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Physiology Metabolism > Metabolism 1 2 > Flashcards

Metabolism 1 2 Flashcards

1
Q

What processes are involved in metabolism?

A

catabolism and anabolism

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2
Q

What is catabolism

A

breakdown of complex molecules into simpler molecules and release of energy via ATP

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3
Q

What is anabolism

A

assembling simple substances to form new complex molecules via energy from ATP

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4
Q

Where are the energy stored in ATP?

A

High energy bonds of the three phosphates

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5
Q

What happens when ATP is used for energy?

A

It is hydrolyzed to ADP and inorganic phosphate

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6
Q

What is oxidation?

A

loss of electron such as when you add oxygen or remove a hydrogen

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7
Q

What is reduction?

A

addition of an electron such as when you add hydrogen or remove oxygen

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8
Q 
Name the following compounds in terms of their oxidation status from least to greates
Methane
Formic Acid
Formaldehyde
Methanol
Carbon Dioxide
A 
CH4 (methane)
CH3OH(Methanol)
CH2O (Formaldehyde)
HOCHO (Formic Acid)
CO2 (Carbon Dioxide)
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9
Q

What are the most important electron carriers and their reduced forms ?

A

NAD+ =>NADH

NADP+ => NADPH

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10
Q

What is the common product that the major products of digestion of carbs, lipids, and proteins in the metabolic pathway lead to?

A

Acetyl CoA

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11
Q

What is the primary function of Acetyl-CoA

A

Convey carbon atom within the acetyl group to the TCA Cycle to be oxidized for energy production

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12
Q

Where is Acetyl CoA generated?

A

In the mitochondrial matrix

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13
Q

Where does the conversion of pyruvate to Acetyl CoA take place?

A

Mitochondrial Matrix

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14
Q

What are the 4 fates for Acetyl CoA and which is the primary fate?

A
  1. Oxidize acetyl groups in CAC for energy generation and produce ATP, CO2, H2O (Primary fate)
  2. Lipogenesis: Form fatty acids -> esterification -> form triacylglycerol
  3. Ketogenesis: Form ketone bodies
  4. Cholesterologenesis: form cholesterol to synthesize steroids
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15
Q

Can all components of metabolism (fat, protein, carbs) give rise to the synthesis and storage of fat?

A

Yes, by first converting into acetyl CoA

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16
Q

How are fructose and galactose metabolized?

A

Converted to intermediates in the same glycolysis pathway as glucose

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17
Q

What happens to excess carbohydrates?

A

stored in glycogen

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18
Q

Which organs have the largest stores of glycogen?

A

liver, heart, skeletal muscle

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19
Q

What happens to fatty acids?

A

Go through beta oxidation in mitochondria to form Acetyl-CoA

Otherwise, they form Triacylglycerols to be stored in adipose tissue

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20
Q

Can cell without a mitochondria have beta oxidation?

A

No because it require mitochondria to beta-oxidize fatty acids to form Acetyl-CoA

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21
Q

What happens to amino acids in metabolism?

A

Metabolized to form either Acetyl-CoA or an intermediate in the CAC

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22
Q

What is the downside to the metabolism of amino acids

A

Formation of ammonia which is toxic at high levels if not converted to uera

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23
Q

How are amino acids stored?

A

As proteins

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24
Q

What are the fuel preferences for the liver?

A

fatty acids
glucose
amino acids

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25
Q

What are the fuel preferences for adipose tissue?

A

Fatty acids

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26
Q

What are the fuel preferences for skeletal muscle

A

At rest: fatty acids

Exertion: glucose

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27
Q

What are the fuel preferences for heart muscle?

A

Fatty acids (still uses everything though just prefers this)

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28
Q

What are the fuel preferences for the brain?

A

Fed state: glucose

Starvation: ketone bodies/glucose

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29
Q

What is the driving force for the coordination of metabolism?

