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Biochemistry Fall MS1 > Exam II cards > Flashcards

Exam II cards Flashcards

1
Q

fructose is synthesized in the body from glucise via the

A

polyol pathway

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2
Q

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

A

fructose

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3
Q

how is fructose metabolized

A

conversion to intermediates of glycolysis

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4
Q

fructose enters cells via

A

GLUT 5 transporter

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5
Q

fructose is converted to fructose 1 phosphate via

A

fructokinase (uses an ATP)

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6
Q

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

A

dihydroxyacetone-P and glyceraldehyde 3-P

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7
Q

where does fructose metabolism occur

A

liver

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8
Q

function of aldolases in fructose metabolism

A

all cleave F1,6 bisphoophate

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9
Q

what enzyme is soley responsible for cleaving fructose 1 phosphate

A

aldolase B

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10
Q

what is the rate limiting enzyme of fructose metabolism

A

aldolase B

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11
Q

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

A

fructose is converted to fructose 6 phosphate

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12
Q

aldolase A is found

A

muscle

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13
Q

essential fructosuria

A

deficiency in fructose kinase

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14
Q

hereditary fructose intolerance

A

deficiency in aldolase B

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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

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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

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17
Q

the polyol pathway is important in

A

seminal vesicles

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18
Q

what population has a very high rate of galactose metabolism

A

neonates

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19
Q

galactose is converted to galactose 1 phosphate via

A

galactokinase (uses atp)

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20
Q

galactose 1 phosphate is converted to glucose 1 phosphate via

A

galactose 1 phosphate uridylyltransferase

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21
Q

UDP galactose can be converted to UDP glucose via

A

Epimerase

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22
Q

when lactose is cleaved in is converted to

A

glucose and galactose

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23
Q

function of PPP

A

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

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24
Q

______is the only source of NADPH for RBC’s

A

PPP

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25
Q

what is the substrate for PPP

A

glucose 6 phosphate

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26
Q

pentose intermediates are reversibly interconverted to what

A

intermediates of glycolysis

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27
Q

1 Glucose 6 phosphate produces what through PPP

A

2 NADPH, one co2 and one ribulose 5 phosphate

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28
Q

what is the enzyme called that oxidizes aldehyde at C1 of G6P to produce NADPH

A

G6PD

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29
Q

what are the 4 key enzymes involved in nonoxidative PPP

A

isomerase, epimerase, transketolase, and transaldolase

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30
Q

type of reaction of nonoxidative phase to produce ribose 5 p

A

ketose to aldose conversion

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31
Q

what are the 2 pathways of Ribose 6 phosphate

A

nucleotide synthetic pathway or glycolytic intermediates in the non-oxidative phase of PPP

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32
Q

_________transverse a 2 carbon unit

A

transketolase

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33
Q

what cofactor does transketolase require

A

thiamine

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34
Q

what type of deficiency is common in alcoholics

A

thiamine deficient

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35
Q

xylose 5 phosphate and ribose 5 phosphate can be converted to what and what

A

glyceraldehyde 3 phosphate and sedoheptulose 7 phosphate

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36
Q

____________transferse a three carbon unit

A

transaldolase

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37
Q

sendohelptulse 7 phosphate and G3P can be converted to what via transaldolase

A

erythrose 4 phosphate and fructose 6 phosphate

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38
Q

what is the net result of nonoxidative PPP from 3 moles of ribulose 5P

A

2 frucot 6P
1 G3P
3 rib 5P

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39
Q

overal net result of PPP

A

3 G6P to 6 NADPH, 3 CO2, 2 fructose 6P, and 1 g3P

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40
Q

what is the rate limiting step in PPP

A

glucose 6P dehydrogenase

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41
Q

if a cell needs NADPH only

A

oxidative reactions to produce NADPH

non oxidative to convert r5P to G6P to produce more NADPH

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42
Q

cell needs NADPH and rib 5P

A

oxidative reactions

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43
Q

cell needs rib 5 phosphate

A

only nonaxidative reactions, high NADPH inhibits g6PD

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44
Q

cell needs NADPH and pyruvate

A

both oxidative and nonoxidative reactions are used

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45
Q

Heinz bodies

A

NADPH needed for GSSG to GSH, G6PD deficiency leads to formation of these in RBC’s and can lead to hemolysis

