Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Dragon > Pearl > Flashcards

Pearl Flashcards

1
Q

nucleoside

A

pentose covalently bonded to nitrogenous base at C-1’

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

nucleotide

A

nucleoside with phosphate attached at C-5’

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

why are ADP and ATP high energy compounds?

A

repulsion between proximate, negatively charged phosphate groups

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

the sugar included in RNA

A

ribose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

the sugar included in DNA

A

deoxyribose (ribose with 2’-OH replaced by -H)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

nucleotides are joined by

A

3’-5’ phosphodiester bonds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is found at the 5’ end versus 3’ end of a strand of nucleic acids

A

at 5’, free hydroxyl or phosphate bonded to C-5’; at 3’, free hydroxyl bonded to C-3’

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

the mnemonic for purines and pyrimidines

A

CUT the PYe: C, U, and T are pyrimidines

PURe As Gold: A and G are purines. Weddings rings are gold. You need two.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

which bases are aromatic

A

all

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

the four requirements of aromaticity

A

cyclic, planar, conjugated (alt lone pairs or double bonds), 4n+2 pi electrons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

the nitrogenous bases are found here relative to the phosphodiester backbone

A

within the double helix

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

number of hydrogen bonds per pair

A

3 for G and C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

length of the turn of a double helix

A

4.2 nm, 10 BP per turn

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Z-DNA

A

high GC content or high salt concentration may contribute to its formation, difficulty to study b/c it is unstable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How denaturing agents work

A

disrupt H-bonds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

number of xsomes humans have

A

46

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

nucleosome

A

200 BPs DNA wrapped around 4 histones. DNA is sealed of by a fifth histone, as it leaves/enters the nucleosome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

histones are basic/acidic

A

basic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

nucleoproteins

A

proteins which assoc with DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

heterochromatin

A

dark and dense under microscope. often composed of highly repetitive sequences. High GC. transcriptionally silent. remains compacted even during interphase.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

type of chromatin which is transcriptionally active

A

euchromatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

telomerase

A

a reverse-transcriptase enzyme which carries its own RNA template. helps prevent loss of telomeres.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what are five histone proteins in eukaryotic cells? which one is not part of the histone core around which DNA wraps to form chromatin?

A

H1, H2A, H2B, H3, H4; H5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

replisome

A

i.e. replication complex. set of specialized proteins which assist DNA polymerases. prevent unwound DNA from reannealing or being degraded by nucleases.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

helicase

A

unzips DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

topoisomerases

A

works ahead of helicase, nicking one or both strands, to reduce torsional strain of supercoiling during replication. reseals.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

de novo synthesis

A

not needing another molecule to “hook on” to

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

primase

A

builds RNA primer on parent strand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

DNA pol III

A

begins synthesizing daughter strand in prokaryotes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

begins synthesizing daughter strand in prokaryotes

A

DNA pol III

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

begins synthesizing daughter stand in eukaryotes

A

DNA polymerases alpha and delta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

DNA polymerases alpha and delta

A

begins synthesizing daughter stand in eukaryotes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

incoming nucleotides during synthesis

A

triphosphates (gives energy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

DNA pol I

A

removes primer and replaces it with DNA nucleotides in prokaryotes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

RNase H

A

removes primer in eukaryotes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

after primer is removed, adds DNA nucleotides to daughter strand in eukaryotes

A

DNA pol delta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

function of DNA pol theta

A

euk: work with alpha in synthesis, fill in gap left by primer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

DNA pol for repair in euk

A

beta and epsilon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

DNA pol for mitochondrial DNA

A

gamma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

sliding clamp assists

A

delta and epsilon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

PCNA

A

sliding clamp

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

topoisomerase also called ___ in prok

A

gyrase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

oncogene

A

mutated genes that cause cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

proto-oncogene

A

potential to cause cancer if mutated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

antioncogenes

A

tummor supressors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

is it “harder” for an oncogene or antioncogene mutation to cause cancer

A

oncogene, as only one allele need mutate. one copy of the antioncogene is usually enough for good protein activity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

proofreading

A

DNA pol looks back for mismatched BPs. It can tell which base to replace b/c the one belonging to the parent/template is more heavily methylated (it’s been around longer).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

which strand is more prone to mutation

A

lagging. more start/stop. DNA ligase doesn’t proofread.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

when is proofreading concluded?