A

To provide the normal range of glucose levels for hte brain as nerve cells die in a very short period of time

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30
Q

What happens in a fasted state (starvation)

A

low blood insulin -> activate lipolysis in adipose tissue -> raise blood levels of fatty acids -> used in preference to glucose via beta oxidation of fatty acid in liver for ATP used for gluconeogenesis
Brain uses ketone bodies as alternative when ketone body levels iin blood are high enough, BUT brain will never lose its requirement for glucose

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31
Q

What are hte kcal/g for carbs, proteins, fats?

A

Carbs:4
Fats:9
Protein:4

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32
Q

Carbs/Source/Enzymes:

Amylopectin

A

Source; Potatoes, rice, corn, bread

Enzyme: Isomaltase

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33
Q

Carbs/Source/Enzymes::

Amylose

A

Source; Potatoes, rice, corn, bread

Enzyme: Maltase

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34
Q

Carbs/Source/Enzymes:

Starch

A

Mix of amylose and amylopectin

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35
Q

Carbs/Source/Enzymes:

Sucrose

A

Source; Table Sugar, desserts

Enzyme: Sucrase

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36
Q

Carbs/Source/Enzymes:

Lactose

A

Source: Milk, milk products
Enzyme: Lactase

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37
Q

Carbs/Source/Enzymes:

Fructose

A

Source: Fruit, honey
Enzyme: none

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38
Q

Carbs/Source/Enzymes:

Glucose

A

Source: Fruit, hooney, grapes
Enzyme: none

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39
Q

Carbs/Source/Enzymes:

Maltose

A

Source: Barley
Enzyme: Maltase

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40
Q

Carbs/Source/Enzymes:

Trehalose

A

Source: Young Mushroom
Enzyme: Trehalase

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41
Q

Carbs/Source/Enzymes:

Cellulose

A

Source: Fiber in plant foods
Enzyme: none; not digestible by humans, forms bulk of feces

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42
Q

What is starch

A

Polymer of glucose

Mix of alpha 1-4 and alpha 1-6 linkages

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43
Q

What breaks down starch?

A

Amylase (Salivary and pancreatic)

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44
Q

What are the major disaccharides and their components?

A

Sucrose: glucose and fructose
Lactose: glucose and galactose

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45
Q

What breaks down disacchrides?

A

disaccharidases (Sucrase, Lactase) found in brush border of small intestine

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46
Q

What happens to sacchrides that are not hydrolyzed?

A

Cannot be absorbed, and reach lower tract of intestine at which point past the lower ileum are bacteria

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47
Q

What causes lactose intolerance and what problems does it cause?

A

Deficiency in lactase enzyme production
Dietary lactose not sufficiently hydrolyzed/absorbed -> stays in intestine and causes osmosis of water into the intestine
Intestinal Bacteria can also metabolize lactose to form lactic acid, H+, CO2, CH4 gas, causes bloating, flatulence, and diarrhea

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48
Q

What is the treatment for lactose intolerance?

A

Avoid milk and milk products from diet

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49
Q

Whats the difference in lactose intolerance between infants and adults

A

Infants: congenital lactase deficiency starting at birth causing changes in the secondary structure of the enzyme and truncating it abnormally

Adults: lactose intolerance caused by gradual decrease in activity of hte LCT gene

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50
Q

Insulin

A

Peptide hormone
Secreted by beta cells of pancreas
Function: maintain low blood glucose and promote glycolysis on long term basis and glycogen synthesis

Hyperglycemia => inc insulin

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51
Q

Glucagon

A

Peptide homrone
Secreted by alpha cells of pancreas when blood glucose too low
Causes liver to release glucose into the blood

Hypoglycemia => inc glucagon

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52
Q

Glycogenesis

A

Breakdown of glycogen to G1P and glucose in liver and muscles by enzyme glycogen phosphorylase

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53
Q

Glycolysis

A

Metabolic pathway in cytoplasm in which a single glucose is converted to : 2 pyruvic acid, 2 ATP, 2 NADH and 2 water

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54
Q

Gluconeogenesis

A

Generation of glucose from non-carb carbon substrates like pyruvate, lactate, glycerol, glucogenic amino acids

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55
Q

Glycogenesis

A

Formation of glycogen from glucose

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56
Q

Fed State induces what?

A

Increased glycogen formation
Increased pyruvate and lactate formation via glycolysis
Increased formation of Acetyl-CoA from pyruvate oxidation which feeds into the TCA cycle
Increased insulin release from pancreatic beta cells in response to influx of glucose
No gluconeogenesis by liver

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57
Q

Fasted/Starved state induces what?

A

Increased levels of glucagon by alpha pancreatic cells
Increased levels of epinephrine by adrenal medulla
Increased glycogen degradation to produce G6P
Increased gluconeogenesis

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58
Q

How is carbohydrate metabolized in RBCs?

A

RBCs lack mitchondria so it cannot use amino acid or fatty acid metabolism. Depend entirely on glycolysis

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59
Q

How is carbohydrate metabolized in brain tissue cells?

A

Brain has an absolute requirement for glucose and a very minimal reserve of glycogen. Can carry out TCA cycle

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60
Q

How is carbohydrate metabolized in muscle/heart cells?

A

Have major stores for glycogen. Muscles cannot mobilize glycogen or glucose into circulation. Can carry out TCA and also produce lactic acid from pyruvate

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61
Q

How is carbohydrate metabolized in adipose tissue cells?

A

Convert excess glucose into fat. Can form glycogen but does not carry out TCA

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62
Q

How is carbohydrate metabolized in liver cells?

A

glycolysis, gluconeogenesis, glycogen synthesis, PP Pathway

63
Q

What hexose transporter move down a concentration gradient?

A

GLUT1-4

64
Q

What hexose transporters move agasint a concentration gradient and what does it use for energy?

A

SGLT1, SGLT2, uses electrochemical gradient of sodium to co-transport with hexose

65
Q

Which transporters have a high affinity for glucose?

A

GLUT 1,3,4

66
Q

Which transporters have a low affinity for glucose and why is this important?

A

GLUT2; allows it to change transport rate in proportion ot increasing glucose concentrations after a meal

67
Q

Which GLUT transporters are glucose transporters?

A

Class I: GLUT 1-4

68
Q

Which GLUT transproters are fructose transporters?

A

Class II : GLUT 5,7,9,11

69
Q

SGLT1

A

Co-transport 1 glucose or galactose with 2 sodium ions
Does not transport fructose
Insulin independent

70
Q

SGLT2

A

Co-transports glucose and sodium ions

Does not transport fructuse of galactose

71
Q

GLUT1

A

Insulin independent

Found in RBCS, brain, endothelial cells

72
Q

GLUT2

A

Insulin independent and low affinity
Found in liver(bring in glucose) , intestines (glucose out), kidney
Serves as glucose sensor in pacreatic beta cells

73
Q

GLUT4

A

Insulin DEPENDENT High affinity
Found in muscle, heart, adipocytes
Not active during fasting state

74
Q

GLUT 5

A

Fructose transporter

75
Q

What are the 3 enzymes that catalyze the regulated steps of glycolysis?

A

Hexokinase/Glucokinase: Glucose to G6P
Phosphofructokinase-1: F6P to F1,6bisphosphate
Pyruvate Kinase: PEP to pyruvate

76
Q

How are the enzymes of glycolysis regulated?

A

Allosterically
Covalent modifications
Amount/synthesis of enzymes

77
Q

Does glycolysis require a mitochondria?

A

No. Takes place in cytoplas. Found in all cell types

78
Q

What does Aldolase A do in glycolysis?

A

It’s the most highly regulated part of glycoclysis that carries out the splitting stage to produce dihydroxyacetone phosphate and glyceraldehyde3-phosphate

79
Q

What is allosteric regulation?

A

molecule or ligand interacts with enzyme active site to either speed it up or slow it down
Reversible and quick/transient

80
Q

What is covalent modification

A

Example: phosphorylation and dephosphorylation by kinase/phosphatase causing conformational changes that alter the activity of the enzyme

Insulin activates phosphatases to inhibit epinephrine and glucagon activity

81
Q

Where can hexokinase be found in?

A

All cells

82
Q

What regulates hexokinase?

A

Allosterically inhibited by its product, glucose-6 phosphate

83
Q

Is Hexokinase a constitutive enzyme?

A

Yes. Constitutive, non-inducible, constant amount with low Km for glucose (high affinity)

84
Q

Can hexokinase handle high levels of glucose?

A

No

85
Q

Where can glucokinase be found?

A

Liver and pancreas

86
Q

What’s unique about glucokinase?

A

Translocate between nucleus (inactive) and cytosol (active)

87
Q

How is glucokinase regulated?

A

Fructose 6-phosphate, a downstream product, decreases its activity by promoting translocation to nucleus

Glucose increases its activity by promoting translocation to cytosol

88
Q

Is glucokinase constitutive?

A

No; It is an inducible enzyme and it’s synthesis is induced by INSULIN
Has a high Km

89
Q

Can glucokinase handle high levels of glucose?

A

Yes

90
Q

What reaction does PFK-1 (Phosphofructokinase 1) catalyze?

A

Frcutose 6 phosphate -> Fructose 1,6 bisphosphate

91
Q

What are the positive regulators for PFK1

A

Fructose-2,6 bis phosphate, AMP, ADP

92
Q

What are then negative regulators for PFK1

A

ATP, citrate

93
Q

How is Fructose 2,6 bis phosphate formed and what is its role?

A

Major activator of hepatic PFK1

Formed from fructose-6-phosphate by a non-glycolitic step catalyzed by PFK-2

94
Q

What is the reaction forming fructose 2,6 bisphosphate

A

F6P –PFK2+ATP –>Fructose 2,6 bisphosphate

95
Q

When is fructose 2,6 bisphosphate formed?

A

When blood glucose and insulin levels are high

It is NOT formed when blood glucose is low

96
Q

What inhibits the formation of fructose 2,6 bisphosphate in the liver?

A

Glucagon and epinephrine indirectly by stimulation formation of cAMP and activating PKA to phosphorylate the kinase domain of PFK-2 and inhibiting it.

97
Q

What does PFK2 do?

A

Forms Fructose 2,6 bisphosphate from Fructose 6 phosphate

98
Q

What inhibits PFK2

A

Phosphorylation by PKA

99
Q

Is PFK-2 uni or bi directional?

A

Bidirectional. It can make fructose 2,6 bisphosphate as well as convert it back to fructose 6 phosphate

100
Q

How can PFK-2 carry out both the forward and reverse reactions?

A

It has both a kinase domain and a phosphatase domain

101
Q

What happens when formation of Fructose 2,6 bis phosphate is blocked?

A

Hepatic glycolysis is blocked since Fructose 2,6 bisphosphate is a positive regulator of PFK-1 reaction to form Fructose 1,6 bisphosphate from F6P in the glycolysis pathway

102
Q

What is citrate and what does it do with regards to PFK-1

A

CAC intermediate formed in the mitochondria that accumulates when ATP production in mitochondria is high -> isocitrate dehydrogenase (CAC enzyme) inhibited -> leading to buildup

Inhibits PFK-1 enzyme to signal that there is enough ATP generation going on and to halt progression of glycolysis

103
Q

Why does ATP inhibit PFK-1?

A

It signals that there is enough cytosolic ATP

104
Q

Why are AMP and ADP activators of PFK-1

A

Associated with low energy and low cytoplasmic ATP and aneed for glycolysis to replenish ATP

105
Q

Under normal conditions, what role does fructose-26 bisphosphate play in PFK-1 activity?

A

It is essential. If it is not present, PFK-1 is inhibited under normal conditions

106
Q

How does regulation of heart/skeletal muscle differ from hepatic cells?

A

Epinephrine inhibits hepatic glycolysis but stimulates hear/skeletal muscle glycolysis ( activates PFK-2 in heart and skeletal muscle and thus activates glycolysis by favoring F2,6BP formation)
There are no glucagon receptors in heart and skeletal muscles

107
Q

Why does epinephrine activate PFK-2 in heart/skeletal muscle but opposite in hepatic cells?

A

PFK-2 is of a different form in heart and skeletal muscle than hepatic cells. Lacks a hydroxyl group in the kinase domain and has a hydroxyl in the phosphatase domain -> allows kinase activity and thus formation of F26BP

108
Q

What reaction does pyruvate kinase catalyze in glycolysis?

A

PEP -> pyruvate and formation of ATP

109
Q

What activates pyruvate kinase?

A

Fructose 1,6 bisphosphate (feeds forward reaction)

110
Q

What inhibits pyruvate kinase?

A

ATP

alanine: amino acid that increases in fasting mode and serves as precursor for gluconeogenesis

111
Q

What effect do glucagon and epinephrine have on pyruvate kinase?

A

Act vai cAMP and PKA to phosphorylate and thus inactivate hepatic pyruvate kinase

112
Q

What is needed to activate an inactivated pyruvate kinase?

A

Phosphoprotein phosphatase (remove phospho group)

113
Q

At low blood glucose what is the state of pyruvate kinase?

A

phosphorylated (inactive)

114
Q

At high blood glucose, what is the state of pyruvate kinase?

A

dephosphorylated (active)

115
Q

What genetic condition results from a deficiency of pyruvate kinase?

A

hemolytic anemia

116
Q

What are the counter-enzymes to the 3 allosterically regulated enzymes in the glycolytic pathway favoring gluconeogenesis?

A

Hexokinase: Glucose-6phosphatase
Phosphofructokinase-1 : Fructose 1,6 bisphosphatase
Pyruvate Kinase: PEP Carboxylase

117
Q

What effect do glucagon and epinephrine have on hepatic glycolysis?

A

inhibits it

118
Q

Where are glucagon’s effects most prominent at?

A

Liver. Glucagon receptors are present in the liver but not in skeletal muscle or heart; Released by alpha pancreatic cells at times of low blood glucose

119
Q

Where are epinephrine’s effects most promienent at?

A

Generally everywhere; Not limited to liver like glucagon
Inhibitiion of glycolysis in other cells preserves glucose for use by tissues that highly prefer glucose over other sources

120
Q

How does glucagon/epi regulate hepatic glycolysis?

A

Covalent modification (phosphorylation) of :
PFK-1: indirectly via inhibition of PFK-2
Pyruvate Kinase : direct

Decreases synthesis of the 3 irreversible enzymes of glycolysis

121
Q

What does increased insulin or decreased cAMP result in?

A

Increased synthesis of the 3 irreversible enzymes of glycolysis (Glucokinase, PFK-1, Pyruvate Kinase)

122
Q

What must be regenerated in order for glycolysis to continue?

A

NAD+
NAD/NADH is in limited supply in cytoplasm
NADH is oxidized when pyruvate is converted to lactate

123
Q

How can cytoplasmic NAD+ be regenerated?

A

LDH (cytosolic)
Malate-Aspartate Shuttle (Cytosolic + Mitochondria)
Glycerol-Phosphate Shuttle (Cytosolic + Mitochondria)

124
Q

Lactate Dehydrogenase

A

Catalyze conversion of Pyruvate +NADH to form Lactate and NAD+ (Overall: Get 2 lactate, 2 ATP, 2 H2O in this path)
Is present in all cells
Lactate is acidic and can lead to acidosis if accumulates

125
Q

What are the LDH Isozymes

A

LDH-5: M4: found in skeletal muscle and prefers catalyzing the conversion of pyruvate to lactate for high bursts of energy

LDH-4: kidneys, placenta, pancreas

LDH-3: lungs

LDH-2: ciruclatory system

LDH-1: H4: Heart muscle; Prefers conversion lactate to pyruvate to allow more sustained energy production via Acetyl-CoA and TCA

126
Q

What is the normal ratio in serum of lactate/pyruvate?

A

10/1

127
Q

What is Pyruvate Dehydrogenase (PDH)?

A

Multienzyme that catalyzes conversion of Pyruvate to Acetyl-CoA

128
Q

What are the isozymes of PDH

A

E1: pyruvate dehydrogenase activity
E2: dihydrolipoyl transacetylase
E3: dihydrolipoyl dehydrogenase

129
Q

What happens to pyruvate by PDH?

A

Decarboxylated to a 2C compound and added to thiamine pyrophosphate, which donates the acetyl group to the E2 -> eventually transfers to become Acetyl-CoA

Lipoic acid is then alternated between ox and red forms by E3

130
Q

What does PDH deficiency lead to?

A

Inability to make Acetyl CoA -> impairs tissue function and survival. Brain and heart mainly affected

131
Q

What does arsenic poinson cause?

A

Prevents the shuttling of the lipoic acid between ox and red forms and thus mimics PDH deficiency, leading to pyruvate and lactate accumulations in the blood

132
Q

Does glucagon and epi inhibit PDH?

A

No

133
Q

What inhibits PDH?

A

End products via allosteric regulation (NADH, Acetyl COA)

Phosphorylation of PDH inhibits its activity

134
Q

What does LDH-1>LDH-2 indicate?

A

Potential MI

135
Q

Which enzyme complex of PDH requires which vitamin cofactor to be active?

A

E1 (PDH): Thiamine (B1)
E2(DHL Transacetylase): Pantothenate (B5)
E3 (DHL dehydrogenase): Riboflavin (B2) + Niacin (B3)

136
Q

What happens if have deficiency of Vitamins B1, B2, B3, B5?

A

Less active PDH

137
Q

What happens in LDH deficiency?

A

Pts cant exercise due to inability to use glycolysis for ATP under anaerobic conditions

NAD+ levels are insufficient due to inability to carry out glycolysis.

138
Q

What are the inputs and outputs of glycolysis?

A

Inputs: glucose, 2NAD+, 2 ATP, 4ADP
Output: 2 pyruvate, 2 NADH, 4 ATP, 2 ADP

139
Q

Does lactate formation require oxygen?

A

No. Glycolysis does not require O2 as well

140
Q

Does PDH and TCA require oxygen?

A

YEs. Aerobic

141
Q

What processes require O2?

A

REoxidation of mitochondrial NADH from PDH enzyme

Reoxidation of cytosolic NADH by the shuttles

142
Q

What does low levels of cellular NADH lead to?

A

decreased lactate formation

143
Q

How can we metabolize galactose and fructose?

A

Enzymes to convert them to a glycolytic intermediate

144
Q

What enzymes are needed for galactose metabolism

A

Galactokinase + Gal-1-P Uridyltransferase

Galactose ->Galactose1P -> Glucose 1P -> G6P

145
Q

What is galactosemia?

A

genetic disorder caused by deficiency of either galactokinase or Gal-1-P-uridyltransferase

146
Q

What forms in galactosemia?

A

Galactitol (toxic)

147
Q

What sx are found in galactosemia?

A

Cataracts, increased blood galactose, galactosuria

148
Q

Whats the main difference between galactokinase deficiency and Gal-1P-uridyl Transferase deficiency (classical galactosemia)

A

Autosomal Recessive
See Galactose 1 Phosphate accumulation in addition to the typical sx of galactosemia
Leads to hepatic and brain dysfunctions

149
Q

How do you treat galactosemia?

A

rapid detection and removal of galactose (lactose) from diet

150
Q

What enzymems are needed for fructose metabolism?

A

Fructokinase: produce F1P

Aldolase B: cleaves F1P to glyceraldehyde3 phosphate or DHAP(a glycolytic intermediate)

151
Q

What happens in Aldolase B deficiency?

A

Accumulation of fructose 1 phosphate (toxic) and depletion of ATP (P tied up in F6P)

Low glucose levels

152
Q

What are sx seen with fructose intolerance? Treatment?

A

hypoglycemia, vomiting, jaundice, liver failure

Tx: avoid foods with fructose

153
Q

What is essential fructosuria?

A

defect in fructokinase; fructose found in blood and urine but benign and asymptomatic

Physiology Metabolism (11 decks)

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