Carbohydrate Metabolism Flashcards
1
Q
To be a carbohydrate must have ___+ carbons
A
3
2
Q
What is the formula for carbohydrate?
A
Cn(H2O)n
3
Q
What are the smallest monosaccharides?
A
aldo and keto trioses (named for the placement of O double bond)
4
Q
_____ is a epimer of glucose
A
galactose
5
Q
what is a epimer?
A
each of two isomers with different configurations of atoms around one of several asymmetric carbon atoms present.
6
Q
Lactose is made of what?
A
galactose and glucose (B 1,4 bond)
7
Q
What happens to monosaccharides with greater than 5 carbons in aqueous solutions?
A
they cyclize
8
Q
WHat is the difference between an a and b isomer?
A
A is below and B is above the plane
9
Q
What kind of bond is on amylopectin?
A
A 1,4
A 1,6
(A 1,6 allows branching)
10
Q
Sucrose is made of what?
A
glucose and fructose (A 1,2 bond)
11
Q
What bond is present on a starch?
A
A 1,4
12
Q
What enzymes break down amylopectin?
A
amylase and isomaltose
13
Q
Why is cellulose indigestible?
A
because we do not have the enzyme needed to break down the B1,4 linkage
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))
15
Q
What is cellulose?
A
most abundant carb in the world, indigestible
16
Q
Humans lack the enzymes to degrade to ________ linkage
A
B 1,4 linkage
17
Q
What are the health benefits of dietary fiber?
A
reduces risk for colon cancer, cardiovascular disease
18
Q
What is soluble dietary fiber?
A
dissolved in water and forms a gel substance that is broken down by gut bacteria
19
Q
What is insoluble dietary fiber?
A
does not dissolve in water, passes intact
20
Q
What is insoluble fiber good for?
A
increases frequency of bowl movements
21
Q
What is soluble fiber good for?
A
slows absorption, lowers glycemic index, lowers cholesterol
22
Q
What type of carbohydrate can be taken up by the GI tract?
A
monosaccharides (bigger must be broken down)
23
Q
where is disaccharidases found
A
brush boarder of SI
24
Q
Salivary amylase breaks down ______ into _____
A
starch into a-dextrins (breaks the a 1,4 link)
25
_______ in the small intestine are brakes disaccharides down into _____
disaccarideases
26
Pancreatic amylase breaks down ____ ____ ____.
a- dextrin's
trisaccharide's
27
What do the glucose transporters of the blood transport?
GLUT 2
glucose, fructose, galactose
28
What are the glucose transporters in lumen? What do they transport?
SGLT 1 (active transport of glucose and galactose)
GLUT 5 (passive of fructose)
29
GLUTs transport goes with or against concentration gradient?
with
30
What transporter transports into tissues?
GLUT
31
SGLT transport goes with or against concentration gradient?
against, coupled to Na which is favorable
32
GLUT 2 receptors are found in which TISSUES?
liver, pancreas, small intestine
glucose sensor (Kt, which is similar to Km for glucose> blood glucose)
33
Rates of ____ transport depend on ____
_____ and _____ follows the second blank above
rates of glucose transport depends on Na concentration and glucose (coupled)
Chloride and water follow the Na absorbed
34
Sucrose is a _________________ for oral dextran
glucose donor
35
Where are glut 4 receptors found, what stimulates them?
in adipose, muscle, heart
directly stimulated by insulin
36
carbohydrates are polyhydroxy- _____
aldehydes or ketones
37
where are disaccharides broken down to monosaccharides?
small intestine
38
How does insulin increase glucose uptake?
increasing the amount of GLUT4 transporters at the cell surface
39
Insulin directly promotes________________ ______________________
glucose uptake by the tissues in adipose, skeletal heart muscle
40
for glycogen synthesis _____ must be converted to _____
G6P to G1P (by isomerase)
41
What is the structure of glycogen?
polymer of glucose with a 1,4 glycosidic bonds and a 1,6 bonds at branches
42
What is the difference in usage of glycogen in skeletal muscle vs liver?
