Exam II cards Flashcards

(223 cards)

1
Q

fructose is synthesized in the body from glucise via the

A

polyol pathway

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

in the lens of the eye if it accumulates can lead to cataracts

A

fructose

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

how is fructose metabolized

A

conversion to intermediates of glycolysis

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

fructose enters cells via

A

GLUT 5 transporter

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

fructose is converted to fructose 1 phosphate via

A

fructokinase (uses an ATP)

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

fructose is phosphorylated and cleaved to yield what two intermediates of glycolysis

A

dihydroxyacetone-P and glyceraldehyde 3-P

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

where does fructose metabolism occur

A

liver

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

function of aldolases in fructose metabolism

A

all cleave F1,6 bisphoophate

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

what enzyme is soley responsible for cleaving fructose 1 phosphate

A

aldolase B

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

what is the rate limiting enzyme of fructose metabolism

A

aldolase B

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

what is the function of muscle and adipose hexokinase when glucose is low

A

fructose is converted to fructose 6 phosphate

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

aldolase A is found

A

muscle

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

essential fructosuria

A

deficiency in fructose kinase

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

hereditary fructose intolerance

A

deficiency in aldolase B

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

why is aldolase B deficiency or hereditary fructose intolerance fatal

A

no aldolase B so fructose 1-6 cannot be cleaved but is also inhibits breakdown of glycogen and gluconeogenesis and results in hypoglycemia, high lactate and low ATP

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

what are the two steps to the polyol pathway

A

1) reduction of C1 by aldolase reductoase

2) oxidation of C2 by sorbitol dehydrogenase

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

the polyol pathway is important in

A

seminal vesicles

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

what population has a very high rate of galactose metabolism

A

neonates

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

galactose is converted to galactose 1 phosphate via

A

galactokinase (uses atp)

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

galactose 1 phosphate is converted to glucose 1 phosphate via

A

galactose 1 phosphate uridylyltransferase

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

UDP galactose can be converted to UDP glucose via

A

Epimerase

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

when lactose is cleaved in is converted to

A

glucose and galactose

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

function of PPP

A

generated NADPH for redcuing equivalents and ribose 5 phosphate for nucleotide biosynthesis

