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OS 201 Reviewer > Exam 2 - Metabolism > Flashcards

Exam 2 - Metabolism Flashcards

1
Q

location of TCA

A

mitochondria

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2
Q

location of glycolysis

A

cytosol

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3
Q

ATP yield of one cycle of glycolysis

A 
7 ATP 
(given NADH = 2.5 ATP)
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4
Q

regulation of glycolysis

A

product inhibition
allosteric control
covalent modulation

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5
Q

Fats can be converted to glucose. T/F?

A

F, it can only be converted as far as acetyl CoA due to irreversibility

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6
Q

Glycolysis and gluconeogenesis are both regulated at the same time. T/F?

A

F, both processes have different rate-limiting steps

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7
Q

Alanine is used as a substrate for glycolysis in the glucose-alanine cycle. T/F?

A

F, it is converted back to pyruvate for use in gluconeogenesis.

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8
Q

Glucose to pyruvate conversion requires a lot of energy. T/F?

A

T

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9
Q

hormone initiating glycolysis

A

insulin

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10
Q

hormone initiating gluconeogenesis

A

glucagon

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11
Q

Enzyme:

Fructose-6-P → Fructose-1,6-biP

A

PFK (phosphofructokinase)

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12
Q

Enzyme:

Fructose-1,6-bisphosphate → Fructose-6-Phosphate

A

fructose-1,6-biPase

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13
Q

Enzyme:

PEP → pyruvate

A

pyruvate kinase

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14
Q

absorption pathway of short- and medium-chain FAs

A

enter portal blood directly from enterocytes (readily absorbed)
bound to albumin
oxidized in the liver

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15
Q

absorption pathway of long-chain FAs

A

form chylomicrons and lipoproteins
drain into lymphatics via lacteals
enter bloodstream via thoracic duct into SCV

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16
Q

lipoproteins with the least and most proteins

A

most: HDL
least: chylomicron

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17
Q

lipoproteins with the least and most lipids

A

most: chylomicron
least: HDL

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18
Q

lipoproteins with the least and most fats

A

most: chylomicron
least: HDL

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19
Q

lipoproteins with the least and most free and esterified cholesterol

A

most: LDL
least: chylomicron

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20
Q

lipoproteins with the least and most phospholipids

A

most: HDL
least: chylomicron

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21
Q

LDL marker apoprotein

A

Apo B100

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22
Q

cofactor for LCAT

A

Apo A-I

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23
Q

cofactor for LPL

A

Apo C-II

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24
Q

enzyme inhibitors for LPL

A

Apo A-II and Apo C-III

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25
Q

ennzyme inhibitor for CETP

A

Apo C-I

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26
Q

ligands for LDL receptor

A

Apo B100 and Apo E

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27
Q

ligand for HDL receptor

A

Apo A-I

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28
Q

apoprotein with highest affinity to LDL receptor

A

Apo B100

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29
Q

enzyme catalyzing RLS in FA oxidation

A

acyl CoA synthetase

esterifies FA to CoA

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30
Q

net ATP produced from beta oxidation of 14-C saturated FA

A

formula: 14(n-1) + 10 - 2; where n = C/2

net ATP = 14(6) + 10 - 2 = 92 ATP

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31
Q

sources of acetyl CoA for FA synthesis

A

oxidative decarboxylation of pyruvate from glucose
oxidative degradation of some proteins
beta-oxidation of long-chain FA

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32
Q

sources of cholesterol

A

dietary - 0.4g/day

biliary/de novo - 2g/day

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33
Q

enzyme regulating cholesterol synthesis

A

HMG-CoA reductase

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34
Q

process involving HMG-CoA synthase and HMG-CoA lyase

A

ketogenesis

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35
Q

glucose hydrolysis intermediate converted to glycerol

A

DHAP

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36
Q

derivatives of cholesterol

A

corticosteroids
steroid hormones
bile salts and acids
Vit D

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37
Q

function of serum albumin

A

carrier protein for steroids, FAs, thyroid hormones

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38
Q

sources of N incorporated into urea during urea cycle

A

aspartate and ammonia

majority derived from glutamate

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39
Q

links urea cycle to TCA

A

fumarate

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40
Q

Why should essential AA be part of the diet?

A

The body cannot synthesize essential AA de novo and thus relies on external sources.

