Carbohydrates: Digestion/absorption Flashcards

(136 cards)

1
Q

Oligosaccharide aka

A

Disaccharide

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2
Q

Monosaccharides in Oligosaccharide vs polysaccharide

A

O = 2-20
P = more than 20

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3
Q

Glycoconjugates =

A

Linked to proteins or lipids

Glycoprotein
Or
Glycolipids

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4
Q

Glycoproteins =

A

More protein than sugar

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5
Q

Proteoglycans =

A

More sugar than protein

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6
Q

Where are glycoproteins bound

A

Membrane

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7
Q

Examples of proteoglycans

A

Mucins (mucus)

Lectins (cell to cell interactions)

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8
Q

Glycolipids example

A

Blood types

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9
Q

Trioses are ____ and examples are _______

A

The smallest sugars

Aldose and Ketose

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10
Q

Basic idea of enantiomers

A

Mirror images of one another
Connecting 4 different groups off the main carbon
the main carbon is called the chiral carbon

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11
Q

Most monosaccharides are in _ form

A

D

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12
Q

The most oxidized carbon in aldose and ketose

A

A = C1

K = C2

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13
Q

Which is more common, pentoses or hexoses

A

Hexoses

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14
Q

_______ are _____ that have the _______ molecular formula but _______

A

Isomers

Molecules

Same

Different arrangements of atoms

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15
Q

Interconverted just rotating a group on a single bond ______

A

Conformational isomers

α vs β

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16
Q

To make a disaccharide you take a _____ and a ____

A

α glucose

β glucose

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17
Q

When you make a disaccharide what is the product

A

H2O

Two glucose molecules connected by glycosidic bond

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18
Q

Disaccharide has what kind of ends and their characteristics

A

reducing end = 1 carbon next to 1 oxygen

NonReducing end = 1 carbon next 1 carbon

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19
Q

Amylose and amylopectin are examples of

A

Polysaccharides

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20
Q

Common polysaccharides

A

Cellulose

Starch = amylose, amylopectin

Glycogen

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21
Q

Sources of common polysaccharides

A

Cellulose = plants

Starch = plants

Glycogen = animals

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22
Q

Subunits of common polysaccharides

A

Cellulose = β-glucose

Starch and glycogen = α-glucose

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23
Q

Branches and shapes of common polysaccharides

A

Cellulose = no branches, parallel lines

Starches
amylose = no branches, top of hostess cupcakes
amylopectin = yes branches, 20ish subunits

