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Biochemistry > MCM - Carb Metabolism > Flashcards

MCM - Carb Metabolism Flashcards

1
Q

What chemical reaction do all cells carry out for energy?

A

Glycolysis

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2
Q

What are 3 major monosaccharides that can be used in Glycolysis

A

Glucose, Fructose, and Galactose

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3
Q

Which cell group can only use Glycolysis

A

Red Blood Cells

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4
Q

Whats the brain’s primary source of energy when in “fed” state

A

Glycolysis

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5
Q

How does Glucose enter a cell

A

Through the use of GLUT transporters; facilitated diffusion

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6
Q

How many types of GLUT are there for uptake of solely Glucose

A

GLUT 1, GLUT 2, GLUT 3, GLUT 4

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7
Q

GLUT 1 characteristics

A

Found everywhere, but high concentration in RBC’s and Brain; high affinity

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8
Q

GLUT 2 Characteristics

A

Main transport in liver; low affinity. But picks up any source of glucose

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9
Q

GLUT 3 Characteristics

A

Main transporter in neurons; High Affinity

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10
Q

GLUT 4 Characteristics

A

Present in skeletal muscle, heart, adipose tissue; Insulin Dependent

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11
Q

Where is GLUT 4 located in the cell

A

Sequestered in vesicles until insulin is bound

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12
Q

What enables GLUT 4

A

Binding of insulin, which releases GLUT 4 to the plasma membrane

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13
Q

Basic Steps of Glycolysis

A

1 molecule of glucose -> generate 2 molecules of pyruvate; generate 2 ATP; generate 2 NADH

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14
Q

Is glycolysis Anaerobic or Aerobic

A

Anaerobic

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15
Q

Where does glycolysis occur in the cell

A

Cytoplasm

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16
Q

First Part of Glycolysis

A

Phosphorylation of Glucose to Glucose-6 Phosphate by Hexokinase/Glucokinase

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17
Q

What main energy source does Glycolysis require

A

One molecule of ATP

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18
Q

Differences between Hexokinase and Glucokinase

A

Hexokinase is the general enzyme; glucokinase is specific to the liver and pancreatic Beta cells

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19
Q

What is the Rate Limiting Step of Glycolysis

A

The phosphorylation of Fructose-6 Phosphate to Fructose 1,6-biphosphate

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20
Q

What enzyme performs the first reaction of Glycolysis

A

Hexokinase/Glucokinase

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21
Q

What enzyme performs the Rate Limiting Step of Glycolysis

A

Phosphofructokinase-1; PFK-1

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22
Q

What does Phosphofructokinase do

A

Phosphorylates Fructose 6-Phosphate to Fructose 1,6-biphosphate

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23
Q

Does Phosphofructokinase use ATP

A

Yes

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24
Q

What does the phosphorylation of G3P produce

A

One NADH; no use of ATP

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25
Q

Where does the first pay off of Glycolysis occur

A

When G3P is phosphorylated

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26
Q

What is the second pay off stage of Glycoysis

A

Conversion of 1,3-BPG to 3-PG; 2 ATP created

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27
Q

What is the third and final pay off stage of Glycolysis

A

Formation of Pyruvate from Pyruvate Kinase; 2 ATP created; also irreversible

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28
Q

What are the 3 pay-off stages of Glycolysis

A
  1. Phosphorylation of G3P; 1 NADH
  2. Conversion of 1,3BPG to 3-PG; 2 ATP
  3. Formation of Pyruvate; 2 ATP
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29
Q

What enzyme phosphorylates Glucose to Glucose 6-Phosphate

A

Hexokinase (general)/ glucokinase (liver and pancreas)

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30
Q

What enzyme Phosphorylates Fructose 6-P to Fructose-1,6- Biphosphate

A

Phospofructokinase-1

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31
Q

Which enzymes in Glycolysis use ATP

A

Phospofructokinase-1 and Hexokinase (general)/ glucokinase (liver and pancreas)

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32
Q

Which enzyme takes 1,3-BPG to 3-phosphogylcerate

A

Phosphoglycerate Kinase

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33
Q

Which enzyme takes Phosphoenolpyruvate to Pyruvate

A

Pyruvate Kinase

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34
Q

Which enzymes in Glycolysis produce ATP via their reaction

A

Pyruvate Kinase and Phoshoglycerate Kinase

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35
Q

Which enzyme takes Glyceraldehyde 3-P to 1,3-Bisphosphoglycerate

A

Glyceraldehyde 3-P dehydrogenase

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36
Q

Which enzyme in Glycolysis produces one NADH

A

Glyceraldehyde 3-P dehydrogenase

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37
Q

What are the three irreversible steps of Glycolysis

A
  1. Hexokinase/Glucokinase (Trap Glucose)
  2. Phosphofructokinase (Add another Phosphate)
  3. Pyruvate Kinase (Split the 6 Carbon molecule to two 3 carbon molecules)
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38
Q