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41
Q

cofactor to forward homoCys –> Met

A

Vit B12

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42
Q

cofactor to forward homoCys –> Cys

A

Vit B6

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43
Q

possible condition following Vit B12 and B6 deficiency

A

homocystinuria

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44
Q

AA needing supplementation in diet of Px with phenylketonuria

A

tyrosine

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45
Q

impaired pathway in phenylketonuria

A

phenylalanine –> tyrosine

thus, tyrosine is deficient and needs supplementation in diet

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46
Q

principal action of thyroxine

A 
increase O2 production
increases metabolism (BMR)
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47
Q

factor directly related to BMR

A

lean body mass

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48
Q

importance of dietary proteins

A

provide essential amino acids for protein synthesis

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49
Q

suggested food to lower cholesterol

A

oat bran and other soluble fibers that reduce LDL levels

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50
Q

dietary fibers

A

decrease TAGs
increase stool bulk
improves chyme transmission

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51
Q

kwashiorkor

A 
grossly underweight (<70% below normal)
edema
loss of pigmentation in hair and skin
hypoalbuminemia
moon facie and wet form
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52
Q

marasmus

A

extremely low weight
extreme wasting - loss of fat and muscle
dry form and geriatric face

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53
Q

cause of marasmus

A

calorie, protein, and nutrient deficiency

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54
Q

cause of kwashiorkor

A

protein deficiency despite adequate intake of calories

e.g. substituting milk for cassava

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55
Q

optimal proportion of carbs, fats, and proteins in diet

A

55~70% carbohydrates
20~30% fat
10~15% proteins

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56
Q

glycemic index

A

measure of blood glucose levels in response to food with respect to a standard food

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57
Q

glycemic load

A

glycemic index * carbohydrate concentration of food

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58
Q

food with relatively high glycemic index

A

bread > pasta and rice

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59
Q

biochemical measure of obesity/overnutrition

A

serum LDL

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60
Q

deficiencies resulting in anemia

A

folic acid

Vit B12

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61
Q

reaction associated with Vit C

A

hydroxylation - oxidizes the iron

oxidized Vit C is less/no longer effective

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62
Q

treatment for megaloblastic anemia from Vit B12 deficiency

A

folic acid

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63
Q

retinal

A

active form of Vit A

stored in liver

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64
Q

product of B-carotene hydrolysis

A

retinal

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65
Q

Vit D deficiency in children

A

rickets

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66
Q

Vit D deficiency in adults

A

osteomalacia

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67
Q

fat-soluble vitamins

A

Vit A, D, E, K

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68
Q

precursor of thiamine pyrophosphate

A

Vit B1

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69
Q

thiamine

A

Vit B1

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70
Q

riboflavin

A

Vit B2

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71
Q

Vit B6

A

pyridoxal, pyridoxine, pyridoxamine

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72
Q

thiamine deficiency

A

beri-beri

Wernicke-Korsakoff Syndrome

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73
Q

pellagra

A

can result from niacin deficiency

can lead to 3Ds - dermatitis, diarrhea, dementia

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74
Q

ascorbic acid

A

Vit A

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75
Q

precursor of lycopene and B-carotene

A

plant carotenoids

76
Q

reason for regulation of metabolism

A

energy source does not have the same distribution as energy stores

77
Q

importance of glucose phosphorylation to G6P

A

keep glucose inside cells

RLS in glycolysis

78
Q

GLUT4 insulin dependence

A

insulin dependent

1, 2, 3, 5 are insulin INdependent

79
Q

enzyme forming fructose-2,6-biP

A

Enzyme II

80
Q

effect of phosphorylation of Enzyme II

A

decrease of fructose-2,6-biP concentration

81
Q

energy change with PEP –> pyruvate

A

large negative delta-G

82
Q

energy consumption of PEP –> pyruvate

A

2 ADP

83
Q

location of PEP –> pyruvate

A

cytosol

84
Q

Catabolic enzymes are usually active when phosphorylated. T/F?

A

T

…and anabolic enzymes are active when DEphosphorylated

85
Q

catabolism

A

breakdown
oxidation
exergonic

[think: CAT bOx]

86
Q

anabolism

A

synthesis
reduction
endergonic

87
Q

ATP yield of NADH

A

2.5 ATP

88
Q

ATP yield of FADH2

A

1.5 ATP

89
Q

process not involving net influx of energy from other sources

A

catabolism

exergonic reaction: releases energy to other sources

90
Q

step involved in substrate level phosphorylation in TCA cycle

A

succinyl CoA –> succinate

91
Q

ATP produced in ETC by complete glucose oxidation

A

glycolysis: 2 NADH = 5 ATP
oxidative phosphorylation: 2 NADH = 5 ATP
TCA cycle: 2 FADH2 + 6 NADH = 3 + 15 ATP
total: 5 + 5 + 3 + 15 = 28 ATP

92
Q

predominant glycerol derivative in intestinal lumen after Orlistat discontinuation

A

2-MAG

93
Q

intermediates of odd-chain FAs entering TCA

A

succinyl CoA + acetyl CoA

94
Q

What is acetyl CoA converted into for transport into cytoplasm from mitochondria (and v.v.)?

