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****UNIT 7 > MCP > Flashcards

MCP Flashcards

1
Q

glycosidic bonds

A

covalent linkages between monosaccharides that can be cleaved by digestive enzymes and are named according to alpha/beta configuration of the anomeric carbon and the numbers of connecting carbons

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2
Q

major dietary carbohydrates

A
  1. amylose: linear, a1-4 linkage
  2. amylopectin: branched, a1-4 linkage with a1-6 branches
  3. lactose: disaccharide (galactose + glucose), B1-4 linkage
  4. sucrose: disaccharide (fructose + glucose), a1-2 linkage, non-reducing sugar
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3
Q

cellulose

A

cannot be digested by humans since it has B1,4 linkages between glucose residues which is not recognized by any of our enzymes (lactose also has this linkage but is composed to glucose AND galactose)

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4
Q

3 major glycosidases

A
  1. endoglycosidases: cleaves internal sugar polymer bonds
  2. exoglycosidases: cleaves terminal sugar polymer bonds
  3. disaccharidases: cleaves the glycosidic bonds of disaccharides

*specificity is based on linkage structure, sugars on each side of linkage and position of linkage within polymer

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5
Q

a-amylase

A

endoglucosidase that cleaves internal a1-4 bonds of starch (amylose and amylopectin)

  1. salivary a-amylase: cleaves starch polymers into smaller polysaccharides in the moth and is inactivated by stomach acid
  2. pancreatic a-amylase: secreted into the duodenum and hydrolyzes the products from salivary a-amylase cleavage into smaller fragments (ex: di- and oligosaccharides)
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6
Q

brush border

A

apical membrane of intestines that has glycosidases synthesized from epithelial cells of the jejunum to digest oligo- and disaccharides into monosaccharides before transportation into the epithelial cells

(there is then transport into the bloodstream by transporters in the basolateral membrane)

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7
Q

glucoamylase

A

exoglucosidase that cleaves terminal a1-4 linkages between glucoses–> produces glucose + isomaltose

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8
Q

maltase

A

cleaves a1-4 linkage in maltose and maltotriose–> produces glucose + maltose

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9
Q

isomaltase

A

cleaves a1-6 linkage in isomaltose and a-dextrins–> produces glucose + glucose polymers

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10
Q

sucrase

A

cleaves a1-2 linkage in sucrose–> produces glucose + fructose

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11
Q

lactase

A

cleaves B1-4 linkage in lactose–> produces galactose + glucose

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12
Q

lactase persistence vs. lactase non-persistence

A

lactase persistence: AD trait that has been positively selected for in which lactase activity continues to be expressed into adulthood

lactase non-persistence: 65% of world’s population has low levels of lactase preventing them from being able to properly digest lactose

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13
Q

lactose intolerance

A

lactase deficiency in which lactose moves to the colon and is digested by bacteria producing products that cause symptoms such as: diarrhea, nausea, cramps, bloating and/or gas

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14
Q

glucose

A

the only fuel that can be used by ALL cells and once it enters (passively) the cells of the tissues, it is converted to glucose-6-phosphate which is trapped in the cell and can enter 3 different pathways

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15
Q

3 pathways that glucose-6-phosphate can enter

A
  1. glycolysis: oxidation to make ATP and pyruvate (converts to acetyl-CoA to enter citric acid cycle)
  2. glycogen synthesis: conversion to glycogen which can be stored for later
  3. pentose phosphate pathway: production of NADPH needed for biosynthetic processes through the oxidation of glucose into a 5-C sugar
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16
Q

citric acid cycle

A

occurs in cells with a mitochondria and oxygen in which acetyl-CoA is oxidized completely to CO2 and H2O producing high-energy electrons that help produce ATP

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17
Q

glycogenolysis and gluconeogenesis

A

ways in which the liver can supply glucose to other tissues via the bloodstream when it is lacking from the diet

glycogenolysis: glycogen–> glucose
gluconeogensis: non-carbohydrate sources (ex: AAs) –> glucose

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18
Q

what happens during fasting and the fed state?

A

fasting: release of glucagon, increased: glycogen breakdown, gluconeogenesis and lipolysis

fed state: release of insulin, increased: glycogen synthesis, fatty acid synthesis and triglyceride synthesis

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19
Q

what converts glucose to glucose-6-phosphate?