A

G2! There are other enzymes for mismatch repair in G2 encoded by MSH2 and MLH1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

when does proofreading occur?

A

G1, S, and G2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What types of proofreading occur outside of S phase?

A

base excision repair and nucleotide excision repair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

nucleotide excision repair

A

Needed if UV induces thymine dimers. Proteins scan DNA for sucha lesion. Excision endonuclease nicks phosphodiester backbone and removes defective oligonucleotide. DNA pol fills in gap. Nick is sealed by DNA ligase.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Base excision repair

A

for small, non-helix-distorting mutations.

  1. affected base removed by glycosylase enzyme. leaves behind apurinic/apyrimidinic (AP) site ie abasic site.
  2. AP endonuclease recognizes/removes damaged sequence.
  3. DNA pol. DNA ligase.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

vectors are usually

A

viral or bacterial plasmids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

restriction enzymes

A

ie restriction endonucleases. isolated from bacteria. recognize certain sequence.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

cDNA comes from

A

reverse-transcribing processed mRNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

transgene

A

cloned gene introduced into transgenic mouse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

transgenic mice creation

A
  1. integrate into germ line (good for studying dominant gene effects, as it coexists with the natural allele)
  2. integrate into embryonic stem cells (now you can select for mice with the gene of interest and breed for heterozygotes)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

homeostasis vs. equilibrium

A

most compounds in the body maintained at homeostatic levels, often different from equilibrium, requiring energy expenditure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

what are the three metabolic states?

A

postprandial, postabsorptive (fasting), prolonged fasting (starvation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

postprandial time frame

A

3-5 hours after eating

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

nutrients flood from the gut, then

A

through hepatic portal vein to liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

major target tissues for insulin

A

liver, muscle, adipose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

effect of insulin on liver

A

glycogen synthesis. once glycogen stores are full, excess glucose is converted to FA and triacylglycerols

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

insulin on muscle

A

glucose entry and protein synth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

insulin on adipose

A

glucose entry and triacylglycerol synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

how are most energy needs of the liver met after a meal?

A

oxidation of excess amino acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

two cell types insensitive to insulin

A

nervous tissue and RBC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

the counterregulatory hormones

A

oppose insulin in SAL: epinephrine, norepinephrine, glucagon, cortisol, growth hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

the counterregulatory hormone which stands out in its relation to liver

A

glucagon stimulates gluconeogenesis in addition to glycogenolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

difference in timeframe between glycogenolysis and gluconeogenesis (liver)

A

glycogenolysis at beginning of postabsorptive state, gluconeo does not reach Vmax until 12 hours later

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

how epinephrine relates to gluconeogenesis

A

release of amino acids from skel muscle and FA from adipose stimulated. carried to liver, providing carbon skeletons and energy for gluconeo.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

how long until gluconeo is predominant glucose source?

A

24 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

describe prolonged fasting

A

during prolonged fasting, lipolysis is rapid. muscle uses FA as major fuel. excess acetyl-CoA is used for ketone body synth. brain relies on ketone bodies for 2/3 energy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

advantage of ketone bodies as fuel

A

less glucose needed. less gluconeo. less degredation of amino acids.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

during what stage is there the greatest decrease in circulating conc of insulin?