A

citrate

95
Q

enzyme affected by enteropeptidase deficiency

A

pepsin

96
Q

Maple Syrup Disease

A

accumulation of V, I, L

97
Q

amplification

A

allows small amount of signal molecule to cause an increased intracellular transduction

98
Q

effect of anaerobic glycolysis on GLUT4

A

increases activity

99
Q

difference of hexokinase and glucokinase

A

glucokinase: in liver, phosphorylation only at high glucose levels, increased by insulin
hexokinase: in extrahepatic tissues, inhibited by G6P

100
Q

location of pyruvate carboxylase

A

only in the mitochondria

101
Q

compounds based on tyrosine

A 
catecholamines (epinephrine, norepinephrine, dopamine)
melanin
thyroid hormones (T3, T4)
102
Q

AA precursor of serotonin

A

tryptophan

103
Q

factor increasing digestibility and absorption of dietary lipids

A

longer FA length

104
Q

precursor FA for other FAs

A

palmitate

105
Q

provides reducing equivalents in lipid synthesis

A

glucose

106
Q

location of lipid synthesis

A

cytoplasm

107
Q

characteristics of essential fatty acids

A

not naturally synthesized by humans
synthesized by plants (and some animals)
help maintain membranes
double bonds at delta-12 and delta-15 (o-6 and o-3)

108
Q

location of double bonds in essential FAs

A

delta-12

delta-15

109
Q

omega-3 precursor

A

linoleic acid

110
Q

entry point of proprionyl CoA into TCA cycle

A

proprionyl CoA –> succinyl CoA

111
Q

odd-numbered FAs enter glucogenic pathway via ___ (intermediate)

A

proprionyl CoA

112
Q

Acetoacetic acid and B-hydroxybutyrate are weak acids. T/F?

A

F, they are rather strong.

113
Q

location of ketogenesis

A

liver mitochondria

114
Q

substrate used in ketogenesis

A

acetyl CoA

115
Q

cofactor/s of lysly oxidase (collagen synthesis)

A

Vit C and iron

116
Q

negative nitrogen balance

A

N intake < N loss

117
Q

conditions presenting negative nitrogen balance

A

burns, fevers, wasting diseases, serious injuries

fasting, malnutrition

118
Q

positive nitrogen balance

A

N intake > N loss

119
Q

conditions presenting positive nitrogen balance

A

growth, tissue repair, pregnanacy

120
Q

Athletes usually have lower BMRs (compared to non-athletes). T/F?

A

F, they have slightly higher BMRs.

121
Q

TCA cycle is purely anabolic. T/F?

A

F, it has both anabolic and catabolic phases.

122
Q

final common pathway for metabolism of glucose, FAs, and AAs

A

TCA cycle

123
Q

The TCA cycle produces oxidizing equivalents for the ETC. T/F?

A

F, it produces reducing equivalents.

124
Q

Carbohydrate energy stores are bulky and not readily available. T/F?

A

F, they are bulky but they are more readily available.

125
Q

Fat stores are bulky and not readily available. T/F?

A

F, they are not readily available but compact.

126
Q

Amino acids are glucose sources but have other uses. T/F?

A

T

127
Q

source of blood glucose replenishment

A

breakdown of dietary CHO

128
Q

methotrexate

A

anticancer drug

primary folate antagonist

129
Q

methorexate mechanism

A

inhibits reduction of dihydrofolate to tetrahydrofolate (THF, which helps in nucleotide formation)

130
Q

First Law of Thermodynamics

A

Energy is neither created nor destroyed but converted into other forms.

131
Q

free energy value in spontaneous metabolic reaction

A

negative free energy value (dG)

132
Q

nervous excitation is (endergonic / exergonic)

A

endergonic

133
Q

active transport is (endergonic / exergonic)

A

endergonic

134
Q

muscular contraction is (endergonic / exergonic)

A

endergonic

135
Q

fuel oxidation is (endergonic / exergonic)

A

exergonic

136
Q

amphibolic pathway

A

TCA cycle

137
Q

products of acetyl CoA oxidation in TCA

A

NADH, FADH2, CO2

138
Q

ATP yield from isocitrate –> fumarate

A

isocitrate -> a-ketoglutarate + NADH = 2.5 ATP
a-ketoglutarate -> succinyl CoA + NADH = 2.5 ATP
succinyl CoA -> succinate + GTP = 1 ATP
succinate -> fumarate + FADH2 = 1.5 ATP

total = 2.5 + 2.5 + 1 + 1.5 = 7.5 ATP

139
Q

(some) pathways producing reducing e- for ETC

A

TCA cycle
B-oxidation
aerobic glycolysis

140
Q

used to form H2O at the end of ETC

A

O2

141
Q

location of ETC

A

inner membrane of mitochondria

142
Q

Phosphorylation reactions synthesize ATP. T/F?

A

T

143
Q

Why does muscle contraction increase the rate of oxidative phosphorylation?

A

ADP concentration is increased.