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

______is the only source of NADPH for RBC’s

A

PPP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
what is the substrate for PPP
glucose 6 phosphate
26
pentose intermediates are reversibly interconverted to what
intermediates of glycolysis
27
1 Glucose 6 phosphate produces what through PPP
2 NADPH, one co2 and one ribulose 5 phosphate
28
what is the enzyme called that oxidizes aldehyde at C1 of G6P to produce NADPH
G6PD
29
what are the 4 key enzymes involved in nonoxidative PPP
isomerase, epimerase, transketolase, and transaldolase
30
type of reaction of nonoxidative phase to produce ribose 5 p
ketose to aldose conversion
31
what are the 2 pathways of Ribose 6 phosphate
nucleotide synthetic pathway or glycolytic intermediates in the non-oxidative phase of PPP
32
_________transverse a 2 carbon unit
transketolase
33
what cofactor does transketolase require
thiamine
34
what type of deficiency is common in alcoholics
thiamine deficient
35
xylose 5 phosphate and ribose 5 phosphate can be converted to what and what
glyceraldehyde 3 phosphate and sedoheptulose 7 phosphate
36
____________transferse a three carbon unit
transaldolase
37
sendohelptulse 7 phosphate and G3P can be converted to what via transaldolase
erythrose 4 phosphate and fructose 6 phosphate
38
what is the net result of nonoxidative PPP from 3 moles of ribulose 5P
2 frucot 6P 1 G3P 3 rib 5P
39
overal net result of PPP
3 G6P to 6 NADPH, 3 CO2, 2 fructose 6P, and 1 g3P
40
what is the rate limiting step in PPP
glucose 6P dehydrogenase
41
if a cell needs NADPH only
oxidative reactions to produce NADPH | non oxidative to convert r5P to G6P to produce more NADPH
42
cell needs NADPH and rib 5P
oxidative reactions
43
cell needs rib 5 phosphate
only nonaxidative reactions, high NADPH inhibits g6PD
44
cell needs NADPH and pyruvate
both oxidative and nonoxidative reactions are used
45
Heinz bodies
NADPH needed for GSSG to GSH, G6PD deficiency leads to formation of these in RBC's and can lead to hemolysis
46
ribulose 5 phosphate to ribose 5 phosphate
ribulose 5 phosphate isomerase
47
ribulose 5 phosphate to xyulose 5 phosphate
ribulose 5 phosphate 3 epimerase
48
gluconeogenesis occurs
in the liver under fasting or starving conditions
49
gluconeogenesis is stimulated by
glucagon
50
glucose 6 phosphate is converted to glucose via
glucose 6 phosphatase
51
fructose 1,6 P is converted to fructose 6 P via
fructose 1,6 bisphosphatase
52
carbon sources for gluconeogenesis are
lactate, amino acids and glycerol (from adipose)
53
ethanol cannot be used for gluconeogenesis becasue
it is metabolized to acetyl CoA
54
G3P is converted to what for gluconeogenssis
dihyddroxy acetone phosphate via glycerol 3 phosphate dehydrogenase (produces NADH)
55
pyruvate to OAA via what enzyme
pyruvate carboxylase
56
what cofactor does pyruvate carboxylase require
biotin
57
PEPCK is found where
mitochondria and the cytosol
58
PEPCK activity
OAA to PEP, uses GTP and releases CO2
59
gluconeogenesis costs how many ATP
6 ATP!
60
pyruvate carboxylase requires
4 ATP
61
phophoglycerate kinase requires
2ATP
62
the most important control point in gluconeoegensis is
between F6P and F1,6BP
63
pyruvate carboxylase regulation
activated by acetyl CoA
64
PEP carboxykinase regulation
induced by glucagon, epinpehrine and glucocorticoids
65
g6 Phosphatase regulation
induced by gene transcritpion during fasting
66
F1,6 Bphosphatase regulation
induced during fasting
67
glucokinase regulation
induced by insulin and high Km for glucose
68
PPFK-1
activated by F2,6, BP. AMP, and inhibited by ATP, citrate
69
pyruvate kinase regulation
activated by F1,6BP, inhibited by ATP, alanine, inhibited by phosphorylation from protein kinase A)
70
where is G6 phosphatase found
ER membrane
71
what is the name of the disease that results from deficiency of glucose 6 phosphatase
von Gierkas disease
72
hyperglycemia
osmotic dehydration of tissues, hyperoxmolar coma from brain dehydration
73
hypoglycemia
depletion of ATP, dizziness, drowsiness, coma, blood loss
74
low F2,6 BP stimulates
F1,6 BPase (gluconeogenssis)
75
at 16 hours after fed what is constributing to glucose levels
glycogenolysis and gluconeogenesis
76
cholesterol is important in what
``` vitamin D membrane formation steroid hormones bile salts lipoproteiins (cholesterol esters) ```
77
what are the two sources of cholesterol in our bodies
synthesis and diet
78
how are lipids transported in the blood
via lipoproteins
79
what are the structures on the protein surface of a lipoprotein
apoproteins phospholipids and cholesterol
80
what gives rise to the lipid core of lipoproteins
triglycerides and cholesterol esters
81
what is the precursos lipoprotein to LDL
IDL
82
what is known as the bad cholesterol
LDL
83
good cholesterol
HDL
84
which lipoproteins have the highest cholesterol content
LDL
85
function ofDL
return endogenous lipids (VLDL) remnants) or are LDL precursors
86
name of the receptor on LDL
ApoB 100
87
what is the major way the body eliminates cholesterol
bile salts
88
HDL is made where
liver
89
where is LDL made
blood stream
90