A

postabsorptive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

the solubility of thyroid hormone

A

fat-soluble amino-acid derivative hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

these tissues require insulin for effective glucose uptake

A

adipose and resting skeletal muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

the effect of insulin in relation to carbs

A

increase glucose uptake and carb metabolism in muscle adn fat. increased glycogen synth in liver.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

effect of insulin on carb metabolism, in liver specifically

A

increase activity of glucokinase and glycogen synthase. decrease activity of glycogen phosphorylase and glucose-6-phosphatase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

insulin as it relates to protein metabolism

A

increases AA uptake by muscle cells to increase protein synthesis and decrease breakdown of essential proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

what insulin increases in relation to fat metabolism

A

fat cells take in glucose and triacylglycerol. increase lipoprotein lipase activity. triacylglycerol synth (lipogenesis) from acetyl-CoA in liver and adipose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

what insulin decreases in relation to fat metabolism

A

triacylglycerol breakdown (lipolysis) in adipose. ketone body formation in liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

source of ketone bodies

A

glycol and beta ox

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

function of lipoprotein lipase

A

clears VLDL and chylomicrons from blood

86
Q

for glucose to promote insulin secretion

A

must enter B cells and be metabolized for ATP

87
Q

how ATP conc in cell relates to insulin conc in blood

A

ATP triggers Ca release in cell, which triggers exocytosis of preformed insulin

88
Q

hormones which cause insulin release

A

glucagon and somatostatin

89
Q

what are the four processes which glucagon increases in hepatocytes?

A

glycogenolysis, gluconeogenesis, ketogenesis, lipolysis

90
Q

what processes does glucagon decrease in the liver?

A

lipogenesis, glycogenesis

91
Q

by what mechanism does glucagon increase glycogenolysis in hapatocytes?

A

activates glycogen phosphorylase. inactivates glycogen synthase

92
Q

by what mechanism does glucagon increase gluconeo in liver?

A

promotes conversion of pyruvate to PEP by pyruvate carboxylase and phosphoenolpyruvate carboxykinase. Also, conversion of fructose 1,6-BP to fructose-6-P by fructose-1,6-bisphosphatase.

93
Q

glucagon causes increased lipolysis in liver, but why is not considered a major fat-mobilizing hormone?

A

this action is on liver and not adipocytes

94
Q

what promotes release of glucagon?

A

low blood sugar, but elevated amino acids

95
Q

after what type of meal, would glucagon levels increase?

A

one rich in proteins

96
Q

from where are glucocorticoids released?

A

adrenal cortex

97
Q

what are glucocorticoids released in response to?

A

stress

98
Q

what type of hormone is cortisol

A

a glucocorticoid and steroid hormone

99
Q

how does cortisol relate to amino acids

A

increased degradation and delivery of them

100
Q

how does cortisol relate to lipolysis?

A

increases

101
Q

how is cortisol useful to nervous tissue?

A

elevates blood glucose

102
Q

what does cortisol inhibit?

A

glucose uptake in muscle, lymphoid, and fat tissue

103
Q

what does cortisol increase

A

hepatic output of glucose via gluconeogenesis, particuarly from amino acids

104
Q

all glucocorticoids are also

A

steroid hormones

105
Q

what is the permissive function of cortisol

A

enhances activity of glucagon, epinephrine, other catecholamines

106
Q

what hormones are produced by the adrenal medulla?

A

catecholamines

107
Q

epinephrine and norepinephrine may be categorized as

A

catecholamines

108
Q

epinephrine and norepinephrine are also called

A

adrenaline and noradrenalline

109
Q

what is the effect of catecholamines on skeletal muscle and liver, and by what mechanism

A

increase activity of glycogen phosphorylase, promoting glycogenolysis.

110
Q

what is the difference between the effect of catecholamines on liver vs. skeletal muscle

A

glycogenolysis in both. however, skel muscle does not have glucose-6-phosphatase, so it cannot release glucose into bloodstream

111
Q

what is the effect on adipose of catecholamines

A

increase activity of hormone sensitive lipase, promoting lipolysis

112
Q

how does epinephrine relate to the heart and other target organs in terms of direct effect?

A

increase in metabolic rate via sympathetic nervous stimulation

113
Q

thyroid hormone activity is essentially

A

permissive, levels are kept more or less constant

114
Q

the hormone which requires thyroid hormone in order to have a significant impact

A

epinephrine

115
Q

T3 compared to T4

A

has a more rapid, but short-lived, effect

116
Q

thyroid hormones have their primary effect on the metabolism of what biomolecules?

