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CBFM Final > Carbohydrates: Digestion/absorption > Flashcards

Carbohydrates: Digestion/absorption Flashcards

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
Q

Starch and glycogen RE vs NRE

A

Only 1 RE

TONS of NRE going every which way!

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26
Q

How are cellulose fibrils connected

A

Hydrogen bonds

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27
Q

We cannot ______ carbs so we _______

A

Absorb long polymer

Use glycosidases to Hydrolyze/break them down

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28
Q

What breaks down carbs in mouth
And what does it break

A

α-amylase

Cleaves 1-4

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29
Q

α-amylase creates

A

α-dextrins which have a lot of α 1,6 glycosidic bonds

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30
Q

When you hear 1,6 think

A

Branching!!!

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31
Q

What does our stomach acid do to α-amylase

A

Inactivates it

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32
Q

____ releases _____ into the duodenum to ______

A

Pancreas

HCO3- (bicarbonate)

Neutralize it

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33
Q

Why do we want to neutralize the duodenum

A

So enzymes can be functional again

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34
Q

What is secreted in duodenum from pancreas

A

Bicarb and α-amylase

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35
Q

What is formed in small intestine due to cleavages

A

Maltose(disaccharide), isomaltose, maltotriose

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36
Q

When and where do sucrose and lactose get acted on

A

When they contact the brush border in the intestines

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37
Q

Bacteria in colon can do what and what do they get in return

A

Breakdown small sugars

They get energy in return

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38
Q

______ cleaves sucrose to ______

A

Sucrase
Glucose and fructose

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39
Q

_____ cleaves lactose to ____

A

Lactase
Glucose and galactose

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40
Q

When bacteria breakdown sugars what do they form

A

Gases and short chain FA

FA are what is used for energy

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41
Q

GLUT 1-4 are

A

Glucose facilitated

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42
Q

GLUT 5 is

A

Fructose facilitated

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43
Q

Which GLUT is insulin dependent

A

4

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44
Q

Where are all the GLUTs located

A

1 = most tissues
2 = liver, kidney, pancreatic β
3 = brain, placenta, fetal muscle
4 = skeletal/heart muscle, adipocytes
5 = small intestine

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45
Q

Which GLUT affects vmax

A

4

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46
Q

Cellulose in our diet goes out as

A

Fiber

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47
Q

GLUT 1 has a _____ km which means

A

Low
Takes glucose up readily

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48
Q

SGLT1 is ____ and needs ______and needs _____ to regulate sodium

A

Sodium glucose transporter
Sodium needs to come in with glucose
Na+/k+ ATPase

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49
Q

Why is GLUT2 not in intestines

A

Because it has a HIGH km and has a hard time brining in glucose

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50
Q

Where are SGLT1 and what do they do there

A

In kidney cells

For glucose reabsorption

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51
Q

SGLT1 transport glucose from ____ to ______ in

A

Lumen

Capillaries

Kidneys

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52
Q

The ___ of a transporter is inversely proportional to its affinity to its ____

A

KM

Substrte

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53
Q

GLUT 1 and 3 are really bad at what and why

A

Removing glucose from the blood quickly

Because they have a low KM, the slope change is minimal

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54
Q

What is significant about GLUT2 and its location

A

Liver, kidney, pancreatic β

It removes glucose from the blood quickly when the concentration is high

it is proportional to extracellular glucose concentration
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55
Q