function of LCAT
uses lecithin to convert cholesterol into a cholesterol ester
91
CEPT function in cholesterol biochemistry
functions to transport cholesterol ester from HDL to VLDL
92
functions to deliver cholesterol to liver
HDL
93
functions to deliver cholesterol to tissues
LDL
94
what percentage of cholesterol comes from our diet
1/3 or 15%
95
what percentage of our cholesterol comes from liver
85% or 2/3
96
cholesterol is made primarily in the
liver cytosol
97
what is the key step in cholsterol synthesis
HMG-CoA reductase
98
in the blood cholesterol is initially cared by
VLDL
99
cholesterol is made from
acetyl CoA
100
What are the steps in cholesterol synthesis
``` acetyl CoA Mevalonate isoprene squalene cholesterol ```
101
what are the three ways HMG-CoA reductase can be regulated
transcriptional proteolysis covalent modification
102
HMG-CoA reductase is inactive when it is
phosphorylated
103
what activates AMP protein kinase
AMP and glucagon and sterols
104
what inhibits AMP protein kinase
insulin
105
what step of cholesterol synthesis uses ATP
mevalonate to isoprenes
106
what step of cholesterol synthesis uses NADPH
isoprenes to squalene
107
what is the last intermediate in cholesterol synthesis that does not have a ring
squalene
108
function of ACAT
converts a cholesterol to cholesterol ester so that it can be packaged into VLDL
109
CE is more
hydrophobic
110
what are the two bile acids made from cholesterol synthesis
chenodeoxychlolic acid and cholic acid
111
what is the rate limiting step of cholesterol synthesis
7 alpha hydroxylase
112
what two processes occur that allow for cholesterol to accumulate in plaques
oxydized or glycolyated
113
function of statins
inhibit HMG CoA reductase
114
Ezetimble
decreases absorption of cholesterl
115
when there is increased blood glucose from type 2 diabets what happens to cholesterol
LDL-R can become glcated inhibitng its activity
116
how many carbon longs are eicosanoids
20 hydrocarbon molecules
117
the most abudant precursor for eicosanoid metabolism is
arachidonic acid
118
what compound found in plant cells are important precurss for arachidonic acid
linoleate
119
arachidonic acid can be released by
PLA2 or PLC
120
what are the three enzymes associated with the arachidonic acid pathway
cyclooxygenase lipooxygenase cytochorme P450
121
cytochorme P450 produces
epoxides
122
lipooxygenase produces
HPETE
123
cyclooxygenase produces
prostaglandins and thromboxanes
124
function of thromboxanes
produced by platelets, stimulates platent aggregation causes vasoconstriction (would healing) bronchoconstriction
125
function of prostacyclins
vasodilation INFLAMMATION
126
irreversible inhibit of COX
aspirin
127
acetaminophen and ibuprofen bind
reversible to COX
128
primary function of COX1
platelet aggregation and stomach cytoprotection
129
primary function of COX2
inflammation and hyperalgsia
130
steroids only have an effect on which COX
COX 2
131
examples of COX-2 inhibitors
vioxx and celebrex
132
function of leukotrienes (LTB4
increases vascular permeability, T cell proliferation, Leukocyte aggregation, inflmmatory cytokines
133
function of LTC4 and LTD4
bronchoconstriction, vascular permeabilty and IFN-Gamma
134
cortocoid steroids and leukotrienes
supress inflammatory genes and inhhibits cytokine production
135
leukotriene modifies
may inhibit synthesis or binding to a receptor
136
singular
blocks cysteinyl luekotrienes
137
inhaled steroids
block steroid sensitive mediators
138
LIPOXIN
induces chemotaxis and stimulates superoxide production in leukocytes
139
which eicosanoids act by the AC-cAMP PKA system
PGe, PGD, and PGI
140
altered intracellular calcium is mechanism action for what major eicosnaoids
PGF2-alpha TXA 2 leukotrienes
141
cytochrome P450 pathway
acts on endocrine, ocular, renal and vascular systems | in some cases inhibits sodium/potassium ATPase
142
isoprostanes
produced by action of free radicals not by enzymes
143
what can beused to measure oxidative stress
isoprotane concentration in urine
144
endocannabinoids
ligands for nervous sistem, retrograde messenger, have an analgesic effect
145
where is most of ethanol metabolized
in the liver
146
if ethanol is not metabolismed in the liver where does it goe
enters GI tract or is excreted through the lungs or kidneys
147
what are the two major pathways of ethanol metabolism in the liver
ADH and MEOS
148
when alcohol is absorbed in the gut it passes where
liver
149
ethanol is converted to acetyladehyde via what enzyme
ADH, produces NADH
150
what enzyme is used during low levels of alcohol consumption
ADH
151
what enzyme concerts ethanol to produce acetyladehyde but uses NADPH
MEOS in ER
152
what enzyme is used at high levels of alcohol intake
MEOS
153
specifically which ADH is associated with low km and is active onlt with ethanol, high tissue capacity
ADH1
154
what ADH specifically is found primarily in the liver and lower levels of GI tract
ADH2
155
Where is ADH4 found
highest levels in upper GI tract, gingiva, mouth, esophagus and down to the stomach, not present in the liver
156
which ADH is not found in the liver
ADH4
157
MEOS is part of what