Hexokinase has a low or high affinity

A

High affinity; binds all glucose

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39
Q

Glucokinase has a low or high affintiy

A

Low affinity

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40
Q

What is Hexokinase inhibited by

A

G6P; the product of this enzymes action

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41
Q

What is Glucokinase inhibited by

A

Nothing really, but Glucagon

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42
Q

When is Glucokinase most active

A

High Glucose

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43
Q

Insulin induces the synthesis of

A

Glucokinase

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44
Q

Glucagon inhibits the synthesis of

A

Glucokinase

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45
Q

PFK-1 Activators

A

AMP, Fructose 2,6-Bisphosphate

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46
Q

What makes Fructose 2,6-Bisphosphate

A

PFK-2

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47
Q

PFK-1 Inhibitors

A

ATP, Citrate (TCA Cycle)

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48
Q

When is PFK-1 Activated; when its phosphorylated or dephosphorylated

A

Dephosphorylated

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49
Q

Hormonal Regulation of PFK-1

A

Glucagon Inhibits; Insulin Activates

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50
Q

What activates Pyruvate Kinase

A

Fructose 1,6-Bisphosphate and Glucagon

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51
Q

What inhibits Pyruvate Kinase

A

ATP, Alanine, and Glucagon

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52
Q

High Insulin Effect on Pyruvate Kinase

A

Stimulates protein phosphatase, dephosphorylation of PK, activate

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53
Q

High Glucagon Effect on Pyruvate Kinase

A

cAMP activates PKA, phosphorylation, PK Inhibited

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54
Q

Glucose 6-Phosphate Use in Other Pathways

A

Precursor for the PPP
Can be converted to Glucose 1-Phosphate
{used in galactose metabolism, glycogen synthesis, ironic acid pathway}

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55
Q

Glucose 6-Phosphate’s Outcome in the Pentosephosphate Pathway

A

Ribose and NADPH

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56
Q

Use of Ribose

A

For DNA Synthesis

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57
Q

Use of NADPH

A

Resythesizing Glutathione, a Selenium co-factor for getting rid of Hydrogen Peroxide

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58
Q

What are some fates of Pyruvate

A
  1. Reduced to lactate; to regenerate NAD+ in anaerobic conditions
  2. Oxidized in TCA cycle to Acetyl CoA and the CO2
  3. Converted to Alanine; used in gluconeogenesis and protein synthesis
  4. Converted to ethanol
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59
Q

Disorders of Glycolysis effect what two areas the most

A

The brain and the RBC’s

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60
Q

What do disorders of glycolysis usually cause

A

hemolytic anemia; because RBC’s cannot maintain there molecular gradients

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61
Q

Which enzyme is most affected in glyosis disorders

A

Pyruvate Kinase (95%)

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62
Q

What are the 2 types of Diabetes

A
  1. Type 1- autoimmune disorder affecting the Beta Cells of the Pancreas in the Langhorn area
  2. Type 2: Insulin resistance, usually caused by being extremely overweight
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63
Q

Other Potential causes of Diabetes than obesity

A

mutations, aberrant conversion of proinsulin to mature insulin, defective insulin receptor

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64
Q

What is the normal blood glucose range; fasting

A

70-100 mg/dL

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65
Q

What is the normal blood glucose range; fed

A

<140 mg/dL

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66
Q

Prediabetic glucose range; fasting

A

100-125 mg/dL

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67
Q

Prediabetic glucose range; fed

A

> 125 mg/dL

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68
Q

Tarui Disease

A

Deficient in PFK-1; least common Glycolysis Disorder; exercise induced muscle cramps and weakness