Where are GLUT4 and what makes them move to where

A

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
Q

What 3 steps of glycolysis are regulated

A

Step 1 = hexokinase/glucokinase

Step 3 = phosphofructokinase 1

Step 10 = pyruvate kinase

57
Q

What are the two phases of glycolysis

A

I = energy investment/energy input

II = energy generation/energy output

58
Q

Which steps are ATP consuming and irreversible

A

1: glucose —hexokinase—->G6P

3: F6P ——phosphofructokinase1—->F16BP

59
Q

G6P is a _____ to hexokinase

A

Allosteric inhibitor

Negative feedback

60
Q

Which carbons get phosphates added to them at step 1

A

Carbon 6 gets a phosphate

61
Q

Which carbons get a phosphate added to them at step 3

A

Carbon 1 gets a phosphate added

62
Q

What inhibits step 3 and why

A

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
Q

How does citrate inhibit PFK1 since the TCA is in mitochondria

A

It leaks out to cytosol

64
Q

What do AMP and ADP signal in the energy investment phase of glycolysis and why

A

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
Q

______ cleaves F16BP into ______ and _____

A

Aldose - big al

G3P - glacier aldehyde

DHAP - don’t handle apparatus please

66
Q

Which two products of Aldolase wants to look more like the other

A

DHAP wants to look like G3P

67
Q

Before step 10 of glycolysis what is our ATP status

A

We’ve used 2 ATP and we’ve made 2 ATP

So net = 0

68
Q

What steps are ATP generating and irreversible

A

Step 10

69
Q

What inhibits pyruvate kinase

A

ATP
And
Acetyl CoA

70
Q

What does acetyl CoA indicate for glycolysis

A

That we have enough energy and it can cool its jets

71
Q

What activates pyruvate kinase

A

F16BP

72
Q

What does substrate level phosphorylation mean?

A

ATP is made without using ETC and ATP synthase

73
Q

Which is favored between 1,3BPG or 3PG

A

3PG

74
Q

During glycolysis _____ are generated from _____ glucose molecule through ______

A

2 net ATP

Each

Subrtrate level phosophrylation

75
Q

What doesn’t glycolysis use and what does that make it

A

Doesn’t us O2

ANAEROBIC

76
Q

Which enzyme/step commits glucose to glycolysis

A

PFK-1
Step 3

77
Q

How is glucose kept in a cell and how does it work

A

By Hexokinase or glucokinase turning it into G6P

G6P cannot cross plasma membrane easily

78
Q

Hexokinase exists _____ and is inhibited by ____

A

In most tissues

G6P

79
Q

Glucokinase exists in ____ and is inhibited by ____

A

Liver/pancreatic β cells

F6P

80
Q

Hexokinase has a ____ km and that makes it _____

A

Low

Constitutive. Very efficient

81
Q

What do high concentrations of G6P tell hexokinase

A

“Hey we have plenty of glucose for energy rn, don’t bring any more in from the blood”

82
Q

Glucokinase has a ____ km and that makes it

A

High

Inducible. Which means it will only be active if we have high glucose concentration

83
Q

How does the liver utilize glucose

A

It maintains the levels in the blood! Doesn’t use it for itself. Because our liver loves us

84
Q

What is hexokinase IV

A

Another name for glucokinase

85
Q

What triggers glucokinase to leave the nucleas and work

A

Glucose

86
Q

What tells glucokinase to go back to the nucleas

A

F6P

87
Q

How do you inactivate glucokinase

A

Attach it to regulator protein (RP) in nucleus

88
Q

When our liver starts to form F6P what does that tell us

A

We are at capacity for storing glycogen at the G6P phase so it moves to the next phase, making F6P

89
Q

What step is important for glycogen storage

A

G6P

90
Q

If ____ isn’t around PFK-1 wont be active. It is the main regulator

A

PFK-2

91
Q

When you have allosteric acitvators for F6P what does that do to KM

A

It lowers the km, making it more active

92
Q

_____ ———PFK2———-> ______

A

F6P

F2,6bisP

93
Q

What enhances PFK1 activity

A

F2,6bisP

94
Q

What determines F2,6bisP levels

A

PFK2 and F2,6bisPase

95
Q

Insulin is associated with

A

Phosphatases

96
Q

If glucagon is high (when would that be?) what happens

A

When we’re fasting
Liver wants to put glucose out in our body
sooooo it inhibits glycolysis

97
Q

How does our liver inhibit glycolysis

A

By phosphorylation get F26bisPase and making it active
F26bisPase turns F26P to F6P which then wants to go do gluconeogenesis