A

hexokinase (phosphorylates glucose by using ATP) with the help of Mg2+

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20
Q

liver glucokinase

A

has a lower affinity for glucose than hexokinase so that the liver can transport glucose when it is low in tissues

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21
Q

phosphoglucose isomerase (PGI) and its purpose

A

isomerizes G6P into F6P (fructose-6-phosphate) by moving the carbonyl group from C1 to C2 creating a 5-C ring (aldose–> ketose)

purpose: sets stage for aldol cleavage which will create two equal 3-C fragments after C1 hydroxyl is phosphorylated

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22
Q

phosphofructokinase (PFK) and its role

A

phosphorylates the C1 hydroxyl group of F6P using a P from ATP creating fructose-1, 6 bisphosphate (FBP)

role: central in glycolysis regulation

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23
Q

aldolase

A

cleaves FBP into DHAP (ketose) and GAP (aldose)–> both are trioses

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24
Q

triose-P isomerase and why it catalyzes an unfavored reaction

A

converts DHAP (ketose) from aldolase reaction into GAP (aldose) with an enediol intermediate

*even though DHAP is favored, it is converted to GAP since GAP is being removed

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25
Q

GAPDH (glyceraldehyde-3-phosphate dehydrogenase) and what its mechanism involves

A

oxidizes and phosphorylates GAP into 1,3-bisphosphoglycerate (1,3-BPG) utilizing NAD+ and Pi (becomes NADH and H+)

  • mechanism involves: enzyme-substrate complex, thiohemacetal intermediate and acyl-thioester intermediate
  • steps: Cys residue S- will attack carbonyl after its H is removed, - on oxygen will drop down and donate H to NAD+ (oxidation reaction), O- on Pi will attack carbonyl and detach from S
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26
Q

phosphoglycerate kinase (PGK)

A

substrate level phosphorylation in which 1,3-BPG is converted to 3-phosphoglycerate (3PG) producing 2 ATP since P is donated to ADP by the 1,3-BPG

*makes up for the ATP used by hexokinase and PFK

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27
Q

phosphoglycerate mutase

A

moves the P on the C3 of 3PG to the C2 forming 2PG using a His residue with a P that will donate to the C2 and then remove from the C3

*phosphohistidyl intermediate is involved

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28
Q

enolase and its purpose

A

removal of H2O (dehydration reaction) from 2PG to form a double bond between C2 and C3 creating phosphoenolpyruvate (PEP)

purpose: to create a double bond that will result in the molecule’s P becoming a good leaving group (transferred to ADP in the next step)

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29
Q

pyruvate kinase (PK)

A

substrate-level P that is the last step in the glycolytic pathway which uses ADP in order to remove a P from PEP to create pyruvate and ATP

*the double bond between C2 and C3 has now become a single bond and C2 has a double bond to O instead of a single bond to OPO3

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30
Q

three pathways that can be taken by pyruvate

A
  1. citric acid cycle–> CO2 + H2O
  2. homolactic fermentation–> lactate
  3. alcoholic fermentation–> CO2 + ethanol
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31
Q

lactate dehydrogenase (LDH)

A

conversion of pyruvate + NADH into L-lactate and NAD+ in which the carbonyl of C2 in pyruvate receives a hydride transfer and resulting hydroxyl oxygen is protonated

*reversible reaction and occurs in anaerobic conditions (i.e. RBCs since they have no nucleus)

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32
Q

metabolism of galactose, mannose and fructose

A

they are converted into glycolytic intermesiates and metabolized by the glycolytic pathway instead of forming independent pathways

galactose–> G6P
mannose–> F6P
fructose (muscle)–> F6P (with help of hexokinase)
fructose (liver)–> GAP (with help of fructokinase)

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33
Q

what is the difference between the pathway of fructose in the muscle and fructose in the liver to get to a product fit for glycolysis?

A

muscle: fructose is converted to fructose-6 P by hexokinase with the help of ATP
liver: fructose is converted to fructose-1 P by fructokinase and then glyceraldehyde by fructose-1-P aldolase and finally into GAP by glyceraldehyde kinase and ATP

34
Q

how do we convert mannose into fructose-6 P?

A

hexokinase with the help of ATP converts mannose into mannose-6 P and then an aldose-ketose isomerization using phosphomannose isomerase converts mannose-6 P into fructose-6 P

35
Q

how do we convert galactose into glucose-6 P?

A

galactose is converted into galactose-1 P by galactokinase and ATP which is then converted into glucose-1 P with the addition of UDP-glucose by galactose-1 P uridylyl transferase and then the glucose 1-P is converted into glucose-6 P by phosphoglucomutase

36
Q

enzymes needed for glycogen synthesis from G6P and what is cleaved off:

A

phosphoglucomutase converts it to G-1P which is then acted on by UDP-glucose pyrophosphorylase, then PPi is cleaved (forming UDP-glucose) off and then glycogen synthase removes a UDP and with the help of branching enzyme, glycogen is formed

37
Q

what does branching enzyme do?