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46
Q

ribulose 5 phosphate to ribose 5 phosphate

A

ribulose 5 phosphate isomerase

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47
Q

ribulose 5 phosphate to xyulose 5 phosphate

A

ribulose 5 phosphate 3 epimerase

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48
Q

gluconeogenesis occurs

A

in the liver under fasting or starving conditions

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49
Q

gluconeogenesis is stimulated by

A

glucagon

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50
Q

glucose 6 phosphate is converted to glucose via

A

glucose 6 phosphatase

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51
Q

fructose 1,6 P is converted to fructose 6 P via

A

fructose 1,6 bisphosphatase

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52
Q

carbon sources for gluconeogenesis are

A

lactate, amino acids and glycerol (from adipose)

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53
Q

ethanol cannot be used for gluconeogenesis becasue

A

it is metabolized to acetyl CoA

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54
Q

G3P is converted to what for gluconeogenssis

A

dihyddroxy acetone phosphate via glycerol 3 phosphate dehydrogenase (produces NADH)

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55
Q

pyruvate to OAA via what enzyme

A

pyruvate carboxylase

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56
Q

what cofactor does pyruvate carboxylase require

A

biotin

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57
Q

PEPCK is found where

A

mitochondria and the cytosol

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58
Q

PEPCK activity

A

OAA to PEP, uses GTP and releases CO2

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59
Q

gluconeogenesis costs how many ATP

A

6 ATP!

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60
Q

pyruvate carboxylase requires

A

4 ATP

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61
Q

phophoglycerate kinase requires

A

2ATP

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62
Q

the most important control point in gluconeoegensis is

A

between F6P and F1,6BP

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63
Q

pyruvate carboxylase regulation

A

activated by acetyl CoA

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64
Q

PEP carboxykinase regulation

A

induced by glucagon, epinpehrine and glucocorticoids

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65
Q

g6 Phosphatase regulation

A

induced by gene transcritpion during fasting

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66
Q

F1,6 Bphosphatase regulation

A

induced during fasting

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67
Q

glucokinase regulation

A

induced by insulin and high Km for glucose

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68
Q

PPFK-1

A

activated by F2,6, BP. AMP, and inhibited by ATP, citrate

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69
Q

pyruvate kinase regulation

A

activated by F1,6BP, inhibited by ATP, alanine, inhibited by phosphorylation from protein kinase A)

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70
Q

where is G6 phosphatase found

A

ER membrane

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71
Q

what is the name of the disease that results from deficiency of glucose 6 phosphatase

A

von Gierkas disease

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72
Q

hyperglycemia

A

osmotic dehydration of tissues, hyperoxmolar coma from brain dehydration

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73
Q

hypoglycemia

A

depletion of ATP, dizziness, drowsiness, coma, blood loss

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74
Q

low F2,6 BP stimulates

A

F1,6 BPase (gluconeogenssis)

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75
Q

at 16 hours after fed what is constributing to glucose levels

A

glycogenolysis and gluconeogenesis

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76
Q

cholesterol is important in what

A 
vitamin D
membrane formation
steroid hormones
bile salts
lipoproteiins (cholesterol esters)
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77
Q