Glycogen = yes branches, 10ish subunits

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24
Q

Amylose vs amylopectin bonds logic

A

Amylose shape is hostess cupcake, pretty basic so only 1-4 bonds

Amylopectin is branching so needs more variety, so 1-4, and 1-6

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25
Starch and glycogen RE vs NRE
Only 1 RE TONS of NRE going every which way!
26
How are cellulose fibrils connected
Hydrogen bonds
27
We cannot ______ carbs so we _______
Absorb long polymer Use glycosidases to Hydrolyze/break them down
28
What breaks down carbs in mouth And what does it break
α-amylase Cleaves 1-4
29
α-amylase creates
α-dextrins which have a lot of α 1,6 glycosidic bonds
30
When you hear 1,6 think
Branching!!!
31
What does our stomach acid do to α-amylase
Inactivates it
32
____ releases _____ into the duodenum to ______
Pancreas HCO3- (bicarbonate) Neutralize it
33
Why do we want to neutralize the duodenum
So enzymes can be functional again
34
What is secreted in duodenum from pancreas
Bicarb and α-amylase
35
What is formed in small intestine due to cleavages
Maltose(disaccharide), isomaltose, maltotriose
36
When and where do sucrose and lactose get acted on
When they contact the brush border in the intestines
37
Bacteria in colon can do what and what do they get in return
Breakdown small sugars They get energy in return
38
______ cleaves sucrose to ______
Sucrase Glucose and fructose
39
_____ cleaves lactose to ____
Lactase Glucose and galactose
40
When bacteria breakdown sugars what do they form
Gases and short chain FA FA are what is used for energy
41
GLUT 1-4 are
Glucose facilitated
42
GLUT 5 is
Fructose facilitated
43
Which GLUT is insulin dependent
4
44
Where are all the GLUTs located
1 = most tissues 2 = liver, kidney, pancreatic β 3 = brain, placenta, fetal muscle 4 = skeletal/heart muscle, adipocytes 5 = small intestine
45
Which GLUT affects vmax
4
46
Cellulose in our diet goes out as
Fiber
47
GLUT 1 has a _____ km which means
Low Takes glucose up readily
48
SGLT1 is ____ and needs ______and needs _____ to regulate sodium
Sodium glucose transporter Sodium needs to come in with glucose Na+/k+ ATPase
49
Why is GLUT2 not in intestines
Because it has a HIGH km and has a hard time brining in glucose
50
Where are SGLT1 and what do they do there
In kidney cells For glucose reabsorption
51
SGLT1 transport glucose from ____ to ______ in
Lumen Capillaries Kidneys
52
The ___ of a transporter is inversely proportional to its affinity to its ____
KM Substrte
53
GLUT 1 and 3 are really bad at what and why
Removing glucose from the blood quickly Because they have a low KM, the slope change is minimal
54
What is significant about GLUT2 and its location
Liver, kidney, pancreatic β It removes glucose from the blood quickly when the concentration is high it is proportional to extracellular glucose concentration
55
Where are GLUT4 and what makes them move to where
Muscle and adipose INTRACELLULAR vesicles Insulin moves them to the outside of the cell onto the plasma membrane So they can pump sugar into muscles
56
What 3 steps of glycolysis are regulated
Step 1 = hexokinase/glucokinase Step 3 = phosphofructokinase 1 Step 10 = pyruvate kinase
57
What are the two phases of glycolysis
I = energy investment/energy input II = energy generation/energy output
58
Which steps are ATP consuming and irreversible
1: glucose —hexokinase—->G6P 3: F6P ——phosphofructokinase1—->F16BP
59
G6P is a _____ to hexokinase
Allosteric inhibitor Negative feedback
60
Which carbons get phosphates added to them at step 1
Carbon 6 gets a phosphate
61
Which carbons get a phosphate added to them at step 3
Carbon 1 gets a phosphate added
62
What inhibits step 3 and why
ATP inhibits step 3 because its saying “HEY we have a TON of ATP so stop making them” Citrate also inhibits step 3 because its saying “HEY our citrate levels are HIGH, so our TCA cycle is well and full. Don’t make any more pyruvate please”
63
How does citrate inhibit PFK1 since the TCA is in mitochondria
It leaks out to cytosol
64
What do AMP and ADP signal in the energy investment phase of glycolysis and why
They tell PFK1 to rev up!!! Cuz they are the products when ATP get used. So they say we have low levels of ATP
65
______ cleaves F16BP into ______ and _____
Aldose - big al G3P - glacier aldehyde DHAP - don’t handle apparatus please
66
Which two products of Aldolase wants to look more like the other
DHAP wants to look like G3P
67
Before step 10 of glycolysis what is our ATP status
We’ve used 2 ATP and we’ve made 2 ATP So net = 0
68
What steps are ATP generating and irreversible
Step 10
69
What inhibits pyruvate kinase
ATP And Acetyl CoA
70
What does acetyl CoA indicate for glycolysis
That we have enough energy and it can cool its jets
71
What activates pyruvate kinase
F16BP
72
What does substrate level phosphorylation mean?
ATP is made without using ETC and ATP synthase
73
Which is favored between 1,3BPG or 3PG
3PG
74
During glycolysis _____ are generated from _____ glucose molecule through ______
2 net ATP Each Subrtrate level phosophrylation
75
What doesn’t glycolysis use and what does that make it
Doesn’t us O2 ANAEROBIC
76
Which enzyme/step commits glucose to glycolysis
PFK-1 Step 3
77
How is glucose kept in a cell and how does it work
By Hexokinase or glucokinase turning it into G6P G6P cannot cross plasma membrane easily
78
Hexokinase exists _____ and is inhibited by ____
In most tissues G6P
