH + 2H+ + 4ATP + 2H2O

34
Q

net rxn

A

glc + 2NAD+ + 2Pi + 2ADP –> 2Pyr + 2NADH + 2H+ + 2ATP + 2H2O

35
Q

2,3-BPG

A

from 1,3-BPG mutase; cleaved by phosphatase–>2-PGA that feeds into glycolysis at enolase rxn

36
Q

molecs phos by hexokinase using ATP as P donor

A

glucose, fructose, mannose

37
Q

type I galactosemia

A

GALT deficiency; classic (t change UDP-glucose to UDP-galactose)

38
Q

type II galactosemia

A

GALK deficiency (can’t change galactose to galactose-1P)

39
Q

type III galactosemia

A

GALE deficiency (can’t interconvert UDP-glc and UDP-galac)

40
Q

hypoglycemia

A

inhibition of phosphoglucomutase

41
Q

pentose phosphate pathway, oxid branch

A

alt path of G6P metab; gen NADPH and ribulose 5-P

42
Q

nonoxid PPP

A

ops as shunt if pentose-5-P levels sufficient in cell; for every 18C used to prod NADPH, 3 lost as CO2 and 15C captured as intermeds for glycolysis

43
Q

glucose-6-phosphate dehydrogenase

A

G6P–>6-phosphoglucolactone; NADP+ to NADPH + H+

44
Q

lactonase

A

add H2O; 6-phosphoglucolactone–>6-phosphogluconate

45
Q

6-phosphogluconate dehydrogenase

A

6-phosphogluconate–>ribulose 5P; NADP+ to NADPH and H+; release CO2 (decarboxylation)

46
Q

ribulose 5P

A

used by all cells to make phosphoribosylpyrophosphate (PRPP)

47
Q

G6PDH inhibition

A

high intracellular [NADPH]

48
Q

pentose phosphate shunt

A

sugar rearr to convert excess pentose-5-P into glycolytic intermeds; involve ketose donor, aldose acceptor; 2 enz’s are link back to glycolysis (transketolase, transaldoslase); need 2 xylulose and 1 ribose 5P

49
Q

transketolase

A

catalyzes 2-C transfers (TPP (vit B1) enz)

50
Q

transaldolase

A

catalyzes 3-C transfers

51
Q

G6PDH and pyruvate kinase deficiency

A

non-spherocytic hemolytic anemias

52
Q

defective PK

A

ATP deficiency in RBCs

53
Q

defective G6PDH

A

NADPH defic, impairs RBC abil to neutralize intracell radicals via GSH

54
Q

deficiency of NADPH or NADH

A

interferes w/heme fxn directly; jaundice, Heinz bodies in RBCs

55
Q

defective RBC pyruvate kinase

A

dec flux thru glycolysis; higher 2,3-BPG levels, lower Hb affin for O2 such that reduc in RBC number compensated by inc efficency in O2 deliv to tissues

56
Q

G6PD deficiency

A

X-linked; diff mutations in gene w/diff levels of enz activity assoc w/range of biochem and clin phenos; asymp for years until take drugs (antimalarial, sulfonamide, aspirin and NSAIDs)/ingest fava beans (need GSH); global dist sim to malaria; hemolytic anemia reduces blood O2 and parasites fail to thrive