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69
Q

How much glucose does the brain need in one day

A

120 grams

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70
Q

How much glucose is present in body fluids

A

20 grams

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71
Q

How much glycogen is readily available in the body

A

190 grams

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72
Q

How long can glycogen stores supply the body

A

About one day without eating glucose

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73
Q

Where does Gluconeogenesis Occur

A

Liver, Kidney, and Small Intestine

74
Q

What does Gluconeogenesis accomplish

A

converts pyruvate back to glucose

75
Q

What can be fed into gluconeogenesis

A

lactate, amino acids, and glycerol

76
Q

What are the two enzymes where gluconeogenesis converts (2x) pyruvate

A

Pyruvate Carboxylase and PEP Carboxylase

77
Q

What enzyme does Gluconeogenesis use to bypass PFK-1 process

A

Fructose 1,6-bisphosphatase

78
Q

What enzyme does Gluconeogenesis use to bypass hexokinase/glucokinase

A

glucose 6-phosphatase

79
Q

Positive Regulators of Gluconeogenesis

A

Glucagon, citrate, cortisol, thyrozine, acetyl CoA

80
Q

Positive regulators of Glycolysis

A

Glucose, insulin, AMP, Fructose 2,6-BP, Fructose 1,6-BP

81
Q

Negative regulators of Gluconeogenesis

A

ADP, AMP, Fructose 2,6-BP`

82
Q

Negative regulators of Glycolysis

A

Glucagon, ATP, citrate, Glc 6-P, Fructose 6-P, Alanine

83
Q

4 enzymes that gluconeogenesis uses to bypass glycolysis irreversible steps

A
  1. Pyruvate Carboxylase
  2. Phosphoenolpyruvate Corboxykinase
  3. Fructose 1,6-BP
  4. Glucose 6-phosphatase
84
Q

What is Pyruvate Carboxylase

A

Mitochondrial Enzyme; activated by acetyl CoA and Cortisol

85
Q

Can Oxaloacetate leave the mitochondria

A

No; its impermeable

86
Q

How does Oxaloacetate need to be altered to leave mitochondria

A

Reduced to malate

87
Q

How is Malate changed once it leaves the mitochondria

A

Re-Oxidized to Oxaloacetate

88
Q

PEP Carboxykinase

A

Decarboxylation and phosphorylation of Oxaloacetate to PEP

89
Q

What activates PEP Carboxykinase

A

Cortisol, Glucagon, Thyroxine

90
Q

What is the Rate Limiting step of Gluconeogenesis

A

Fructose 1,6-Bisphosphatase

91
Q

What is Fructose 1,6-Bisphosphatase Activated by

A

Cortisol and Citrate

92
Q

What is Fructose 1,6-Bisphosphatase Inhibited by

A

AMP and F 2,6-BP

93
Q

What is the last step of Gluconeogenesis

A

Dephosphorylation of Glucose 6-Phosphate to Glucose

94
Q

What enzyme takes Glucose 6-Phosphate to Glucose

A

Glucose 6-Phosphatase

95
Q

What activates Glucose 6-Phosphatase

A

Cortisol

96
Q

Where is Glucose 6-Phospatase found

A

Liver, Kidney, Small Intestine and Pancreas

I.E. Where Gluconeogenesis occurs

97
Q

Where in the cell is Glucose 6-Phosphatase found

A

The lumen of the ER

98
Q

How does glucose 6-P get into the lumen of the ER to get to Glucose 6-Phosphatase and get back glucose back out

A

G6P Transporter
and
GLUT7 transporter back into the cytoplasm

99
Q

Cori Cycle Process

A

2 lactate from the muscle transported to the liver
Once in the liver 2 lactate into 2 pyruvate
Once 2 pyruvate you get Glucose with a 4 ATP investment via Gluconeogenesis

100
Q

Name Four Precursors to Gluconeogenesis

A
  1. Glycerol (Carb)
  2. Propionate (from odd-numbered fatty acids)
  3. Alanine (Protein Degradation)
  4. Amino Acids (Protein Degradation)
101
Q