what are the two sources of cholesterol in our bodies

A

synthesis and diet

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78
Q

how are lipids transported in the blood

A

via lipoproteins

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79
Q

what are the structures on the protein surface of a lipoprotein

A

apoproteins
phospholipids and
cholesterol

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80
Q

what gives rise to the lipid core of lipoproteins

A

triglycerides and cholesterol esters

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81
Q

what is the precursos lipoprotein to LDL

A

IDL

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82
Q

what is known as the bad cholesterol

A

LDL

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83
Q

good cholesterol

A

HDL

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84
Q

which lipoproteins have the highest cholesterol content

A

LDL

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85
Q

function ofDL

A

return endogenous lipids (VLDL) remnants) or are LDL precursors

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86
Q

name of the receptor on LDL

A

ApoB 100

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87
Q

what is the major way the body eliminates cholesterol

A

bile salts

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88
Q

HDL is made where

A

liver

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89
Q

where is LDL made

A

blood stream

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90
Q

function of LCAT

A

uses lecithin to convert cholesterol into a cholesterol ester

91
Q

CEPT function in cholesterol biochemistry

A

functions to transport cholesterol ester from HDL to VLDL

92
Q

functions to deliver cholesterol to liver

A

HDL

93
Q

functions to deliver cholesterol to tissues

A

LDL

94
Q

what percentage of cholesterol comes from our diet

A

1/3 or 15%

95
Q

what percentage of our cholesterol comes from liver

A

85% or 2/3

96
Q

cholesterol is made primarily in the

A

liver cytosol

97
Q

what is the key step in cholsterol synthesis

A

HMG-CoA reductase

98
Q

in the blood cholesterol is initially cared by

A

VLDL

99
Q

cholesterol is made from

A

acetyl CoA

100
Q

What are the steps in cholesterol synthesis

A 
acetyl CoA
Mevalonate
isoprene
squalene
cholesterol
101
Q

what are the three ways HMG-CoA reductase can be regulated

A

transcriptional
proteolysis
covalent modification

102
Q

HMG-CoA reductase is inactive when it is

A

phosphorylated

103
Q

what activates AMP protein kinase

A

AMP and glucagon and sterols

104
Q

what inhibits AMP protein kinase

A

insulin

105
Q

what step of cholesterol synthesis uses ATP

A

mevalonate to isoprenes

106
Q

what step of cholesterol synthesis uses NADPH

A

isoprenes to squalene

107
Q

what is the last intermediate in cholesterol synthesis that does not have a ring

A

squalene

108
Q

function of ACAT

A

converts a cholesterol to cholesterol ester so that it can be packaged into VLDL

109
Q

CE is more

A

hydrophobic

110
Q

what are the two bile acids made from cholesterol synthesis

A

chenodeoxychlolic acid and cholic acid

111
Q

what is the rate limiting step of cholesterol synthesis

A

7 alpha hydroxylase

112
Q

what two processes occur that allow for cholesterol to accumulate in plaques

A

oxydized or glycolyated

113
Q

function of statins

A

inhibit HMG CoA reductase

114
Q

Ezetimble

A

decreases absorption of cholesterl

115
Q

when there is increased blood glucose from type 2 diabets what happens to cholesterol

A

LDL-R can become glcated inhibitng its activity

116
Q

how many carbon longs are eicosanoids

A

20 hydrocarbon molecules

117
Q

the most abudant precursor for eicosanoid metabolism is

A

arachidonic acid

118
Q

what compound found in plant cells are important precurss for arachidonic acid

A

linoleate

119
Q

arachidonic acid can be released by

A

PLA2 or PLC

120
Q

what are the three enzymes associated with the arachidonic acid pathway

A

cyclooxygenase
lipooxygenase
cytochorme P450

121
Q

cytochorme P450 produces

A

epoxides

122
Q

lipooxygenase produces

A

HPETE

123
Q

cyclooxygenase produces

A

prostaglandins and thromboxanes

124
Q

function of thromboxanes

A

produced by platelets, stimulates platent aggregation causes vasoconstriction (would healing) bronchoconstriction

125
Q

function of prostacyclins

A

vasodilation INFLAMMATION

126
Q

irreversible inhibit of COX

A

aspirin

127
Q

acetaminophen and ibuprofen bind

A

reversible to COX

128
Q

primary function of COX1

A

platelet aggregation and stomach cytoprotection

129
Q

primary function of COX2

A

inflammation and hyperalgsia

130
Q

steroids only have an effect on which COX

A

COX 2

131
Q

examples of COX-2 inhibitors

A

vioxx and celebrex

132
Q

function of leukotrienes (LTB4

A

increases vascular permeability, T cell proliferation, Leukocyte aggregation, inflmmatory cytokines

133
Q

function of LTC4 and LTD4

A

bronchoconstriction, vascular permeabilty and IFN-Gamma

134
Q

cortocoid steroids and leukotrienes

A

supress inflammatory genes and inhhibits cytokine production

135
Q

leukotriene modifies

A

may inhibit synthesis or binding to a receptor

136
Q

singular

A

blocks cysteinyl luekotrienes

137
Q

inhaled steroids

A

block steroid sensitive mediators

138
Q

LIPOXIN

A

induces chemotaxis and stimulates superoxide production in leukocytes

139
Q

which eicosanoids act by the AC-cAMP PKA system

A

PGe, PGD, and PGI

140
Q

altered intracellular calcium is mechanism action for what major eicosnaoids

A

PGF2-alpha
TXA 2
leukotrienes

141
Q

cytochrome P450 pathway

A

acts on endocrine, ocular, renal and vascular systems

in some cases inhibits sodium/potassium ATPase

142
Q

isoprostanes

A

produced by action of free radicals not by enzymes

143
Q

what can beused to measure oxidative stress

A

isoprotane concentration in urine

144
Q

endocannabinoids

A

ligands for nervous sistem, retrograde messenger, have an analgesic effect

145
Q

where is most of ethanol metabolized

A

in the liver

146
Q

if ethanol is not metabolismed in the liver where does it goe

A

enters GI tract or is excreted through the lungs or kidneys

147
Q

what are the two major pathways of ethanol metabolism in the liver

A

ADH and MEOS

148
Q

when alcohol is absorbed in the gut it passes where

A

liver

149
Q

ethanol is converted to acetyladehyde via what enzyme

A

ADH, produces NADH

150
Q

what enzyme is used during low levels of alcohol consumption

A

ADH

151
Q

what enzyme concerts ethanol to produce acetyladehyde but uses NADPH

A

MEOS in ER

152
Q

what enzyme is used at high levels of alcohol intake

A

MEOS

153
Q

specifically which ADH is associated with low km and is active onlt with ethanol, high tissue capacity

A

ADH1

154
Q

what ADH specifically is found primarily in the liver and lower levels of GI tract

A

ADH2

155
Q

Where is ADH4 found

A

highest levels in upper GI tract, gingiva, mouth, esophagus and down to the stomach, not present in the liver

156
Q

which ADH is not found in the liver

A

ADH4

157
Q

MEOS is part of what

A

cytochorme P450 family

158
Q

which cytochrome is most active to ethanol

A

CYP2E1

159
Q

does MEOS have a higher Km or lower Km than ADH

A

higher Km, low affinity

160
Q

where is MEOS found

A

endoplasmic reticulum

161
Q

in alcohol metabolism what enzyme is responsible for converted acetalaldehyde to acetate

A

ALDH

162
Q

80% of ALDH is found

A

mitochondria

163
Q

what converts acetate to acetyl CoA

A

acetylCoA synthetase I liver and II in skeletal muscle

164
Q

where is morelikely for acetyl CoA to be syntheiszed from acetate

A

skeletal muscle MORE than liver

165
Q

how much energy does ADH produce per ethanol

A

13 ATP’s

166
Q

how many ATP’s per ethanol molecule is produced by the MEOS pathway

A

8 ATPS

167
Q

most of the toxic effects of alcohol are due to what

A

acetyladehyde production and NADH

168
Q

what are the four main effeccts of increasd NADH production in ethanol metabolism

A

inhibits fatty acid oxidation and promotes VLDL
ketoacidosos-not citrate synthesis
inhibits lactate dehydrogenase- decreases uric acid excretion
inhibits gluconeogenesis

169
Q

effects of accumulation of acetyladehyde

A

decreased hepatic protein synthesis

loss of protection against damage from oxidation

170
Q

methanol is a possible substrate for

A

ADH

171
Q

ADH and methanol forms

A

formaldehyde which is then converted to formate via ALDH

172
Q

what is the compound that produces methanol toxicity

A

formate

173
Q

(T/F) ethanol is both lipid and water soluble

A

True!

174
Q

How does olestra work

A

pancreatic lipase is NOT able to hydrolyze the fatty acids attached to sucrose

175
Q

when does digestion of lipids take place

A

not until the intestine

176
Q

lingual lipase is high in

A

children who drink alot of cow’s milk

177
Q

lipids are absorbed by intestinal epithelium and resynthesized to

A

triacylglycerols

178
Q

how are lipids transported

A

via chylomicrons in the lymph

179
Q

function of colipase

A

binds to fat and lipase activating pancreatic lipase

180
Q

function of esterases and phosphilipase A2

A

removes fatty acids and phosphilipids

181
Q

pancreatic lipase and colipase are secreted in response to what

A

cholectyokinin

182
Q

secretin is secreted in response to

A

HCL in the intestine and signals for bicarb secretion

183
Q

what is phospholipase A2 activated by

A

trypsin

184
Q

tryglyceride is converted to monoglyceriade and fatty acids via

A

lipase

185
Q

bile salts are synthesized where

A

liver

186
Q

what is the major component of bile salts

A

cholic aicd

187
Q

what is the rate limiting step of bile acid synthesis

A

first step of 7-alpha hydroxylase, inhibited by bile acids

188
Q

bile salts are reabsorbed where

A

illeum

189
Q

bile salts are stored where

A

gallbladder

190
Q

what type of fatty acids do not need bile salts

A

short and medium chain fatty acids

191
Q

what are packagaed into micells by bile salts

A 
fatty acids
monoacylgylcerols
cholesterol
lysophospholipids
fat soluble vitamins
192
Q

how are triacylglycerols resynthesized

A

free fatty acids are esterifired to 2 monoacyglycerol which requires 2 ATP molecules and CoA

193
Q

which apoprotein is associated with activation of lipoprotein lipase

A

apoCII

194
Q

apoB100 and abpoB 48 are related how

A

located on the same gene

195
Q

what is the major source of acetyl CoA

A

dietary glucose

196
Q

how is OAA produced from pyruvate

A

pyruvate carboxylase

197
Q

how is acetyl CoA produced from pyruvate

A

pyruvate dehydrogenase

198
Q

what has a higher percentage of triacylglycerols VLDL or chylomicrons

A

chylomicrons

199
Q

lipoprotein lipase is activated by

A

apoprotein CII

200
Q

in muscle LPL has a low or high Km

A

low

201
Q

in adipose LPL has a low or high Km

A

high

202
Q

LPL is made in response to

A

insulin

203
Q

what causes the release of fatty acids

A

insulin low, high cAMP, activates protein kinase A

204
Q

glycerol 3 phosphate reacts with two fatty acids to produce

A

phosphatidic acid

205
Q

how is phosphatidylyglycerol produced

A

condendation of CDP-DAG and G3phopshate

206
Q

how is a ceramide formed

A

serine and palmitory CoA

207
Q

how is the double bond formed in sphingolipids

A

FAD

208
Q

short chain fatty acid site of activation

A

cytosol and mitochondria

209
Q

medium chain fatty acid site of activation

A

mitochondrial matrix (kidney and liver)

210
Q

long chain fatty acid site of activation

A

ER, outer mito membrane, peroxisomal membrane

211
Q

very long chain fatty acids site of actiation

A

peroxisomes

212
Q

when beta oxidation of fatty acids is blocked where to excess FA go

A

triacylglycerol synthesis

213
Q

longchian fatty acids require what to get into the mitochondria

A

carnitine

214
Q

Sources of carnitine

A

comes from the diet, but can also be synthesized from lysinne

215
Q

beta oxidation of long chain fatty acids is inhibited by

A

malonyl CoA

216
Q

what part of beta oxidation does malonyl CoA inhibit

A

carnitine palmitory transferse I

217
Q

reaction of propionyl CoA to succinyl CoA requires

A

propioyl Coa, bicarb, ATP, biotin, and conezyme B12

218
Q

wehre does omega oxidation of fatty acids occur

A

endoplasmic reticulum

219
Q

citrate inhibits

A

PFK-1

220
Q

what are the three ketone bodies

A

acetoacetate
beta hdyrogxy butyrate
acetone

221
Q

OAA has what affect on ketone body synthesis

A

decreases synthesis

222
Q

what are the strictly ketogenic amino acids

A

leucine and lysine

223
Q

what are the ketogenic and glucogenic amino acid

A

phenyalalanine, trophophan and tyrosine

Biochemistry Fall MS1 (12 decks)

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