98
Q

Why would our liver want to inhibit glycolysis

A

Because we want to be making sugar, not breaking it down

99
Q

What does F26P do in liver vs adipose tissue

A

In liver it regulates glycolysis and gluconeogenesis

In adipose it regulates glycolysis

100
Q

PFK2 in liver active vs inactive

A

INactive = phosphorylated

ACTIVE = dephosphorylated

101
Q

F2,6bisPase in liver active vs inactive

A

INactive = dephosphorylated

ACTIVE = phosphorylated

IF fia talks about P she’s activated

102
Q

A lactose intolerance would be determined by

A

A lactase deficiency

103
Q

What enzyme decreases with age

A

Lactase

104
Q

What inhibits pyruvate kinase

A

Alanine and ATP
Acetyl CoA
Long chain FA

105
Q

What activates pyruvate kinase

A

F1,6bisP

106
Q

Alanine indicates what about energy

A

We have enough so cool the jets on glycolysis

107
Q

Glucagon signals what in the blood

A

Low blood sugar

108
Q

Pyruvate kinase active vs inactive

A

INactive = phosphorylated
ACTIVE = dephosphorylated

109
Q

What’s the first and second most enzyme deficiency

A

1st = G6PDH

2nd = pyruvate kinase deficiency

110
Q

When you have a pyruvate kinase deficiency what is vulnerable

A

RBC

111
Q

What levels are important to note for pyruvate deficiency, what happens to them

A

ATP decreases

2,3 bisphosophoglycerate increases

112
Q

Pyruvate K deficiency is dominant or recessive

A

Autosomal recessive

113
Q

With strenuous exercise what is O2 like

A

Anaerobic

114
Q

During anaerobic conditions pyruvate makes

A

NAD+ and Lactate

115
Q

Why is NAD+ important

A

It can be used for GAPDH

116
Q

What’s the whole point of forming lactate

A

It regenerates NAD+ concentrations SOOO we can’t continue glycolysis at step 6
glyceraldehyde-3-phosphate ——GADPH—-> 1,3bisphophoglycerate

117
Q

Enzyme used to turn pyruvate to lactate

A

Lactate dehydrogenase

118
Q

Accumulation of pyruvate =

A

Hemolysis
Muscle cramping during strenuous exercise

119
Q

If you’re in an aerobic condition what’s going on with pyruvate

A

It will continue on to be made into Acetly CoA

120
Q

The Warburg effect is

A

Aerobic glycolysis in cancer

121
Q

Even with O2 what do cancer cells do

A

Convert pyruvate to lactate

122
Q

When cancer makes lactate why is this beneficial

A

Acidity helps cancers invade and escape our immune system

123
Q

During Warburg effect ____ intermediary molecules can be used for ____ and cell growth

A

More

Anabolism

124
Q

Galactose key enzymes

A

GALK
GALT
GALE

125
Q

Deficiency in GALK, GALT, GALE lead to

A

Galactosemia = accumulation of galactose in your blood

GALK especially

126
Q

Fructose enzymes

A

Fructokinase = rapid

Aldolase B = rate limiting

127
Q

Fructokinase deficiency vs Aldolase B deficiency

A

F = benign
accumulation of fructose

AB = hereditary fructose intolerance
damages liver
reduced ATP/ADP ratio
trap pi in F1P form

128
Q

Where is fructose mainly used

A

Liver

129
Q

____ cannot be used for glycogen synthesis

A

Fructose

130
Q

Why is fructose less regulated

A

It bypasses PFK1 rate limiting step

131
Q

Why is consuming TONS of fructose bad?

A

Because we can’t regulate it (no rate limiting step)
Leads to fatty liver and hyperglycemia

132
Q

Too much glucose can lead to

A

Glycosylation (HbA1C)
Glucose turning to fructose
Cataracts, retinopathy, peripheral neuropathy

133
Q

Glycosylation

A

Excessive chemical attachment of glucose to proteins with out involvement of enzymes

134
Q

Why does too much glucose lead to neural stuff/eye stuff

A

Certain cells lack/have low sorbitol dehydrogenase
Sooo they cant ???

135
Q

Inducible vs constitutive enzymes. Give examples of each

A

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
Q

A few days on breast milk can lead to

A

Deficiency in GALK or GALT

CBFM Final (18 decks)

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