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Metabolism > Lecture I & II > Flashcards

Lecture I & II Flashcards

1
Q

What is metabolism?

A

Series of chemical reactions in which foodstuff is converted to usable energy forms. Can be catabolism or anabolism

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2
Q

What is catabolism?

A

Breakdown of complex organic molecules into simple molecules

Process releases ATP

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3
Q

What is anabolism?

A

Assebly of simple molecules into complex organic molecules

Requires use of ATP/energy

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4
Q

How does ATP create energy?

A

Cleaving third phosphate in energetically favorable reaction forming ADP
Forming ATP is not energetically favorable
Reaction is hydrolysis leaving ADP and inorganic phosphate behind

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5
Q

What is oxidation?

A

Loss of electron from atom as a result of adding oxygen or removing hydrogen

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6
Q

What is reduction?

A

Gain of electron resulting from gain of hydroden or loss of oxygen

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7
Q

What are the most important electron transporters?

A

NAD+ and NADP+
These are oxidized forms of NADPH and NADH
NAD+/NADP+ are oxidizing agents

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8
Q

Difference between NADP & NAD?

A

Phosphate group at the 2 prime position of ribose ring

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9
Q

What does drinking alcohol to to NAD+ in body?

A

Removes it from the system to it can no longer be used in glycolysis
This is why drinking makes you feel so hungry even though glucose is high

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10
Q

What must carbohydrates be converted into?

A

Fructose
Glucose
Galactose

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11
Q

What must lipids be converted into?

A

Glycerol and fatty acids

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12
Q

Where can proteins enter metabolic cycle?

A

Pyruvate
AcCoA
TCA

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13
Q

Where can lipids enter metabolic cycle?

A

Pyruvate

AcCoA

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14
Q

Main function of AcCoA?

A

Convey carbon atoms from acetyl groups to TCA

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15
Q

Where is AcCoA generated?

A

Micohondrial matrix

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16
Q

What can give rise to AcCoA?

A

Proteins, carbs, and lipids

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17
Q

4 Fates of AcCoA?

A

Lipogenesis
TCA
Ketone Bodies
Cholesterol

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18
Q

Primary fate of AcCoA?

A

TCA

Oxidation of acetyl groups in a combustion reaction producting water, CO2, ATP

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19
Q

What is lipogenesis?

A

Formation of fatty acids from AcCoA, carbs or Aas

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20
Q

What is esterification?

A

Formation of triacylglycerol (fats) from fatty acids

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21
Q

Where does glycolosis occur?

A

Cytoplasm

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22
Q

What is ketogenesis?

A

Formation of ketone bodies from AcCoA

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23
Q

What is cholesterogenesis?

A

Formation of cholesterol from AcCoA

Chosterol can then be converted to steroids

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24
Q

What is steroidogenesis?

A

Creation of steroids from cholesterol

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25
Q

What dietary items can fat storage?

A

Proteins, carbs, and lipids as they can all become AcCoA then become fat via lipogenesis and esterification

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26
Q

What is Beta Oxidation?

A

Creating AcCoA from Fatty acids

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27
Q

Primary metabolization of carbs?

A

As glucose, fructose and galactose become intermediates in glycolytic pathway

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28
Q

What has largest glycogen stores?

A

Liver, heart, skeletal muscle

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29
Q

Where does beta oxidation occur?

A

Mitochondria forming AcCoA from fatty acids

Only cells with mitochondria can perform this

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30
Q

What are triacylglyerols?

A

Stored form of fatty acids in adipose tissue

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31
Q

What does protein metabolism yield?

A

NH4 (ammonia)

Toxic in large amounts so liver must turn into urea

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32
Q

Preffered fuel of Liver?

A

Fatty Acids
Glucose
Amino Acids

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33
Q

Preffered fuel of Adipose Tissue?

A

Fatty Acids

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34
Q

Preffered fuel of skeletal muscle?

A

Glucose under exertion

Fatty acids at rest

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35
Q

Preffered fuel of heart muscle?

A

Fatty acids

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36
Q

Prefferred fuel of brain?

A

Normally glucose but can also use ketone bodies in starvation

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37
Q

What does liver do while fasting?

A

Uses energy to create glucose from fatty acids

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38
Q

What occurs in fasted state?

A

Low insulin initiates lypolisis in adipose tissue increasing serum fatty acids
Fatty acids used preferentially by some tissues or converted to glucose by liver

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39
Q

What happens to AcCoA generated from fatty acid oxidation in liver?

A

Oxidized to form ketone bodies in liver mitochondria

Brain will use these when levels are high enough but still always needs glucose

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40
Q

How many calories does a gram of fat provide?

A

9 Kilo cals

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41
Q

How many calories does a gram of carbs provide?

A

4 Kilo cals

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42
Q

How many calories does a gram of protein provide?

A

4 Kilo cals

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43
Q

Amylose source and enzyme?

A

Potatoes, rice, corn, bread

Maltase

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44
Q

Sucrose source and enzyme?

A

Table sugar & desserts

Sucrase

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45
Q

Lactose source and enzyme?

A

Milk products

Lactase

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46
Q

Fructose source and enzyme?

A

Fruit & Honey

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47
Q

Glucose source and enyme?

A

Fruit Honey & Grapes

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48
Q

What does maltase do?

A

Digests amylose

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49
Q

What is starch?

A

Polymer of glucose which is form most foods enter body

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50
Q

What digests starches?

A

Amylase in pancreas and saliva

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51
Q

What is sucrose?

A

Glucose/fructose molecule

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52
Q

What is lactose?

A

Galactose and glucose molecule

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53
Q

Where are disaccharides digested?

A

Brush border of smal lintestine

Final digestion of them occurs on luminal surface of SI epithelial cells

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54
Q

Can disaccharides be absorbed?

A

No

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55
Q

What must acids be turned into to enter TCA?

A

Alpha keto acids

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56
Q

What is lactose intolerance?

A

Decrease in intestinal lactase prohibiting lactose from being absorbed
Causes water to follow lactose leading to diarrhea
Gut bacteria also digests into gases causing bloating

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57
Q

What can be confused with lactose intolerance?

A

Milk alergy induced anaphylaxis

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58
Q

What does insulin do and where is it produced?

A

Pancreatic beta cells
Promotes glycolysis and glycogen sysnthesis
Main function is to keep blood sugar low

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59
Q

What is glucagon and where is it made?

A

Pancreatic alpha cells

Causes liver to release glucose into blood via glycogenolysis

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60
Q

What is glycogenolysis?

A

Break down of glycogen by liver and muscle cells

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61
Q

What enzyme is used to convert glycogen in muscles?

A

Glycogen phosphorylase

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62
Q

What does glycolysis create?

A

Single glucose molecule yields 2 ATP, 2 Pyruvate 2 molecules water and 2 molecules NADH

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63
Q

What is gluconeogenesis?

A

Creation of glucose from con carbohydrate sources such as pyruvate, lactate, glycerol, and glucogenic Aas

64
Q

Bodies glucose requirements?

A

Brain: 120g per day
Muscles: 40g per day

65
Q

What must blood glucose be kept above to keep brain functioning?

A

6omg/100ml

66
Q

What is chronic hyperglycemia?

A

Blood glucose above 110mg/100ml

67
Q

What happens in fed state?

A

Glycogen storage
Insulin release
ATP production via pyruvate and lactate production
AcCoA or tiacylglycerol can be created

68
Q

What are serum levels like just after eating?

A

High glucose and insulin

Low glucagon, fatty acids, and ketones low

69
Q

Where is epinephrine release from?

A

Adrenal medulla

70
Q

Are there glucagon receptors on liver?

A

No

71
Q

What does the pentose phosphate pathway produce?

A

NADPH

72
Q

What is protein in milk causing allergy?

A

S1 Casein

73
Q

What is product of Glycogenlysis?

A

Glucose-6-P

74
Q

What does adding phosphate to glucose do?

A

Traps it in cell

75
Q

What is Oxaloacetate use for?

A

To create glucose-6-P in gluconeogenesis

76
Q

What do epinephrine and glucagon do?

A

Block glycolyis and encourage gluconeogenesis to keep blook leves high

77
Q

Can glucose be created from lactate and pyruvate?

A

From lactate by not pyruvate

78
Q

What is special of RBC metabolism?

A

No mitochondria
Only can metabolize carbs no proteins or fats
Lactace made as no mitochondria and is released from cell
Pentose phosphate pathway prevalent

79
Q

Brain metabolism?

A

Pentose phosphate pathway
Nearly all glucose in TCA
Very small glycogen store

80
Q

Muscle metabolism?

A

TCA
Pentose pathway
Glycogen stores but only to be used by cell not sent into circulation

81
Q

Adipose metabolism?

A

No TCA

Excess glucose becomes fats

82
Q

Liver metabolims?

A 
Pentose
TCA
Gluconeogenesis
Glucogen synthesis
Glucogenolysis for body
Glucouronide production
83
Q

What are glucouronide?

A

Produced in liver

Responsible for drug and bilirubin detoxification

84
Q

SGLTI

A

One molecule of glucose or galactose with 2Na
Na fructose
Found in intestinal mucosa and kidney tubule
Down gradient

85
Q

SGLT2

A

One glucose and 1 Na
Found in kidney tubule
No galactose or glucose
Down gradient

86
Q

Glut2

A 
Low affinity, high Km
Inulin independent
Liver intestines, kidney
Moves in both directions: into cell in fed out, out in starved 
Serves as glucose sensor in beta cells
87
Q

Glut4

A 
Insulin Dependent
High glucose affinity, low KM
Heart, mucle, adipose
Not active during resting state 
Gets glucose after we have eaten
88
Q

What does glucokinase do?

A

Turns glucose into glucose 6 phosphate trapping it in cell

89
Q

What does gluco-6 phosphotase do?

A

Removes phosphate from glucose allowing it to leave cell in starved state

90
Q

What enzyme is found with GLUT4?

A

Hexokinase

91
Q

What enzyme is found with GLUT2?

A

Glucokinase

92
Q

Important steps in glycolysis?

A

Priming step - ATP invested to break glucose
Splitting stage
Ox/redox stage

93
Q

What happens in splitting stage?

A

Fructose-1-6 bisphosphate split into either dihydroxyacetone phosphate or glyceraldehyde 3 phosphate

94
Q

What does Aldolase do?

A

Enzyme responsible for splitting fructose-1-6 bisphosphate into dihydroxyacetone phosphate

95
Q

What happens in the Ox/redux / phosphorylation stage?

A
  • Glyceraldehyde 3 phosphate converted into pyruvate - and ATP
  • ATP earning
  • NADH is created during this step
96
Q

What are the 3 key glycolytic enzymes?

A
  1. Hexokinase /glucokinase
  2. PFK1
  3. Pyruvate kinase
97
Q

What does Hexokinase / glucokinase do?

A
  • Regulates change of glucose to glucose-6-P
  • This is a phosphorylating enzyme
  • Hexokinase found in muscle cells, glucokinase in liver
98
Q

What does PFK1 do?

A
  • Regulates change of fructose-6-P to Fructose-1-6 bisphosphate
  • This is a phosphorylating enzyme
  • PFKI - can be regulated by PFKII
99
Q

What does Pyruvate kinase do?

A
  • Regulates change of phosphoenolpyruvate to pyruvate

Substrate level phosphorylation

100
Q

How many ATP does glycolysis create?

A

4 total

2 net

101
Q

What happens to pyruvate when energy is not needed?

A

Becomes substrate in aa synthesis

102
Q

What are the ways in which enzymes can be modulated?

A
  1. Allosteric regulation
  2. Covalent modification
  3. Induction/repression of gene
103
Q

What is covalent modification?

A

Kinases - phosphorylate

Phosphotases - dephosphorylate

104
Q

Where is hexokinase found? What regulates it? When is it present?

A

All cell types
Modulated by product, glucose-6-P
Always present and non inducible

105
Q

What is km of hexokinase?

A

Very low, easily saturated

106
Q

Where is glucokinase found? How is it moldulated

A

Present in liver and pancreas

Active when moved to cytoplasm, inactive in nucleus

107
Q

What regulates glucokinase?

A

Glucose - increases
Insulin - increases
Fructose 6 - P: decreases

108
Q

What is KM of glucokinase?

A

High, not easily saturated

109
Q

What happens in irreversible rxn 1?

A
  • Glucose becomes glucose-6-p locking it in cell

- ATP required

110
Q

What positively regulates PFK1?

A

ADP
AMP
Fructose-2-6 biphosphate

111
Q

What negatively regulates PFK1?

A

ATP

Citrate

112
Q

What does fructose 2-6 biphosphate regulate?

A

Hepatic PFKI

113
Q

What does PFKII do? When does it do this?

A

Converts fructose-6-P to Fructose-2-6-P in liver

Occurs when insulin and glucose and high and more glycolysis is needed

114
Q

How is hepatic fructose-2-6-P regulated?

A

Inhibitors - epinephrine & glucagon
Stimulate cAMP & PKA
These inhibit kinase domain of PFKII stopping F26P formation and stopping glycolyis

115
Q

Can PFKI function without F26P?

A

No! In absence glycolysis is stopped and gluconeogenesis occurs

116
Q

What is different about glycolysis in the heart, skeletal muscle?

A
  • Epinephrine activates phosphotase region of PFKII activating enzyme and stimulating glycolysis
  • No glycogen receptors
117
Q

What does phosphorylation of hepatic PFKII do?

A

Inactivates it

118
Q

What regulatory means are used in hepatic PFKII?

A

Hepatic glycolysis is inhibited by epinephrine and glucagon through inhibition of enzymes and repressed mRNA synthesis

119
Q

What inhibitis and encourages pyruvate kinase?

A

Activated: insulin and fructose-1-6-P
Inhibition: epinephrine, alanine, and ATP, glucagon

120
Q

What does pyruvate kinase do?

A
  • Converts phosphoenolpyruvate into pyruvate
121
Q

What form of pyruvate kinase is active?

A

Phosphorylated form is less active

122
Q

What does lack of pyruvate kinase cause?

A

Hemolytic anemia

123
Q

What can pyruvate become?

A

Lactate
AcCoA
Alanine
AxaloacetateW

124
Q

What does Pyruvate dehydrogenase do?

A

Key enzyme for entering TCA cycle by converting pyruvate to AcoA

125
Q

What is microcephally?

A
  • reduced head circumference
126
Q

Symptoms of pyruvate dehydrogenase defect?

A

Microcephaly, poor muscle coordination, mental retardation

127
Q

What does Pyruvate carboxylase do?

A
  • Converts pyruvate to oxaloacetate
128
Q

Where are glucagon receptors located?

A

In liver and not on muscles as only liver metabolizes glucagon for rest of body

129
Q

What does inhibition of Hepatic glycolysis do?

A

Preserves glucose for use by tissues that have fuel prefference

130
Q

What type of cells have epinephrine receptors?

A

Liver, muscle, fat

131
Q

How do epinephrine and glucagon control glycolysis?

A

Indirectly inhibiting PFKI
Directly inhibiting pyruvate kinase
In liver they also slow synthesis of three required enzymes

132
Q

What does gyclolysis require? How do we get it?

A

NAD+

NADH is oxidized in conversion of pyruvate to lactate by LDH

133
Q

How can NAD be regeneraed?

A

Conversion of pyruvate to lactate by LDH

Mitochondrial linked shuttles

134
Q

What does LDH do?

A
  • Enzyme in body that controls conversion of pyruvate and NADH to lactate and NAD+
135
Q

What is LDH5-M4? -

A

Specific LDH molecule in skeletal muscle that preferentially converts pyruvate to lactate to give energy burst during exercise

136
Q

What is LDH1-4H?

A
  • LDH enzyme in heart prefers to convert lactate to pyruvate
  • Allows for prolonged energy creation
137
Q

What is normal lactate/pyruvate ratio?

A

Normal serum concentration of lactate:pyruvate is 10:1

138
Q

What does Pyruvate dehydrogenase do?

A
  • Multienzyme complex that converts pyruvate, NAD+ and coenzyme A to AcCoA in the mitochondrial matrix
139
Q

What are pyruvate dehydrogenase cofactors?

A
  • Thiamine, riboflavin, niacin increase PDH function

- These are B1, B2, B3, B5

140
Q

What happens if you do not have pyruvate dehydrogenase cofactors?

A

Limited movement from pyruvate to AcCoA but you can still have AcCoA from fatty acids and proteins

141
Q

What regulates PDH?

A
  • End products (AcCoA & NADH) allosterically inhibit PDH function by phosphorylation
  • Glucagon and Epinephrine play no role
  • Increased Mg and Ca function to increase activity of PDH via phosphatase action
  • Usually present in increased activity
142
Q

What happens in lactate dehydrogenase deficiency?

A
  • Lack of LDH limits NAD+ levels during exercise so little pyruvate can be created from lactate to undergo glycolysis
  • Moderate exercise cannot be maintained due to lack of energy
  • Must be homozygous to see effects
143
Q

Inputs and outputs of glycolysis?

A

Inputs - Glucose, 2 ATP, 4 ADP, 4 P, 2 NAD+
Output - 4 ATP, 2 NADH, 2 pyruvate, 2 ADP
Net gain of 2 ATP
One glucose yields 2 pyruvate

144
Q

Do RBCs make pyruvate?

A
  • RBCs only make lactate as they do not have mitochondria
145
Q

What reactions require oxygen?

A

Reoxidation of mitochondrial NADH formed in reaction catalyzed by PDH
Reoxidation of cytosolic NADH by mitochondrial linked shuttle
Glycerol phosphate shuttle
Malate aspartate shuttle

146
Q

What do low levels of NADH Do?

A

Low levels of NADH decrease the formation of lactate

147
Q

Enzymes required for galactose metabolism?

A

Galactokinase - converts galactose to galactose 1-P
Gal-1-P uridyltransferase - converts galactose 1 - P to glucose 1-p
Then converted to glucose-6-p by hexo/glucokinase

148
Q

What does Galactokinase do?

A
  • converts galactose to galactose 1-P
149
Q

What does Gal-1-P uridyltransferase?

A
  • converts galactose 1 - P to glucose 1-p
150
Q

What does lactose become?

A

Glucose and galactose

151
Q

What is Galactosemia?

A
  • genetic (autosomal recessive) disorder caused by lack of galactokinase and Gal-1P uridyltransferase leading to buildup of Galactitol and galactose 1-P
152
Q

Which form of galactosemia is more sever?

A

Gal-1P uridyltransferase - more common

153
Q

Symptoms of galactosemia?

A
  • Symptoms: include cataracts, jaundice, brain & kidney damage, enlarged liver, galactosuria
  • In deficiency of galactokinase only galactose urea, cataracts, and galactosemia are seen
154
Q

What is Galactitol?

A

What builds up in body when galactokinase is not present

155
Q

What is required for fructose metabolism?

A

Fructokinase - turns fructose into frutcose-1-P

Aldolase A/B/C - convert fructose-1-P into glyceraldehyde 3 phosphate or dihydroxy acetone phosphate

156
Q

What is special about aldolase B?

A

Found in liver and RBCs, plays crucial role in glycolysis and gluconeogenesis

157
Q

Symptoms of fructose metabolism issues?

A 
Hypoglycemia
Vomiting
Jaundice 
Hepatic failure 
Causes accululatoin of fructose which is toxic and hypoglycemia
Increases lactic and uric acid

Metabolism (17 decks)

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