144
Q

mechanism of hydrogen sulfide

A

inhibits cytochrome oxidases (in complex IV)

leads to loss of consciousness and cardiopulmonary arrest

145
Q

result of oxidative phosphorylation uncoupling by dinitrophenol

A

ATP production stops

oxygen uptake continues

146
Q

ADP

A

product of ATP hydrolysis
positive effector for glycolysis and TCA cycle
signals low enery level in the cell

147
Q

final electron acceptor in the ETC

A

O2

148
Q

direct energy source for ATP synthase to produce ATP

A

proton gradient established in mitochondria

149
Q

changes in metabolism in the heart following MI

A

decreased rate of oxidative phosphorylation
increased rate of lactic acid synthesis
increased use of glucose by muscle tissue

150
Q

cellular compartment becoming acidic (filled with H+) during mitochondrial electron transport

A

space between inner and outer mitochondrial membrane

151
Q

As affinity of the enzyme for substrate decreases, Km also decreases. T/F?

A

F, substrate affinity and Km are inversely proportional.

152
Q

Km

A

substrate concentration at 1/2 Vm

expressed in units of concentration

153
Q

organic precursors of coenzymes

A

vitamins

154
Q

Noncompetitive inhibition is irreversible. T/F?

A

F, both competitive and noncompetitive inhibition are reversible.

155
Q

reverses competitive inhibition

A

addition of excess substrate

156
Q

Reversible inhibition entails covalent bond formation. T/F?

A

F, reversible inhibition involves noncovalent interactions (H-bonds, hydrophobic interactions, ionic bonds) while irreversible inhibition usually involves covalent bonds.

157
Q

electron acceptor of cyt c oxidase

A

O2

158
Q

protein directly catalyzing fibrin hydrolysis

A

plasmin

159
Q

isozymes

A

enzymes with different AA sequences catalyzing same chemical reaction
(e.g. hexokinase and glucokinase)

160
Q

competitive inhibition

A

increases Km
inhibitor is usually a structural analog of substrate
via noncovalent interactions

161
Q

function of pyridoxal phosphate as cofactor

A

amino group carrier

162
Q

organ with highest demand for glucose as fuel

A

brain

163
Q

Why isn’t skeletal muscle glycogen involved in blood glucose regulation?

A

Only the liver has G-6-Pase which allows glucose release into the blood.

164
Q

counter-regulatory hormones to insulin

A

glucagon
epinephrine
cortisol

165
Q

Not all enzymes involved in gluconeogenesis are in the cytosol. T/F?

A

T, some are in the sER and mitochondria.

166
Q

processes regulating glycolysis

A 
covalent modification (pyruvate kinase inhibited by high [ATP])
allosteric control (PFK)
hormonal regulation (role of glucagon)
167
Q

products of anaerobic glycolysis of 1 glucose

A

2 ATP + 2 lactate

168
Q

possible Px presentation of insulinoma (insulin-secreting tumor)

A

obesity

hypoglycemia

169
Q

products of transamination of aspartate and a-ketoglutarate

A

OAA + glutamate

170
Q

AA utilized to transport ammonia to the liver

A

A and Q

171
Q

diet causing high [urea] in urine

A

very low CHO, very high CHON

172
Q

ketogenic AA

A

yields acetoacetyl CoA through ketogenesis
exclusively ketogenic: L, K
keto- and glucogenic: W, I, F, T, Y

173
Q

glucogenic AA

A

yields glucose through gluconeogenesis

~all AA except K and L

174
Q

Why is arginine semi-essential?

A

synthesizable via urea cycle

required intake dependent on health status and stage of development

175
Q

compounds involved in metabolism of 1-C compounds

A

THF
SAM
B12 (methylcobalamin)

176
Q

AA donating amino groups for purine synthesis

A

G, Q, D

177
Q

activated sugar utilized for both purine and pyrimidine de novo synthesis

A

PRPP

178
Q

deficient enzyme in hyperuricemia

A

hypoxanthine-guanine phosphoribosyl transferase (HGPT)

179
Q

disorders associated with hyperuricemia

A

Lesch-Nyhan syndrome

gout

180
Q

mechanism of allopurinol

A

inhibits xanthine oxidase (xanthine –> uric acid)
decreases uric acid formation
inhibits purine synthesis

181
Q

indication/s for allopurinol

A

hyperuricemia

gout

182
Q

mechanism of methotrexate

A 
inhibits DHFR (DHF --> THF)
inhibits synthesis of DNA, RNA, thymidylates, proteins
183
Q

indications of methotrexate

A

cancer

autoimmune diseases

184
Q

mechanism of 5-fluoroacil

A

inhibits thymidylate synthase (dUMP –> TMP)

inhibits RNA synthesis

185
Q

indications for 5-fluoroacil

A

cancer

OS 201 Reviewer (3 decks)

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