A

it removes a 7-residue fragment from chains of at least 11 residues and forms a new a 1,6 glycosidic bond within a chain at least 4 residues from other branches

38
Q

when Glucose is needed, how can we get it from glycogen?

A

phosphorylase brakes the glycosidic bond at the end of a glycogen chain by adding a P (through HPO4 2-) to give G-1 P

*continues until the terminal gluose on the chain is within 4 residues away from a branch point in which glycogen debranching enzyme comes in so further phosphorolysis can take place

39
Q

how is G-1 P converted to G-6 P?

A

phosphoglucomutase acts on it and a G 1,6-bisphosphate intermediate forms before converting to G-6 P

40
Q

difference between phophoglucomutase and phosphoglycerate mutase:

A

phosphoglucomutase: Ser-P intermediate

phosphoglycerate mutase: His-P intermediate

41
Q

Von Gierke disease (type I)

A

defective enzyme: G-6 P (glycogen storage disease)

affects: liver and kidney

glycogen in affected organs: increased

clinical features: enlargement of the liver, hypoglycemia, ketosis, hyperuricemia, hyperlipemia

42
Q

Anderson disease (type IV)

A

defective enzyme: branching enzyme (a 1,4 –> a 1,6)

organ affected: liver and spleen

glycogen in affected organs: normal amount, very long outer branches

clinical features: cirrhosis of liver causing death before age 2

43
Q

McArdle disease (type V)

A

defective enzyme: muscle

affected organ: muscle

glycogen in affected organ: moderately increased, normal structure

clinical features: limited ability to perform strenuous exercise because of cramps

44
Q

epimerase

A

inversion of asymmetric groups

45
Q

enolase

A

OH and double bond conversion

46
Q

isomerase

A

converts to isomer

47
Q

mutase

A

shifting of functional groups

48
Q

aldolase

A

breaks something down

49
Q

substrate level phosphorylation

A

direct transfer of P to form ATP

50
Q

mitochondria’s role in ATP production

A

90% of ATP is produced under aerobic conditions through the CAC and oxidative phosphorylation in mitochondria of eukaryotic cells

51
Q

which cells have a lot of mitochondria?

A
  • heart cells to contract
  • kidney cells for transportation
  • liver cells for biosynthesis
  • need lots of ATP
  • located near structures that need the ATP (to decrease the diffusion path)
52
Q

what are the functions of the citric acid cycle?

A
  • to convert a number of different fuels to a common mobile fuel (NADH)
  • to serve as the final meeting place of nearly all oxidizable substrates
  • to provide intermediates for biosynthesis
53
Q

what is special about citrate in the citric acid cycle?

A

it is the first intermediate (cycle is named after it)

54
Q

what is the connecting link between glycolysis and the CAC?

A

the pyruvate dehydrogenase complex which oxidizes pyruvate to acetyl-CoA in the mitochondrial matrix space

*kinetic advantage since products are not released into solution (not diffusion-limited)

55
Q

enzymes of the pyruvate dehydrogenase complex and the type of reaction they catalyze:

A

pyruvate dehydrogenase (E1)–> condensation/decarboxylation (TPP prosthetic group)

dihydrolipoyl transacetylase (E2)–> oxidative transfer and transacetylation (lipoamide prosthetic group)

dihydrolipoyl dehydrogenase (E3)–> dehydrogenation (FAD prosthetic group)

56
Q

lipoamide

A

prosthetic group of E2 of pyruvate dehydrogenase complex and has a swinging arm resulting in fast kinetics

57
Q

citrate synthase

A

converts oxaloacetate and acetyl CoA to citrate with a citryl CoA intermediate through a condensation and hydrolysis reaction

*hydrolysis step has a delta G of -7.5 kcal/mol

58
Q

aconitase

A

conversion of citrate to isocitrate with cis-aconitate intermediate trhough dehydration and hydration reactions

  • citrate is favored by isocitrate is constantly removed so it is being produced
  • purpose: to move the hydroxyl to the secondary C so it can be oxidized
59
Q

isocitrate dehydrogenase

A

oxidative decarboxylation to produce a-ketoglutarate which has a bottom portion that resembles pyruvate but within a different binding pocket

60
Q

a-ketoglutarate dehydrogenase complex

A

oxidative decarboxylation and formation of a thioester (succinyl CoA is produced) utilizing the same 4 step mechanism as the pyruvate dehydrogenase complex

61
Q

succinyl CoA synthetase

A

thioester cleavage and GTP synthesis with a common intermediate (a phosphohistidyl) is a product of the first reaction then the substrate of the next reaction to couple an exergonic reaction to an endergonic reaction

62
Q

succinate dehydrogenase, fumarase, malate dehydrogenase

A
  • oxidation, hydration, oxidation
  • succinate dehydrogenase transfers electrons to FAD
  • oxidation of malate by NAD+ is difficult (delta G= +7.1) so very little OAA is in equilibrium with a large amount of malate
63
Q

where are the shunt enzymes found?