A

lipid and carbohydrate

117
Q

thyroid hormone clears this, and causes absorption of that

A

clears cholesterol from plasma, increases absorption of glucose from small intestine

118
Q

what is the primary metabolic function of insulin

A

glucose uptake by adipose and muscle, glucose utilization in muscle, and macromolecule storage (glycogenesis, lipogenesis)

119
Q

what is the primary metabolic function of glucagon

A

increases blood glucose levels by promoting glycogenolysis, gluconeo, lipolysis, and ketogenesis

120
Q

what is the primary metabolic function of cortisol

A

increase lipolysis and AA mobilization, decrease glucose uptake in certain tissues, enhance activity of other counterregulatory hormones

121
Q

what is the primary metabolic function of catecholamines

A

increase glycogenolysis in muscle and liver and lipolysis in adipose

122
Q

what is the primary metabolic function of thyroid hormones

A

increase basal metabolic rate and potentiate activity of other hormones

123
Q

what does thyroid storm present with?

A

tachypnea, tachycardia, hypertension, hyperthermia

124
Q

what does liver do with glucose received from hepatic portal vein?

A

extracts excess. replenish glycogen stores, then convert what remains into acetyl-CoA for fatty acid synthesis (both in liver)

125
Q

what is does the liver do with the fatty acids it makes?

A

convert them to triacylglycerols and release into blood as VLDL (very low denisty lipoproteins)

126
Q

what is the main source of energy for the liver in its well-fed state?

A

oxidation of excess amino acids

127
Q

what is the source of carbon skeletons for glucose synthesis?

A

lactate from anaerobic metabolism, glycerol from triacylglycerols, and amino acids

128
Q

insulin, specific to adipose

A

in addition to glucose uptake, fatty acid release from VLDL and chylomicrons.

129
Q

what does adipose do with the fatty acids released from lipoproteins?

A

re-esterify to triacylglycerols

130
Q

where does adipose get the glycerol phosphate needed for triacylglycerol synthesis?

A

comes from glucose metabolism in liver

131
Q

what is the body’s major consumer of fuel

A

skeletal muscle

132
Q

fuel source for skel muscle in fasting state?

A

amino acids and, if prolonged, ketone bodies

133
Q

the most short lived source of energy in active skel muscle

A

creatine phosphate, which transfers P from ADP to ATP

134
Q

in what form is energy stored by muscle

A

glycogen and some triacylglycerols

135
Q

what can muscle take from blood for energy?

A

glucose and free FA’s

136
Q

during short bursts of high-intensity exercise, skel muscle also derives energy from

A

anaerobic glycolysis on stored glycogen

137
Q

after continuous exercise, rate declines to a level that can be supported by

A

oxidation of fatty acids

138
Q

preferred source of energy by cardiac myocytes in well-fed state. in fasting?

A

fatty acids. fatty acids and ketone bodies.

139
Q

cardiac hypertrophy and metabolism in cardiac myocytes

A

glucose oxidation rises, beta oxidation falls

140
Q

what is the source of glucose used by brain?

A

hepatic glycogenolysis and gluconeogenesis

141
Q

what is the preferred fuel for most cells in well-fed state and what is the exception

A

preferred fuel is glucose, exception is cardiac muscle, which prefers fatty acids

142
Q

what organ consumes the greatest amount of glucose relative to its percentage of body mass?

A

brain

143
Q

describe the major metabolic functions of the liver

A

steady-state conc of glucose in blood via glucose uptake and storage, glycogen, gluconeo. cholesterol and fat metabolism. urea cycle. bile synthesis. detox of foreign substances.

144
Q

glucose entry into most cell vs. absorption from digestive tract

A

concentration driven and independent of Na+

145
Q

GLUT2

A

High Km. hepatocytes and beta-islet cells of pancreas. hepatic portal vein glucose.

146
Q

GLUT2 as it relates specifically to pancreas

A

in beta-islet cells, glucose sensor for insulin release, along with glucokinase

147
Q

GLUT4

A

adipose and muscle. peripheral blood. Km close to normal blood glucose, saturated when level is just a bit higher. insulin causes increase in GLUT4 on cell surface.