79
Glucokinase exists in ____ and is inhibited by ____
Liver/pancreatic β cells F6P
80
Hexokinase has a ____ km and that makes it _____
Low Constitutive. Very efficient
81
What do high concentrations of G6P tell hexokinase
“Hey we have plenty of glucose for energy rn, don’t bring any more in from the blood”
82
Glucokinase has a ____ km and that makes it
High Inducible. Which means it will only be active if we have high glucose concentration
83
How does the liver utilize glucose
It maintains the levels in the blood! Doesn’t use it for itself. Because our liver loves us
84
What is hexokinase IV
Another name for glucokinase
85
What triggers glucokinase to leave the nucleas and work
Glucose
86
What tells glucokinase to go back to the nucleas
F6P
87
How do you inactivate glucokinase
Attach it to regulator protein (RP) in nucleus
88
When our liver starts to form F6P what does that tell us
We are at capacity for storing glycogen at the G6P phase so it moves to the next phase, making F6P
89
What step is important for glycogen storage
G6P
90
If ____ isn’t around PFK-1 wont be active. It is the main regulator
PFK-2
91
When you have allosteric acitvators for F6P what does that do to KM
It lowers the km, making it more active
92
_____ ———PFK2———-> ______
F6P F2,6bisP
93
What enhances PFK1 activity
F2,6bisP
94
What determines F2,6bisP levels
PFK2 and F2,6bisPase
95
Insulin is associated with
Phosphatases
96
If glucagon is high (when would that be?) what happens
When we’re fasting Liver wants to put glucose out in our body sooooo it inhibits glycolysis
97
How does our liver inhibit glycolysis
By phosphorylation get F26bisPase and making it active F26bisPase turns F26P to F6P which then wants to go do gluconeogenesis
98
Why would our liver want to inhibit glycolysis
Because we want to be making sugar, not breaking it down
99
What does F26P do in liver vs adipose tissue
In liver it regulates glycolysis and gluconeogenesis In adipose it regulates glycolysis
100
PFK2 in liver active vs inactive
INactive = phosphorylated ACTIVE = dephosphorylated
101
F2,6bisPase in liver active vs inactive
INactive = dephosphorylated ACTIVE = phosphorylated IF fia talks about P she’s activated
102
A lactose intolerance would be determined by
A lactase deficiency
103
What enzyme decreases with age
Lactase
104
What inhibits pyruvate kinase
Alanine and ATP Acetyl CoA Long chain FA
105
What activates pyruvate kinase
F1,6bisP
106
Alanine indicates what about energy
We have enough so cool the jets on glycolysis
107
Glucagon signals what in the blood
Low blood sugar
108
Pyruvate kinase active vs inactive
INactive = phosphorylated ACTIVE = dephosphorylated
109
What’s the first and second most enzyme deficiency
1st = G6PDH 2nd = pyruvate kinase deficiency
110
When you have a pyruvate kinase deficiency what is vulnerable
RBC
111
What levels are important to note for pyruvate deficiency, what happens to them
ATP decreases 2,3 bisphosophoglycerate increases
112
Pyruvate K deficiency is dominant or recessive
Autosomal recessive
113
With strenuous exercise what is O2 like
Anaerobic
114
During anaerobic conditions pyruvate makes
NAD+ and Lactate
115
Why is NAD+ important
It can be used for GAPDH
116
What’s the whole point of forming lactate
It regenerates NAD+ concentrations SOOO we can’t continue glycolysis at step 6 glyceraldehyde-3-phosphate ——GADPH—-> 1,3bisphophoglycerate
117
Enzyme used to turn pyruvate to lactate
Lactate dehydrogenase
118
Accumulation of pyruvate =
Hemolysis Muscle cramping during strenuous exercise
119
If you’re in an aerobic condition what’s going on with pyruvate
It will continue on to be made into Acetly CoA
120
The Warburg effect is
Aerobic glycolysis in cancer
121
Even with O2 what do cancer cells do
Convert pyruvate to lactate
122
When cancer makes lactate why is this beneficial
Acidity helps cancers invade and escape our immune system
123
During Warburg effect ____ intermediary molecules can be used for ____ and cell growth
More Anabolism
124
Galactose key enzymes
GALK GALT GALE
125
Deficiency in GALK, GALT, GALE lead to
Galactosemia = accumulation of galactose in your blood GALK especially
126
Fructose enzymes
Fructokinase = rapid Aldolase B = rate limiting
127
Fructokinase deficiency vs Aldolase B deficiency
F = benign accumulation of fructose AB = hereditary fructose intolerance damages liver reduced ATP/ADP ratio trap pi in F1P form
128
Where is fructose mainly used
Liver
129
____ cannot be used for glycogen synthesis
Fructose
130
Why is fructose less regulated
It bypasses PFK1 rate limiting step
131
Why is consuming TONS of fructose bad?
Because we can’t regulate it (no rate limiting step) Leads to fatty liver and hyperglycemia
132
Too much glucose can lead to
Glycosylation (HbA1C) Glucose turning to fructose Cataracts, retinopathy, peripheral neuropathy
133
Glycosylation
Excessive chemical attachment of glucose to proteins with out involvement of enzymes
134
Why does too much glucose lead to neural stuff/eye stuff
Certain cells lack/have low sorbitol dehydrogenase Sooo they cant ???
135
Inducible vs constitutive enzymes. Give examples of each
Inducible = expressed under specific conditions. Can be turned on(induced) or turned off(repressed) in response to changes in our bodies concentration of the substrate example = glucokinase Con = always on no matter the substrate concentration example = hexokinase
136
A few days on breast milk can lead to
Deficiency in GALK or GALT