muscle: fuel source for ATP generation in muscle itself
Liver: source of glucose for other tissues
43
What can G6P be used for
-glycolysis
-glycogen synthesis
-enter pentose phosphate pathway
44
What does G 1 P to UDP glucose do for glycogen synthesis?
donates glucose
45
What are glycogen degradation products
G1P and glucose
46
What does UDP glucose do?
donates glucose for syn of glycogen
47
What is the rate limiting step of glycogenesis?
glycogen synthase step (forms a a1,4 bond (cant form 1,6, branching enzyme does this))
48
What two enzymes are needed for glycogen synthesis?
branching enzyme
glycogen synthase (RLS)
49
What elongates the glycogenin primer?
glycogen synthase
50
Synthesis of glycogen requires what?
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)
51
What is the rate limiting step for glycogenolysis?
glycogen phosphorylase
52
how does glycogen phosphorylase work?
usues inorganic phosphate to cleave the a1,4 bond and release G1P (major product, but CANT break a1,6 bond)
53
How is liver glycogen metabolism regulated in the muscle, in the fasting state?
stress and exercise favor muscle glycogenolysis
-epinephrine inhibits glycogen synthase
-Ca, AMP, epinephrine: activate glycogen phosphatase
54
How does debranching enzyme work?
uss H2O to cleave the a1,6 glycosidic bond and release free glucose (minor product cause not many 1,6)
55
How is liver glycogen metabolism regulated, in the liver, in the fed state?
INSULIN: favors glycogen synthesis,
activates glycogen synthase, inhibits glycogen phosphorylase
56
How is liver glycogen metabolism regulated in the liver, in the fasting state?
GLUCAGON/EPINEPRINE
favors glycogenolysis, inhibits glycogen synthase, activates glycogen phosphorylase
57
How is liver glycogen metabolism regulated in the muscle, in the FED state?
INSULIN: favors glycogen synthesis,
activates glycogen synthase, inhibits glycogen phosphorylase (SAME AS LIVER)
58
What are the steps of muscle glycogen phosphorylase during exercise?
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
59
Glycogen is the animal storage form of glucose with glucose
linked together in _____ and _____ glycosidic bonds
a-1,4- and a-1,6
60
Glycogen synthesis requires:
a primer (glycogenin), UDP-glucose, glycogen synthase (rate-limiting step) and branching enzyme.
61
Glycogenolysis products are ______ and _____.
glucose-1-phosphate (major) and
glucose (minor)
62
the debranching enzyme uses _______ to break _____
water to break a-1,6-linkage
63
Glycogen phosphorylase breaks _____ with _______.
a-1,4-linkages with a phosphate (rate limiting);
64
____ and _____ increase glycogenolysis by increasing glycogen phosphorylase activity and decreasing glycogen synthase activity
Glucagon and epinephrine
65
Liver glycogenolysis occurs in the _____ state and ______
glucose to the blood.
fasting, releases
66
Muscle glycogenolysis provides glucose for glycolysis and is
stimulated by _____, ______, and _____
epinephrine, increases in AMP and Ca 2+.
67
what can happen if blood glucose gets too high?
coma, dehydration of brain cells
68
______ promotes glycogen synthesis in liver and muscle by
increasing glycogen synthase acctivity and decreasing glycogen
phosphorylase activity.
insulin
69
What are some physiological effects of low glucose?
low- sweating/trembling
very low- convulsions/coma
extremely low- brain damage/death
70
increased levels of glucagon and epinephrine in the blood favors increase of which processes?
glycogenolysis, gluconeogenesis and lipolysis
71
Glucagon and epinephrine increase glycogenolysis by
increasing glycogen phosphorylase activity and
decreasing glycogen synthase activity
72
what are two precursors for pyruvate?
lactate and alanine
73
what are the steps of fuel metabolism in the fasting state? (theres 4)
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
____ ____ ___ from muscle are quantitatively the most important precursors
Glucogenic amino acids
75
What are four major gluconeogenic precursors? Ei carbon sources
lactate, alanine, glucogenic amino acids and glycerol
76
Can acetyl CoA be converted to glucose?
NO, so fat is not a carbon source for gluconeogenesis
77
What is reciprocal regulation in the liver?