Name two other sugars that can go into Gluconeogenesis

A
  1. Galactose

2. Fructose

102
Q

Fructose 1,6-BP Deficiency Consequences

A

Cannot have the payoff of Gluconeogenesis

103
Q

Von Gierke Disease

A

Mutations in the catalytic site in GSD 1a

Present with hepatomegaly due to buildup of glycogen in the liver

104
Q

Sucrose Structure

A

Fructose and Glucose

105
Q

What is Sucrose Cleaved by

A

Sucrase

106
Q

Lactose Structure

A

Galactose and Glucose

107
Q

What is Lactose cleaved by

A

Lactase

108
Q

Which GLUT Transporter uptakes Fructose

A

GLUT 5

109
Q

SGLT1 uptakes which two sugars

A

Galactose and Glucose

110
Q

Franconi-Bickel Syndrome; Overall effect

A

GLUT 2 mutation; failing to absorb galactose, glucose, and fructose

111
Q

Location of GLUT 2 Tranporter

A

Liver, Pancreatic Beta Cells, Enterocytes, and renal tubular cells

112
Q

What process takes Glucose to Fructose

A

The Polyol Pathway

113
Q

What is the Polyol Pathway

A

Glucose reduced to Sorbitol, Sorbitol oxidized to Fructose

114
Q

What two enzymes are utilized in the Polyol Pathway

A

Aldose Reductase and Sorbitol Dehydrogenase

115
Q

Cells lacking Sorbitol Dehydrogenase allow build up of sorbital triggering what

A

Cataracts

116
Q

Fructose Caviet in entering Glycolysis

A

Can by-pass PFK-1, the rate-limiting step of Glycolysis

This leads to excess Pyruvate, furthering to storage of Fatty Acids into Triacylglycerols, leading to excess Fat

117
Q

High Fructose Corn Syrup Effect

A

Can bypass PFK-1 and be stored as fat easier

118
Q

Deficiency of Galactokinase leads to

A

Build up of Galacitol; leading to cataracts

119
Q

Deficiency in Glucose 1P uridyltransferase

A

Leads to accumulation of Galacitol because of the side reaction that takes place

120
Q

What does the Pentose Phosphate Pathway Produce

A
  1. Sugar needed for DNA and RNA formation

2. NADPH; used to remake Glutathione

121
Q

Where does the P.P.P. take place

A

Cytosol

122
Q

What does G6P Dehydrogenase produce from the Pentose Phosphate Pathway

A

NADPH

123
Q

What is the rate limiting step of the P.P.P.

A

G6P Dehydrogenase

124
Q

G6PD Deficiency

A

Accumulation of hydrogen peroxide, leads to hemolytic anemia

125
Q

Which Part of the P.P.P. is irreversible

A

The Oxidative Phase

126
Q

What does the Oxidative Phase of the P.P.P. produce

A

NADPH and Ribulose 5-P

127
Q

What Part of the P.P.P. is reversible

A

The Non-Oxidative Phase

128
Q

What does the Non-Oxidative Phase Produce

A

Several Metabolites that can go into glycolysis and gluconeogenesis

129
Q

When is the Oxidative side of the P.P.P. favored

A

When cells are rapidly dividing; in need of Ribulose 5-P

130
Q

When there is a high demand for NADPH what does the P.P.P. do

A

Non-Oxidative products channeled into gluconeogenesis for re-entry into the P.P.P. Oxidative Pathway

131
Q

Where is an area where P.P.P. activity is very high

A

Phagocytic Cells

132
Q

What kind of chain is produced with the alpha 1,4

A

Straight chain

133
Q

What kind of chain is produced with the alpha 1,6

A

Branches

134
Q

Which end of glycogen is free to react?

A

The non-reducing end

135
Q

Which end of glycogen is not free to react

A

The reducing end

136
Q

What is the hallmark of the non-reducing end

A

An OH- group at Carbon 4

137
Q

Where does Glycogen Store

A

The Liver and Muscle

138
Q

How is glycogen stored inside the liver and muscle

A

Inside granules; containing the enzymes needed for glycogen metabolism

139
Q

What is the function of Liver Glycogen

A

To regulate blood glucose

140
Q

What is the function of Muscle Glycogen

A

To provide a reservoir of glucose for physical activity

141
Q

What is the first step of Glycogenesis

A

Trapping and Activation of Glucose; hexokinase/Glucokinase phosphorylyze glucose in liver and muscle cells (in the cytosol of the respective cells)

142
Q

What is the rate limiting step of Glycogensis

A

Glycogen Synthase; adds UDP-Glucose to non-reducing end of glycogen chain

143
Q

What branches the growing glycogen chain

A

At about 11 residues a fragment is broken off and the reattached elsewhere to with an alpha 1,6 chain via branching enzyme

144
Q

How does branching effect the solubility of glycogen

A

Increases the solubility as branching is increased

145
Q

What is the rate limiting step of Glycogenolysis

A

Glycogen Phosphorylase

146
Q

What does Glycogen Phosporylase do

A

Catalyzes the cleavage of glucose residues as a G1P from the non-reducing end

147
Q

How does the alpha 1,6 bond break

A

With debranching enzyme, adding the 3 residues back to the straight chain, cleaving the last alpha 1,6 bond that is left to release free glucose