A

in the cytosol like in glycolysis

64
Q

what is an overview of the steps of the pentose phosphate shunt? what are the two products of the shunt?

A

overview:
- steps 1-3: referred to as the oxidative phase and are irreversible in which 2 NADPH are formed and the G6P is converted to a pentose (Ru5P) with the release of CO2

  • steps 4-8: referred to as the nonoxidative phase and are reversible in which intermediated of the glycolytic pathway are created (2 F6P and 1 GAP)
    products: NADPH and ribose-5-phosphate (R5P)
65
Q

products of glycolysis compared to products of pentose P shunt (if we start with 3 Glu)

A

if we start with 3 Glu…

glycolysis–> equivalent to 6 GAP
pentose 5 P–> equivalent to 5 GAP and 6 NADPH (6th GAP leaves as 3 CO2)

66
Q

similarities and differences between NAD+ and NADP+

A

similarities: same redox reactions
differences: C2 hydroxyl oxygen of the ribose has a proton in NAD+ whereas it has a P group in NADP+ allowing enzymes to make a distinction between the two

67
Q

importance of active pentose P pathways in the small intestines and RBC

A

SI: to detoxify xenobiotics (from food poisoning) with the help of cytochrome p450

RBC: to detoxify ROS through reduction

*both are accomplished by NADPH

68
Q

G6PDH’s function and what happens with a deficiency

A

function: G6PDH is responsible for aiding in the conversion of G6P and NADP+ to NADPH and 6-P-gluconolactone
deficiency: hemolytic anemia (favism) and selective advantage against malaria

69
Q

what if we need ribose but not NADPH?

A

run the non-oxidative phase of the shunt in reverse starting with F6P and GAP and ending with R5P

70
Q

what are the biosynthetic uses of ribose?

A
  • RNA/DNA
  • ATP and other energy carrying NTP’s
  • NADH/FAD
  • CoA

*needed for information storage, energy transfer, redox reactions and enzyme catalysis

71
Q

what if the cell needs both NADPH and ribose?

A

you can get 2 NADPH/ribose if you run just the oxidative phase of the shunt and concert all of the Ru5P produced to R5P

72
Q

what percentage of Glu goes down the shunt in the liver?

A

30%

*other 70% goes straight down glycolysis

73
Q

what kicks in when glycogen stores in the liver has been depleted but blood Glu still needs to be maintained?

A

gluconeogenesis

74
Q

irreversible kinases of glycolysis and their bypasses

A

3 of the 4 kinases of glycolysis are irreversible:

  • pyruvate kinase (bypass I: pyruvate carboxylase + PEPCK)
  • PFK (bypass II: FBPase)
  • hexokinase (bypass III: glucose-6-phosphatase)
75
Q

where do the bypasses start?

A

in the mitochondria since pyruvate carboxylase is only present in the mitochondria and then PEPCK is present in the mitochondria and cytosol (where the rest are present)

*exception: glycerol which gets converted to DHAP in the cytosol

76
Q

biotin

A

the prosthetic group that helps bicarbonate be activated by ATP through transfer of PO3 in order to aid pyruvate carboxylase in conversion of pyruvate to oxaloacetate followed by release of PO4 and condensation of CO2 which is transferred from biotin to the -CH3 of pyruvate to give OAA in bypass I

*biotin is made by bacteria in the gut (flora) so there will never be a deficiency

77
Q

which AAs do not contribute to gluconeogenesis?

A

Leu and Lys

78
Q

how is OAA transported?

A

is does not have a transport system but it can exit the mitochondria by the Mal/Asp shuttle running in reverse after first being reduced to malate (by malate dehydrogenase) or aspartate (by aspartate aminotransferase) and then it is converted back to OAA in the cytosol

79
Q

what is the only kinase that is reversible?

A

phosphoglyverate kinase

80
Q

production of lactate

A

when ATP demands in the muscle exceed the capacity of oxidative phosphorylation for generating ATP (or in RBC which lack mitochondria)

81
Q

Corri Cycle

A

lactate is carried to the liver where it is converted to Glu and released back into the bloodstream

  • after exercise, this continues as muscle glycogen stores are replenished
  • oxygen debt
82
Q

oxygen debt

A

the amount of O2 consumed in the liver during the Corri Cycle’s rebuilding of muscle glycogen

****UNIT 7 (5 decks)

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