cytochorme P450 family
158
which cytochrome is most active to ethanol
CYP2E1
159
does MEOS have a higher Km or lower Km than ADH
higher Km, low affinity
160
where is MEOS found
endoplasmic reticulum
161
in alcohol metabolism what enzyme is responsible for converted acetalaldehyde to acetate
ALDH
162
80% of ALDH is found
mitochondria
163
what converts acetate to acetyl CoA
acetylCoA synthetase I liver and II in skeletal muscle
164
where is morelikely for acetyl CoA to be syntheiszed from acetate
skeletal muscle MORE than liver
165
how much energy does ADH produce per ethanol
13 ATP's
166
how many ATP's per ethanol molecule is produced by the MEOS pathway
8 ATPS
167
most of the toxic effects of alcohol are due to what
acetyladehyde production and NADH
168
what are the four main effeccts of increasd NADH production in ethanol metabolism
inhibits fatty acid oxidation and promotes VLDL ketoacidosos-not citrate synthesis inhibits lactate dehydrogenase- decreases uric acid excretion inhibits gluconeogenesis
169
effects of accumulation of acetyladehyde
decreased hepatic protein synthesis | loss of protection against damage from oxidation
170
methanol is a possible substrate for
ADH
171
ADH and methanol forms
formaldehyde which is then converted to formate via ALDH
172
what is the compound that produces methanol toxicity
formate
173
(T/F) ethanol is both lipid and water soluble
True!
174
How does olestra work
pancreatic lipase is NOT able to hydrolyze the fatty acids attached to sucrose
175
when does digestion of lipids take place
not until the intestine
176
lingual lipase is high in
children who drink alot of cow's milk
177
lipids are absorbed by intestinal epithelium and resynthesized to
triacylglycerols
178
how are lipids transported
via chylomicrons in the lymph
179
function of colipase
binds to fat and lipase activating pancreatic lipase
180
function of esterases and phosphilipase A2
removes fatty acids and phosphilipids
181
pancreatic lipase and colipase are secreted in response to what
cholectyokinin
182
secretin is secreted in response to
HCL in the intestine and signals for bicarb secretion
183
what is phospholipase A2 activated by
trypsin
184
tryglyceride is converted to monoglyceriade and fatty acids via
lipase
185
bile salts are synthesized where
liver
186
what is the major component of bile salts
cholic aicd
187
what is the rate limiting step of bile acid synthesis
first step of 7-alpha hydroxylase, inhibited by bile acids
188
bile salts are reabsorbed where
illeum
189
bile salts are stored where
gallbladder
190
what type of fatty acids do not need bile salts
short and medium chain fatty acids
191
what are packagaed into micells by bile salts
``` fatty acids monoacylgylcerols cholesterol lysophospholipids fat soluble vitamins ```
192
how are triacylglycerols resynthesized
free fatty acids are esterifired to 2 monoacyglycerol which requires 2 ATP molecules and CoA
193
which apoprotein is associated with activation of lipoprotein lipase
apoCII
194
apoB100 and abpoB 48 are related how
located on the same gene
195
what is the major source of acetyl CoA
dietary glucose
196
how is OAA produced from pyruvate
pyruvate carboxylase
197
how is acetyl CoA produced from pyruvate
pyruvate dehydrogenase
198
what has a higher percentage of triacylglycerols VLDL or chylomicrons
chylomicrons
199
lipoprotein lipase is activated by
apoprotein CII
200
in muscle LPL has a low or high Km
low
201
in adipose LPL has a low or high Km
high
202
LPL is made in response to
insulin
203
what causes the release of fatty acids
insulin low, high cAMP, activates protein kinase A
204
glycerol 3 phosphate reacts with two fatty acids to produce
phosphatidic acid
205
how is phosphatidylyglycerol produced
condendation of CDP-DAG and G3phopshate
206
how is a ceramide formed
serine and palmitory CoA
207
how is the double bond formed in sphingolipids
FAD
208
short chain fatty acid site of activation
cytosol and mitochondria
209
medium chain fatty acid site of activation
mitochondrial matrix (kidney and liver)
210
long chain fatty acid site of activation
ER, outer mito membrane, peroxisomal membrane
211
very long chain fatty acids site of actiation
peroxisomes
212
when beta oxidation of fatty acids is blocked where to excess FA go
triacylglycerol synthesis
213
longchian fatty acids require what to get into the mitochondria
carnitine
214
Sources of carnitine
comes from the diet, but can also be synthesized from lysinne
215
beta oxidation of long chain fatty acids is inhibited by
malonyl CoA
216
what part of beta oxidation does malonyl CoA inhibit
carnitine palmitory transferse I
217
reaction of propionyl CoA to succinyl CoA requires
propioyl Coa, bicarb, ATP, biotin, and conezyme B12
218
wehre does omega oxidation of fatty acids occur
endoplasmic reticulum
219
citrate inhibits
PFK-1
220
what are the three ketone bodies
acetoacetate beta hdyrogxy butyrate acetone
221
OAA has what affect on ketone body synthesis
decreases synthesis
222
what are the strictly ketogenic amino acids
leucine and lysine
223
what are the ketogenic and glucogenic amino acid
phenyalalanine, trophophan and tyrosine