148
Q

Ratio of Glu-1-P to Glu

A

10:1

149
Q

Fate of Liver Glu-1-P

A

converted to Glu-6-P and then to Glu. Free glucose released to blood

150
Q

Fate of Muscle Glu-1-P

A

Myocytes and cardiac myocytes lack glucose-6-phosphatase. So they use the Glu-1-P to generate energy via glycolysis and the TCA cycle

151
Q

What are 2 important reasons to regulate glycogen metabolism

A
  1. Maintain Blood Sugar

2. Provide Energy to Muscle

152
Q

What are the 2 Key enzymes in regulating glycogen metabolism

A
  1. Glycogen Synthase

2. Glycogen Phosphorylase

153
Q

What does Glycogen Synthase do

A

makes alpha 1,4 links and is the rate limiting step of glycogensis

154
Q

What does Glycogen Phosphorylase do

A

Cuts the alpha 1,4 links and the is the rate limiting step of glycogenolysis

155
Q

When is Glycogen Synthase active

A

When it is in the Dephospho form

156
Q

When is Glycogen Phosphorylase Active

A

When it is in the Phospho form

157
Q

When is Glycogen Synthase Inactive

A

When it is in the Phospho Form

158
Q

When is Glycogen Phosporylase Inactive

A

When it is in the Depospho Form

159
Q

In which state, fed or fasting, is Glycogenesis favored

A

Fed

160
Q

In which state, fed or fasting, is Glycogenolysis favored

A

Fasting

161
Q

Which state is favored while exercising, glycogenolysis or glycogenesis

A

Glycogenolysis

162
Q

What are the four key proteins involved in Insulin Regulation

A
  1. GLUT 4; insulin sensitive GLUT transporter
  2. Protein Kinase B (PKB)
  3. Protein Phosphatase 1 (PP1)
  4. Glycogen Synthase Kinase 3 (GSK 3)
163
Q

Effect of Insulin Binding on Glycogen Synthase

A

Binds, excites PKB. PKB excites PP1 which phosphorylates Glycogen Synthase activating it

164
Q

Effect of Insulin Binding on Glycogen Phosphorylase

A

Insulin binds, excites PKB. PKBB Excites PP1. PP1 inhibits Pyruvate Kinase and dephosphorylates Glycogen Phosporylase

165
Q

Type 2 Diabetes Blood Criteria

A

Normal: 70-100mg fasting; <140mg fed
PreDiabetic: 100-125mg fasting; >140 fed
Diabetic: >126mg fasting; >199mg Fed

166
Q

Key Enzymes and secondary messengers of Glucagon Regulation

A 
G Protein
Adenylate Cyclase and cAMP
Protein Kinase A
Protein Phosphatase 1
Phosphorylase Kinase
167
Q

Net Result of Insulin Binding

A

Glycogen is stored

168
Q

Net Result of Glucagon Binding

A

Glycogen is broken down for glucose

169
Q

Effect of Glucagon Binding on Glycogen Synthase

A

Phosphorylates Glycogen Synthase; deactivating it

170
Q

Effect of Glucagon Binding on Glycogen Phosphorylase

A

Dephosphorylates Glycogen Phosphorylase; activating it

171
Q

Effect of Epinephrine binding to muscle or liver during exercise

A

Same as Glucagon

172
Q

Glycogen Storage Disease; Genetic Traits

A

Autosomal Recessive

173
Q

Glycogen Storage Diseases

A
  1. Glycogen Synthase Defective
  2. Von Gierke Disease
  3. Pompe Disease
  4. Cori Disease
  5. Anderson Disease
  6. McArdle Disease
  7. Hers Disease
174
Q

What enzyme is defective in Glycogen Synthase Defect

A

Glycogen Synthase

175
Q

What enzyme is defective in Von Gierke Disease

A

Glucose 6-Phosphatase

176
Q

What enzyme is defective in in Pompe Disease

A

Acid Maltase

177
Q

What enzyme is defective in Cori Disease

A

Debranching Enzyme

178
Q

What enzyme is defective in Anderson Disease

A

Glucosyl (4:6) Transferase

179
Q

What enzyme is defective in McArdle Disease

A

Muscle Glycogen Phosphorylase

180
Q

What enzyme is defective in Hers Disease

A

Liver Glycogen Phosphorylase

181
Q

Difference between McArdle Disease vs. Hers Disease

A

McArdle: in Muscle GP; muscle form of isozyme is activated by AMP, Ca-CaM, and G Actin
Hers: in Liver GP; inactivated by free glucose and unaffected by AMP

182
Q

G-3-P and DHAP have an equilibrium; DHAP can also go

A

Into FA Synthesis and TAG Synth

Biochemistry (7 decks)

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