1. When glycolysis is increased, gluconeogenesis is decreased.
2. When gluconeogenesis is increased, glycolysis is decreased
78
What enzymes that are unique to glycolysis?
1. hexokinase (liver), glucokinase (pancreas)
2.PFK1
3. pyruvate kinase
79
What unique enzymes are needed for gluconeogenesis to convert pyruvate to phosphonyl pyruvate?
--Pyruvate Carboxylase
--Phosphoenolpyruvate Carboxykinase (PEPCK)
80
What unique enzymes are needed for gluconeogenesis to go from fructose 1,6 bp to F6P?
Fructose-1,6-bisphosphatase (F-1,6-BPase)
81
Conversion of PEP requires ____, ____, and _____.
pyruvate carboxylase, PEPCK, 2 ATP
82
Fructose-2,6-Bisphosphate Reciprocally regulates _______ and ________
Regulates glycolysis and gluconeogenesis
83
What unique enzymes are needed for gluconeogenesis to go from glucose 6 phosphate to glucose?
Glucose-6-phosphatase (liver only)
84
In the liver Insulin stimulates PFK2 to produce
F-2,6-BP
85
In the liver glucagon and epinephrine inhibit
F-2,6-BP formation and stimulate its breakdown
86
In the liver in glycolysis cAMP/PKA (liver) Inhibits
Pyruvate Kinase
87
Insulin in the liver increases expression of ______
glucokinase
88
During gluconeogenesis in the liver Acetyl CoA activates?
Pyruvate Carboxylase
89
During glycolysis in the liver F26BP inactivates? Activates what in gouconeogenesis?
PFK1;
Inhibits F16BPase
90
Epinephrine, Glucagon, (Cortisol)
increase expression of
* Glucose-6-phosphatase
* Fructose-1,6-bisphosphatase
* PEPCK
91
Glycolysis is favored in the fed
state with elevated:
* Blood glucose
* Blood insulin
* Liver F26BP
* AMP
92
Gluconeogenesis is
favored in the fasting
state with decreased:
* Blood glucose
* Blood insulin
* Liver F26BP
* AMP
93
_____ and ___ are the only tissues with glucagon receptors
liver and adipose
94
What are the steps of metabolism in the fed state?
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
What happens during metabolism in the starved state?
1. ↑ ketone bodies promote uptake & utilization in brain
2. ↓ AA degradation ↓ urea production
3. Gluconeogenesis
for RBC, neurotransmitters
96
What happens during metabolism after 12 hours in the fasting state?
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
What changes in blood fuels occur during starving
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
Insulin increases _____; Glucagon, epinephrine, decrease _____.
F26BP, F26BP
99
F26BP increases _______ and decreases _______
glycolysis, gluconeogenesis
100
Summary: Fed State: Increased Insulin/Glucagon (Insulin relative to Glucagon), increases what?
– Increased glucose utilization (glycolysis)
– Increased synthesis of biomolecules & fuels (glycogen, fat, protein)
101
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)
decreased, decreased, increased,
102
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
decreased, reduced, increased
103
In the pentose phosphate pathway the oxidative step is:
is irreversible and generates: NADPH, ribulose- 5-phosphate and CO 2
(glucose is oxidized NO ATP made)
104
In the pentose phosphate pathway the non-oxidative step is:
is reversible and converts 5 carbon sugars such as ribose-5-phosphate to fructose-6-phosphate.
105
Tissues that are doing PPP are active in tissues that are
– 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
Entry into the PPP is determined by the ratio of
NADP+/NADPH
107
1. PPP: Oxidative Phase (irreversible), what is the rate limiting step? What are the products?
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
What are the functions of NADPH from a synthesis standpoint?
* Fatty acid synthesis
* Cholesterol synthesis
* Steroid synthesis
* Nucleotide synthesis
109
What does NADPH do for detoxification?
--Reduction of oxidized gluthathione. (Scavenges ROS)
--Cytochrome P450 monooxygenase
110
What is the starting material for the non-oxidative phase PPP?
Ribose-5-phosphate
111
What helps protect cells from ROS?
reduced glutathione
112
What is the products of the non- oxidative phase of PPP?
glyeraldehyide-3-phosphate
fructose-6-phosphate
113
What do you need to regenerate reduced glutathione (GSH)?
