Carbohydrate Metabolism Flashcards

1
Q

To be a carbohydrate must have ___+ carbons

A

3

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2
Q

What is the formula for carbohydrate?

A

Cn(H2O)n

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3
Q

What are the smallest monosaccharides?

A

aldo and keto trioses (named for the placement of O double bond)

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4
Q

_____ is a epimer of glucose

A

galactose

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5
Q

what is a epimer?

A

each of two isomers with different configurations of atoms around one of several asymmetric carbon atoms present.

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6
Q

Lactose is made of what?

A

galactose and glucose (B 1,4 bond)

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7
Q

What happens to monosaccharides with greater than 5 carbons in aqueous solutions?

A

they cyclize

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8
Q

WHat is the difference between an a and b isomer?

A

A is below and B is above the plane

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9
Q

What kind of bond is on amylopectin?

A

A 1,4
A 1,6
(A 1,6 allows branching)

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10
Q

Sucrose is made of what?

A

glucose and fructose (A 1,2 bond)

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11
Q

What bond is present on a starch?

A

A 1,4

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12
Q

What enzymes break down amylopectin?

A

amylase and isomaltose

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13
Q

Why is cellulose indigestible?

A

because we do not have the enzyme needed to break down the B1,4 linkage

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14
Q

The glucose in oral dextran is derived from _____

A

sucrose (only get cavities from sucrose cause it donates its glucose for a slow growing glucose chain (streptococcal mutagens allows this))

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15
Q

What is cellulose?

A

most abundant carb in the world, indigestible

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16
Q

Humans lack the enzymes to degrade to ________ linkage

A

B 1,4 linkage

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17
Q

What are the health benefits of dietary fiber?

A

reduces risk for colon cancer, cardiovascular disease

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18
Q

What is soluble dietary fiber?

A

dissolved in water and forms a gel substance that is broken down by gut bacteria

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19
Q

What is insoluble dietary fiber?

A

does not dissolve in water, passes intact

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20
Q

What is insoluble fiber good for?

A

increases frequency of bowl movements

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21
Q

What is soluble fiber good for?

A

slows absorption, lowers glycemic index, lowers cholesterol

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22
Q

What type of carbohydrate can be taken up by the GI tract?

A

monosaccharides (bigger must be broken down)

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23
Q

where is disaccharidases found

A

brush boarder of SI

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24
Q

Salivary amylase breaks down ______ into _____

A

starch into a-dextrins (breaks the a 1,4 link)

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25
Q

_______ in the small intestine are brakes disaccharides down into _____

A

disaccarideases

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26
Q

Pancreatic amylase breaks down ____ ____ ____.

A

a- dextrin’s
trisaccharide’s

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27
Q

What do the glucose transporters of the blood transport?

A

GLUT 2
glucose, fructose, galactose

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28
Q

What are the glucose transporters in lumen? What do they transport?

A

SGLT 1 (active transport of glucose and galactose)
GLUT 5 (passive of fructose)

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29
Q

GLUTs transport goes with or against concentration gradient?

A

with

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30
Q

What transporter transports into tissues?

A

GLUT

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31
Q

SGLT transport goes with or against concentration gradient?

A

against, coupled to Na which is favorable

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32
Q

GLUT 2 receptors are found in which TISSUES?

A

liver, pancreas, small intestine
glucose sensor (Kt, which is similar to Km for glucose> blood glucose)

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33
Q

Rates of ____ transport depend on ____
_____ and _____ follows the second blank above

A

rates of glucose transport depends on Na concentration and glucose (coupled)
Chloride and water follow the Na absorbed

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34
Q

Sucrose is a _________________ for oral dextran

A

glucose donor

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35
Q

Where are glut 4 receptors found, what stimulates them?

A

in adipose, muscle, heart
directly stimulated by insulin

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36
Q

carbohydrates are polyhydroxy- _____

A

aldehydes or ketones

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37
Q

where are disaccharides broken down to monosaccharides?

A

small intestine

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38
Q

How does insulin increase glucose uptake?

A

increasing the amount of GLUT4 transporters at the cell surface

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39
Q

Insulin directly promotes________________ ______________________

A

glucose uptake by the tissues in adipose, skeletal heart muscle

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40
Q

for glycogen synthesis _____ must be converted to _____

A

G6P to G1P (by isomerase)

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41
Q

What is the structure of glycogen?

A

polymer of glucose with a 1,4 glycosidic bonds and a 1,6 bonds at branches

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42
Q

What is the difference in usage of glycogen in skeletal muscle vs liver?