148
Q

without insulin, is there glucose absorption?

A

yes, there are basal levels in all cells

149
Q

why does adipose need glucose

A

to form DHAP, which is converted to glycerol phosphate for storage of incoming FA as triacylglycerol

150
Q

which metabolic processes require mitochondria?

A

TCA, ETC, ox-phos, beta-ox (FA metabolism)

151
Q

a special function of glycolysis in liver

A

produce intermediates for FA synth

152
Q

RLE of glycol

A

PFK-1

153
Q

RLE of fermentation

A

lactate dehydrogenase

154
Q

RLE of glycogenesis

A

glycogen synthase

155
Q

glycogenolysis RLE

A

glycogen phosphorylase

156
Q

gluconeogenesis RLE

A

fructose-1,6-bisphosphatase

157
Q

pentose phosphate pathway RLE

A

glucose-6-phosphate dehydrogenase

158
Q

irreversible enzymes of glycolysis

A

glucokinase/hexokinase, PFK-1, pyruvate kinase

159
Q

enzyme that converts glucose to glucose-6-phosphate

A

hexokinase/glucokinase

160
Q

where is glucokinase found?

A

liver cells and B-islet of pancreas

161
Q

difference between glucokinase and hexokinase?

A

hexokinase has a low Km (not proportional to conc) and is inhibited by glucose-6-phosphate. glucokinase has a high Km (proportional to conc). it is activated by insulin.

162
Q

unique insulin sensitivity in liver/pancreas vs. muscle/adipose

A

in liver: glucokinase is insulin-sensitive. in muscle: GLUT4 is insulin sensitive.

163
Q

inhibits PFK-1

A

ATP and citrate

164
Q

activates PFK-1

A

AMP

165
Q

why is special PFK-1 regulation in hepatocytes needed?

A

here, you want a way to override inhibition by ATP. You still want to create intermediates for FA synthesis and create glycogen, even when energy needs of cell are met.

166
Q

how is PFK-1 specially regulated in liver by insulin?

A

PFK-2 is stimulated. this enzyme converts fructose 1,6-bisphosphate to fructose 2,6-bisphosphate. F2,6-BP activates….PFK-1 :)

167
Q

how is PFK-2 specially regulated in liver by glucagon?

A

PFK-2 is inhibited.

168
Q

where is PFK-2 found?

A

mostly in liver

169
Q

what does glyceraldehyde-3-phosphate dehydrogenase do?

A

between glyceraldehyde 3-P and 1,3-bisphosphoglycerate. NAD+ is reduced.

170
Q

what does 3-phosphoglycerate kinase do?

A

between 1,3-bisphosphoglycerate and 3-phosphoglycerate. Substrate-level phosphorylation.

171
Q

what does pyruvate kinase do?

A

PEP to pyruvate. Substrate-level phosphorylation.

172
Q

activates pyruvate kinase

A

fructose 1,6-bisphosphate

173
Q

lactate dehydrogenase

A

fermentation. regenerates NAD+

174
Q

What can we do with DHAP besides continuing glycolysis?

A

It can be isomerized to glycerol 3-phosphate and converted to glycerol for triacylglycerol synthesis in hepatic and adipose

175
Q

mnemonic for irreversibel enzymes of glycol

A 
How Glycolysis Pushes Forward the Process: Kinase
Hexokinase
Glycokinase
PFK-1
Pyruvate Kinase
176
Q

enzyme responsible for difference between maternal and fetal Hb oxygen affinity

A

bisphosphoglycerate mutase

177
Q

bisphosphoglycerate works by

A

producing 2,3-BPG from 1,3-BPG. the former decreases affinity of HbA for oxygen

178
Q

bisphosphoglycerate mutase is found in

A

RBC

179
Q

at high altitudes, pO2 is higher/lower, and you would increase/decrease respiration