NADPH
114
Glutathione is reduced when ____ is reduced
cysteine (GSH is a tripeptide containing system)
115
When are ROS made?
When O2 interacts with substances that give up e-
116
Is the PPP used to produce ATP?
no
117
What are the two enzymes needed for the non-oxidative phase of PPP?
transketolase (required thiamine)
transaldolase
118
What part of the NADP allows the reducing?
Nicotinamide (this pics up the electrons
119
What is the difference between NADH/NAD+ and NADP+/NADPH? Metabolism wise
NADH/NAD+ : catabolism
NADPH/NADP+ : anabolism
120
What does NADPH do for phagocytosis?
creates ROS (purposefully makes ROS to kill/git rid of bacteria)
121
When would you want to use the non-oxidative pathway for PPP?
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
The PPP provides the _____ needed to ______ glutathione
NADPH, reduce
123
What rate limiting enzyme of the PPP produces NADPH?
G6P dehydrogenase
124
IF NADPH is being consumed, what happens to G6P dehydrogenase?
it speeds up/works faster to regenerate the NADPH
125
What happens if you have a G6P dehydrogenase deficiency?
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
When would someone present symptoms of G6PD deficiently?
during oxidative stress like an antimalarial drug, infection or fava bean ingestion
127
What are the most important pathways of carbohydrate metabolism in erythrocytes?
glycolysis, PPP and generation of 2,3BPG
128
How do RBS do glycolysis?
substrate level phosphorylation for maintenance of ion pumps
129
What do ROS do to RBC?
cause lipid peroxidation and leaky membranes leading to hemolysis
130
Why do rBS generate ROS?
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
What is a respiratory burst in phagocytes?
in response to an infectious agent phagocytes rapidly consume O2 to produce ROS to aid in killing the invading pathogen
132
What enzyme causes the respiratory burst?
NADPH oxidase
133
UDP-glucose is a _____ donor
glucose (high energy bond favors donation)
134
UDP-glucoronate is important for _______
drug detoxification and excretion of bilirubin
135
what are the functions of UTP-Glucose?
epimerized to udp-galactose
oxidized to a sugar acid
used to make proteoglycans, glycoproteins and glycolipids
136
UDP-glucuronate can donate
________ to other –OH
containing compounds to
form ________.
glucuronic acid
glucuronide
137
The _________ ______carboxyl
group increases water solubility of
non-polar compounds which can
be excreted in the urine or bile
negatively charged
138
Glucuronides are important for:
Are important in the metabolism of bilirubin, drug detoxification and steroid excretion.
139
How can galactose enter the glycolytic pathway?
it can be concerted to udp-galactose or g6p
140
Fructose metabolism primary happens where?
liver
141
What is the key thing she wants you to know about galactose metabolism?
it can be phosphorated, udp glucose can make it g1p and udp-galactose and become utp-glucose. g1p which can entry glycolytic pathway
142
how can fructose enter the glycolytic pathway
after pfk as DHAP + gly3p
143
What are the steps of galactose metabolism?
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
what is the kinase needed for fructose metabolism?
fructokinase, (fructose gets phosphate much faster than glucose)
145
What special step can fructose bypass?
PFK1, instead aldolase B converts from F1P to glyceraldehyde and DHAP
146
Due to the bypassing of PFK1 what effect happens?
there is no ATP feedback mechanism, if you have an extremely high fructose diet there is no control to stop the process
147
Because fructose bypasses PFK 1, high levels of fructose in the body can cause what?
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
What is the polyol pathway?
pathway used to synthesize fructose
149
What is the first step of the polyol pathway?
sugars are reduced to sugar alcohol by aldose reductase NADPH IS CONSUMED
150
Why is sorbitol dangerous?
it builds up in the cells
151
What health effects can occur from build up of sugar alcohols?
Buildup of the sugar alcohol
and consumption of NADPH in
the lens, nerve and glomerulus
in diabetics may contribute to
tissue damage.
152
To make sorbitol there is consumption of NADPH, what is dangerous about over production of sorbitol?
it can cause depletion of NADPH which would cause an accumulation of ROS