A

muscle: fuel source for ATP generation in muscle itself
Liver: source of glucose for other tissues

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43
Q

What can G6P be used for

A

-glycolysis
-glycogen synthesis
-enter pentose phosphate pathway

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44
Q

What does G 1 P to UDP glucose do for glycogen synthesis?

A

donates glucose

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45
Q

What are glycogen degradation products

A

G1P and glucose

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46
Q

What does UDP glucose do?

A

donates glucose for syn of glycogen

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47
Q

What is the rate limiting step of glycogenesis?

A

glycogen synthase step (forms a a1,4 bond (cant form 1,6, branching enzyme does this))

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48
Q

What two enzymes are needed for glycogen synthesis?

A

branching enzyme
glycogen synthase (RLS)

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49
Q

What elongates the glycogenin primer?

A

glycogen synthase

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50
Q

Synthesis of glycogen requires what?

A

glycogenin primer and UTP glucose

(catalyzes the transfer of glucose from UDP-glucose to the OH group of Try194. glycogenin usually adds 7 more residues to the primer, glycogen synthase then elongates the glycogenin primer)

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51
Q

What is the rate limiting step for glycogenolysis?

A

glycogen phosphorylase

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52
Q

how does glycogen phosphorylase work?

A

usues inorganic phosphate to cleave the a1,4 bond and release G1P (major product, but CANT break a1,6 bond)

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53
Q

How is liver glycogen metabolism regulated in the muscle, in the fasting state?

A

stress and exercise favor muscle glycogenolysis
-epinephrine inhibits glycogen synthase
-Ca, AMP, epinephrine: activate glycogen phosphatase

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54
Q

How does debranching enzyme work?

A

uss H2O to cleave the a1,6 glycosidic bond and release free glucose (minor product cause not many 1,6)

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55
Q

How is liver glycogen metabolism regulated, in the liver, in the fed state?

A

INSULIN: favors glycogen synthesis,
activates glycogen synthase, inhibits glycogen phosphorylase

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56
Q

How is liver glycogen metabolism regulated in the liver, in the fasting state?

A

GLUCAGON/EPINEPRINE
favors glycogenolysis, inhibits glycogen synthase, activates glycogen phosphorylase

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57
Q

How is liver glycogen metabolism regulated in the muscle, in the FED state?

A

INSULIN: favors glycogen synthesis,
activates glycogen synthase, inhibits glycogen phosphorylase (SAME AS LIVER)

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58
Q

What are the steps of muscle glycogen phosphorylase during exercise?

A
  1. amp activates glycogen phosphatase
  2. Ca calmodulin activates phosphorylase kinase
    3.epinephrine activates cAMP/PKA; PKA activates phosphorylase kinase
    4.phospoylase kinase activates glycogen phosphorylase
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59
Q

Glycogen is the animal storage form of glucose with glucose
linked together in _____ and _____ glycosidic bonds

A

a-1,4- and a-1,6

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60
Q

Glycogen synthesis requires:

A

a primer (glycogenin), UDP-glucose, glycogen synthase (rate-limiting step) and branching enzyme.

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61
Q

Glycogenolysis products are ______ and _____.

A

glucose-1-phosphate (major) and
glucose (minor)

62
Q

the debranching enzyme uses _______ to break _____

A

water to break a-1,6-linkage

63
Q

Glycogen phosphorylase breaks _____ with _______.

A

a-1,4-linkages with a phosphate (rate limiting);

64
Q

____ and _____ increase glycogenolysis by increasing glycogen phosphorylase activity and decreasing glycogen synthase activity

A

Glucagon and epinephrine

65
Q

Liver glycogenolysis occurs in the _____ state and ______
glucose to the blood.

A

fasting, releases

66
Q

Muscle glycogenolysis provides glucose for glycolysis and is
stimulated by _____, ______, and _____

A

epinephrine, increases in AMP and Ca 2+.

67
Q

what can happen if blood glucose gets too high?

A

coma, dehydration of brain cells

68
Q

______ promotes glycogen synthesis in liver and muscle by
increasing glycogen synthase acctivity and decreasing glycogen
phosphorylase activity.

A

insulin

69
Q

What are some physiological effects of low glucose?

A

low- sweating/trembling
very low- convulsions/coma
extremely low- brain damage/death

70
Q

increased levels of glucagon and epinephrine in the blood favors increase of which processes?

A

glycogenolysis, gluconeogenesis and lipolysis

71
Q

Glucagon and epinephrine increase glycogenolysis by

A

increasing glycogen phosphorylase activity and
decreasing glycogen synthase activity

72
Q

what are two precursors for pyruvate?

A

lactate and alanine

73
Q

what are the steps of fuel metabolism in the fasting state? (theres 4)

A
  1. Liver glycogenolysis and gluconeogenesis release glucose to the blood.
  2. Fatty acids from adipose are utilized as fuel in liver and muscle
  3. Glycerol from triglycerides provide carbon skeleton for liver gluconeogenesis.
  4. Amino acids from muscle provide carbon skeleton for liver gluconeogenesis.
74
Q

____ ____ ___ from muscle are quantitatively the most important precursors

A

Glucogenic amino acids

75
Q

What are four major gluconeogenic precursors? Ei carbon sources

A

lactate, alanine, glucogenic amino acids and glycerol

76
Q

Can acetyl CoA be converted to glucose?

A

NO, so fat is not a carbon source for gluconeogenesis

77
Q

What is reciprocal regulation in the liver?

A
  1. When glycolysis is increased, gluconeogenesis is decreased.
  2. When gluconeogenesis is increased, glycolysis is decreased
78
Q

What enzymes that are unique to glycolysis?

A
  1. hexokinase (liver), glucokinase (pancreas)
    2.PFK1
  2. pyruvate kinase
79
Q

What unique enzymes are needed for gluconeogenesis to convert pyruvate to phosphonyl pyruvate?

A

–Pyruvate Carboxylase
–Phosphoenolpyruvate Carboxykinase (PEPCK)

80
Q

What unique enzymes are needed for gluconeogenesis to go from fructose 1,6 bp to F6P?

A

Fructose-1,6-bisphosphatase (F-1,6-BPase)

81
Q

Conversion of PEP requires ____, ____, and _____.

A

pyruvate carboxylase, PEPCK, 2 ATP

82
Q

Fructose-2,6-Bisphosphate Reciprocally regulates _______ and ________

A

Regulates glycolysis and gluconeogenesis

83
Q

What unique enzymes are needed for gluconeogenesis to go from glucose 6 phosphate to glucose?

A

Glucose-6-phosphatase (liver only)

84
Q

In the liver Insulin stimulates PFK2 to produce

A

F-2,6-BP

85
Q

In the liver glucagon and epinephrine inhibit

A

F-2,6-BP formation and stimulate its breakdown

86
Q

In the liver in glycolysis cAMP/PKA (liver) Inhibits

A

Pyruvate Kinase

87
Q

Insulin in the liver increases expression of ______

A

glucokinase

88
Q

During gluconeogenesis in the liver Acetyl CoA activates?

A

Pyruvate Carboxylase

89
Q

During glycolysis in the liver F26BP inactivates? Activates what in gouconeogenesis?

A

PFK1;
Inhibits F16BPase

90
Q

Epinephrine, Glucagon, (Cortisol)
increase expression of

A
  • Glucose-6-phosphatase
  • Fructose-1,6-bisphosphatase
  • PEPCK
91
Q

Glycolysis is favored in the fed
state with elevated:

A
  • Blood glucose
  • Blood insulin
  • Liver F26BP
  • AMP
92
Q

Gluconeogenesis is
favored in the fasting
state with decreased:

A
  • Blood glucose
  • Blood insulin
  • Liver F26BP
  • AMP
93
Q

_____ and ___ are the only tissues with glucagon receptors

A

liver and adipose

94
Q

What are the steps of metabolism in the fed state?

A
  1. Increased insulin relative to glucagon.
  2. Insulin stimulates glycolysis in all tissues.
  3. Insulin directly stimulates glucose uptake in adipose and muscle.
  4. Increased FA and TG synthesis in liver.
  5. Increased TG lipolysis on VLDLs, chylomicrons.
    * Increased FA uptake and TG synthesis in adipose.
  6. Increased AA uptake and protein synthesis.
95
Q

What happens during metabolism in the starved state?

A
  1. ↑ ketone bodies promote uptake & utilization in brain
  2. ↓ AA degradation ↓ urea production
  3. Gluconeogenesis
    for RBC, neurotransmitters
96
Q

What happens during metabolism after 12 hours in the fasting state?

A
  1. Increased glucagon.
  2. Liver glycogen diminished.
  3. Gluconeogenesis main source of glucose.
  4. Increased lipolysis yields fatty acids and glycerol.
  5. Increased FA oxidation provides energy for gluconeogenesis
  6. Increased FA utilization, decreased glucose uptake in muscle.
  7. Protein degradation yields glucogenic AA precursors.
  8. Increased urea production and excretion.
97
Q

What changes in blood fuels occur during starving

A
  1. Fasting State (<24hrs)
    Urinary nitrogen high due
    to high gluconeogenesis.
  2. Fasting State (<24hrs)
    Free fatty acids increase
    due to lipolysis of adipose.
  3. Starvation (≥3days)
    Increased ketone bodies (alternate fuel for brain)
  4. Starvation (≥3days)
    Decreased urinary nitrogen, decreased
    gluconeogenesis, protein conservation.
98
Q

Insulin increases _____; Glucagon, epinephrine, decrease _____.

A

F26BP, F26BP

99
Q

F26BP increases _______ and decreases _______

A

glycolysis, gluconeogenesis

100
Q

Summary: Fed State: Increased Insulin/Glucagon (Insulin relative to Glucagon), increases what?

A

– Increased glucose utilization (glycolysis)
– Increased synthesis of biomolecules & fuels (glycogen, fat, protein)

101
Q

Fasting State: Decreased Insulin/Glucagon, Increased Stress Hormones (epinephrine, cortisol) changes what?
– _________ glucose uptake (adipose, muscle)
– _______ glucose utilization (liver)
– _________ mobilization of fuels (glucose output liver, lipolysis, protein degradation/release of amino acids)

A

decreased, decreased, increased,

102
Q

Starved State:
– ________ protein degradation to protect organs (decreased urinary nitrogen)
– Gluconeogenesis is _____, but still occurs.
– _______ reliance on fatty acids by most tissues and ketone bodies by the CNS

A

decreased, reduced, increased

103
Q

In the pentose phosphate pathway the oxidative step is:

A

is irreversible and generates: NADPH, ribulose- 5-phosphate and CO 2
(glucose is oxidized NO ATP made)

104
Q

In the pentose phosphate pathway the non-oxidative step is:

A

is reversible and converts 5 carbon sugars such as ribose-5-phosphate to fructose-6-phosphate.

105
Q

Tissues that are doing PPP are active in tissues that are

A

– rapidly growing (bone marrow, skin, intestinal mucosa, cancerous cells)
– actively synthesizing fatty acids, cholesterol or steroids (liver, lactating mammary gland, adrenal gland, gonads)
– Exposed to O2 (red blood cells, cells of the lens and cornea)

106
Q

Entry into the PPP is determined by the ratio of

A

NADP+/NADPH

107
Q
  1. PPP: Oxidative Phase (irreversible), what is the rate limiting step? What are the products?
A
  1. Glucose-6-phosphate
    dehydrogenase catalyzes the rate-limiting step; generates 1 st NADPH
  2. Products of the oxidative phase: 2 NADPH, ribulose-5-phosphate, CO2 .
108
Q

What are the functions of NADPH from a synthesis standpoint?

A
  • Fatty acid synthesis
  • Cholesterol synthesis
  • Steroid synthesis
  • Nucleotide synthesis
109
Q

What does NADPH do for detoxification?

A

–Reduction of oxidized gluthathione. (Scavenges ROS)
–Cytochrome P450 monooxygenase

110
Q

What is the starting material for the non-oxidative phase PPP?

A

Ribose-5-phosphate

111
Q

What helps protect cells from ROS?

A

reduced glutathione

112
Q

What is the products of the non- oxidative phase of PPP?

A

glyeraldehyide-3-phosphate
fructose-6-phosphate

113
Q

What do you need to regenerate reduced glutathione (GSH)?

A

NADPH

114
Q

Glutathione is reduced when ____ is reduced

A

cysteine (GSH is a tripeptide containing system)

115
Q

When are ROS made?

A

When O2 interacts with substances that give up e-

116
Q

Is the PPP used to produce ATP?

A

no

117
Q

What are the two enzymes needed for the non-oxidative phase of PPP?

A

transketolase (required thiamine)
transaldolase

118
Q

What part of the NADP allows the reducing?

A

Nicotinamide (this pics up the electrons

119
Q

What is the difference between NADH/NAD+ and NADP+/NADPH? Metabolism wise

A

NADH/NAD+ : catabolism
NADPH/NADP+ : anabolism

120
Q

What does NADPH do for phagocytosis?

A

creates ROS (purposefully makes ROS to kill/git rid of bacteria)

121
Q

When would you want to use the non-oxidative pathway for PPP?

A

cells where you are doing reductive biotsyn, need NADPH but not ribose so you want to bring it back to intermediates of glycolysis to be used there

122
Q

The PPP provides the _____ needed to ______ glutathione

A

NADPH, reduce

123
Q

What rate limiting enzyme of the PPP produces NADPH?

A

G6P dehydrogenase

124
Q

IF NADPH is being consumed, what happens to G6P dehydrogenase?

A

it speeds up/works faster to regenerate the NADPH

125
Q

What happens if you have a G6P dehydrogenase deficiency?

A

Inability to produce enough NADPH to get rid of ROS causes hemolysis of RBC.

(one of the most common inherited diseases, malaria do not grow well without it)

126
Q

When would someone present symptoms of G6PD deficiently?

A

during oxidative stress like an antimalarial drug, infection or fava bean ingestion

127
Q

What are the most important pathways of carbohydrate metabolism in erythrocytes?

A

glycolysis, PPP and generation of 2,3BPG

128
Q

How do RBS do glycolysis?

A

substrate level phosphorylation for maintenance of ion pumps

129
Q

What do ROS do to RBC?

A

cause lipid peroxidation and leaky membranes leading to hemolysis

130
Q

Why do rBS generate ROS?

A

because of the iron in the heme of hemoglobin (NADPH produced in the RBC through PPP to scavenge the ROS, if this didnt happen the cell will lyse)

131
Q

What is a respiratory burst in phagocytes?

A

in response to an infectious agent phagocytes rapidly consume O2 to produce ROS to aid in killing the invading pathogen

132
Q

What enzyme causes the respiratory burst?

A

NADPH oxidase

133
Q

UDP-glucose is a _____ donor

A

glucose (high energy bond favors donation)

134
Q

UDP-glucoronate is important for _______

A

drug detoxification and excretion of bilirubin

135
Q

what are the functions of UTP-Glucose?

A

epimerized to udp-galactose
oxidized to a sugar acid
used to make proteoglycans, glycoproteins and glycolipids

136
Q

UDP-glucuronate can donate
________ to other –OH
containing compounds to
form ________.

A

glucuronic acid
glucuronide

137
Q

The _________ ______carboxyl
group increases water solubility of
non-polar compounds which can
be excreted in the urine or bile

A

negatively charged

138
Q

Glucuronides are important for:

A

Are important in the metabolism of bilirubin, drug detoxification and steroid excretion.

139
Q

How can galactose enter the glycolytic pathway?

A

it can be concerted to udp-galactose or g6p

140
Q

Fructose metabolism primary happens where?

A

liver

141
Q

What is the key thing she wants you to know about galactose metabolism?

A

it can be phosphorated, udp glucose can make it g1p and udp-galactose and become utp-glucose. g1p which can entry glycolytic pathway

142
Q

how can fructose enter the glycolytic pathway

A

after pfk as DHAP + gly3p

143
Q

What are the steps of galactose metabolism?

A

1- enters cell becomes Galactose-1-phos
2- reacts with utp glucose to form glucose 1-p and udp galactose
3: UDP galactose epimerized to utp galactose (DONT NEED TO KNOW THIS DETAIL??)
4: glucose 1- phos can enter glycolysis or other metabolic routes for glucose

144
Q

what is the kinase needed for fructose metabolism?

A

fructokinase, (fructose gets phosphate much faster than glucose)

145
Q

What special step can fructose bypass?

A

PFK1, instead aldolase B converts from F1P to glyceraldehyde and DHAP

146
Q

Due to the bypassing of PFK1 what effect happens?

A

there is no ATP feedback mechanism, if you have an extremely high fructose diet there is no control to stop the process

147
Q

Because fructose bypasses PFK 1, high levels of fructose in the body can cause what?

A

High levels of fructose can lead to liver damage, lactic acidosis
and fatty acid synthesis in the liver (too much citrate build up makes a lot of fatty acids which causes the fatty liver)

148
Q

What is the polyol pathway?

A

pathway used to synthesize fructose

149
Q

What is the first step of the polyol pathway?

A

sugars are reduced to sugar alcohol by aldose reductase NADPH IS CONSUMED

150
Q

Why is sorbitol dangerous?

A

it builds up in the cells

151
Q

What health effects can occur from build up of sugar alcohols?

A

Buildup of the sugar alcohol
and consumption of NADPH in
the lens, nerve and glomerulus
in diabetics may contribute to
tissue damage.

152
Q

To make sorbitol there is consumption of NADPH, what is dangerous about over production of sorbitol?

A

it can cause depletion of NADPH which would cause an accumulation of ROS