A

lower, increase

180
Q

four things which cause rightward shift of Hg oxygen dissociation curve

A

High 2,3-BPG, low pH, high H+, high pCO2

181
Q

two prominent monosaccharides other than glucose

A

galactose and fructose

182
Q

galactose comes from

A

lactose = glucose + galactose

183
Q

fructose comes from

A

sucrose = glucose + fructose

184
Q

a monosaccharide which can bypass PFK-1

A

fructose

185
Q

three possible fates of pyruvate

A

conversion to acetyl-CoA by pyruvate, conversion to lactate by lactate dehydrogenase, conversion to OAA by pyruvate carboxylase

186
Q

pyruvate enters mito and is converted to acetyl-CoA. will it be used for TCA or FA synthesis?

A

depends if ATP is present

187
Q

is PDH hormone-responsive

A

in liver, to insulin

188
Q

by what mechanism does PDH convert acetyl-CoA to pyruvate?

A

it can’t, it is an irreversible reaction. acetyl-CoA cannot be converted back to glucose.

189
Q

what cofactors/coenzymes does PDH require?

A

FAD and NAD+, CoA, lip and thigh (lipoic acid and thiamine pyrophosphate)

190
Q

by what mechanism is pyruvate conserved for gluconeo instead of PDH?

A

PDH is inhib by acetyl-CoA

191
Q

in what manner is glycogen stored

A

as granules in cytoplasm

192
Q

difference between glycogen consisting of linear versus branched chains

A

linear will have higher density near core. branched will have higher density on periphery. the latter is better for rapid release.

193
Q

plant version of glycogen

A

starch

194
Q

outline glycogenesis

A

glycogenin is the core protein. then glucose-6-P is converted to glucose-1-P. G1P interacts with UTP to become UDP-glucose and PPi, allowing it to be integrated into glycogen by glycogen synthase.

195
Q

glycogen branching

A

alpha-1,4 moves it forward, alpha-1,6 puts a branch in the mix

196
Q

inhibits glycogen synthase

A

glucagon and epinephrine

197
Q

describe how glycogen branching occurs

A

branching enzyme hydrolyzes an alpha-1,4 and then forms an alpha-1,6 btwn the parent chain and the oligoglucose . then glycogen synthase continues, extending both branches.

198
Q

glucagon enters liver; what happens to glycogen

A

glycogen phosphorylase breaks alpha-1,4 bonds and releases molecules of glucose-1-P. Debranching enzyme cleaves the alpha-1,6’s.

199
Q

difference between activation of glucagon in liver and in skel muscle

A

in liver, by glucagon. in skel muscle, by epinephrine and AMP. Makes sense, since only liver glycogen is broken down to glucose for rest of body.

200
Q

inhibits glycogen phosphorylase

A

ATP

201
Q

is free glucose every produced directly from glycogenolysis?

A

debranching enzyme is really 2 enzymes. the first breaks alpha-1,4 of branch and adds it to parent chain. the other breaks the alpha-1,6, releasing one free glucose.

202
Q

which organs do gluconeo

A

liver and, to lesser extent, kidney

203
Q

inhibits gluconeo

A

insulin

204
Q

stimulates gluconeo

A

epinephrine and glucagon

205
Q

where is galactose and fructose converted to glucose?

A

in liver

206
Q

three substrates for gluconeo and their source

A
  1. glycerol 3-phosphate (adipose)
  2. lactate (anaerobic glycol)
  3. glucogenic amino acids (muscle proteins)
207
Q

glucogenic AA

A

all but leucine and lysine

208
Q

how much glucose can you get from stored fat

A

not much. most becomes acetyl-CoA, which can’t be converted to glucose. The exception is FA with odd number carbons

209
Q

how does acetyl-CoA relate to gluconeo?

A

can’t be used as substrate, but is actually REQUIRED. it is needed to inhibit pyruvate dehydrogenase and stimulate pyruvate carboxylase.

210
Q

how does gluconeo relate to beta-ox

A

gluconeo needs acetyl-CoA from beta ox, not as substrate, but as regulator

211
Q

pyruvate dehydrogenase function

A

pyruvate to Acetyl-CoA

Dragon (23 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions