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Foundations > Metabolism > Flashcards

Metabolism Flashcards

1
Q

Result of one round of fatty acid oxidation/beta oxidation

A

1 Acetyl-CoA, 1 NADH, 1 FADH2, H+, fatty acyl-CoA that is 2 carbons shorter

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2
Q

Dehydrogenase (1/4 fatty acid oxidation)

A

Enzyme: dehydrogenase
Occurs between the second and third carbons of fatty acyl-CoA
Products=trans double bond between C-2 and C-3; FADH2

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3
Q

Hydration(2/4 fatty acid oxidation)

A

Enzyme: hydratase
Water is added to double bond
Products: 3-hydroxy fatty acyl chain

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4
Q

Dehydrogenation (3/4 fatty acid oxidation)

A

Enzyme: dehydrogenase
Two hydrogens are moved to NAD+
Products: NADH + H+; 3-keto fatty acyl chain

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5
Q

Formation of Acetyl-CoA(4/4 fatty acid oxidation)

A

Enzyme: thiolase
Bond between C-2 and C-3 is broken/ free CoA is linked to C-3
Products:a Acetyl-CoA and a fatty acyl-CoA chain that is 2 carbons shorter

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6
Q

Rate-limiting step of fatty acid oxidation/beta oxidation

A

Transport of fatty acid into the mitochondrial matrix via the carnitine shuttle

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7
Q

To make fatty acyl-CoA

A

Enzyme: acyl-CoA synthase
ATP—> AMP +PP
Creates a high energy thioester linkage

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8
Q

What plasma protein is utilized by fatty acids to be transported into cells?

A

Albumin

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9
Q

What happens to the products from fatty acid oxidation/beta oxidation?

A

Acetyl-CoA goes to the CAC

NADH + FADH2 go to the ETC

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10
Q

How many kcal are in 1g of fats?

A

9 kcal

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11
Q

How many kcal are in 1g of carbohydrates?

A

4kcal

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12
Q

Energy yield from 1 Acetyl-CoA

A

10 ATP

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13
Q

Energy yield for 1 NADH

A

2.5 ATP

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14
Q

Energy yield for 1 FADH2

A

1.5 ATP

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15
Q

What is the maximum energy yield for glucose oxidation?

A

32 ATP

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16
Q

Why do lipids have higher energy content?

A

Fatty acids are more reduced than glucose and when they are oxidized the larger amount of protons released and the result of acetyl-CoA leads to lots of ATP production

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17
Q

Ketone bodies

A

Synthesized in the LIVER from EXCESS Acetyl-CoA
Exported from the liver to be used as a fuel source

Acetoacetate(non-physiological) and beta-hydroxybutyrate(physiological)

4 carbon molecules/carboxylic acids —> water soluble

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18
Q

Ketoacidosis

A

High concentration of ketone bodies in the blood

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19
Q

Why are ketone bodies a good source of energy for peripheral tissues?

A

Soluble in water and don’t need a transport protein
Made in the liver in response to HYPOglycemia
Used routinely in extrahepatic tissues(skeletal/cardiac muscle, intestinal mucosa, and renal cortex
Alternative fuel for brain so that is can spare blood glucose and reduce muscle protein loss during extended fasting

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20
Q

Pathological ketoacidosis

A

Seen in Type I Diabetes Mellitus
Concentration of ketone bodies in blood(ketonemia) and urine(ketonuria)
Can lead to fruity smell on the breath due to increased production of acetone

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21
Q

Ketogenesis/Ketone Body Synthesis

A

4 step process to turn excess Acetyl-CoA into ketone bodies

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22
Q

Acetoacetyl-CoA Formation(1/4 ketogenesis)

A

In: 2 Acetyl-CoA
Enzyme: thiolase
Out: 1 Acetoacetyl-CoA and 1 free CoA

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23
Q

HMG-CoA Formation (2/4 ketogenesis)

A

In: 1 Acetoacetyl-CoA and 1 Acetyl-CoA
Enzyme: HMG-Synthase(in any cells that makes cholesterol)
Out: hydroxymethylglutaryl-CoA = HMG-CoA and 1 CoA

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24
Q

Acetoacetate Formation (3/4 ketogenesis)

A

In: HMG-CoA
Enzyme: HMG-CoA Lyase(LIVER ONLY)
Out: Acetoacetate and 1 Acetyl-CoA

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25
Q

Ketone Body Interchange (4/4 ketogenesis)

A

In: Acetoacetate and NADH
Enzyme: beta-hydroxybutyrate dehydrogenase
Out: beta-hyrdroxybutyrate and NAD+

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26
Q

When is ketone body synthesis favored?

A

During fatty acid oxidation—> more NADH is present

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27
Q

Ketone Body Utilization/Ketolysis

A

Ketone bodies go from liver to peripheral cells where they will be converted into acetyl-CoA

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28
Q

Acetoacetyl-CoA Formation(1/2 Ketolysis)

A

PART 1:
In: beta-hydroxybutyrate and NAD+
Enzyme: betaxhydroxybutyrate dehydrogenase
Out: Acetoacetate and NADH

PART 2:
In: Acetoacetate and succinyl-CoA
Enzyme: transferase
Out: acetoacetyl-CoA and succinate

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29
Q

Acetyl-CoA Formation (2/2 Ketolysis)

A

In: Acetoacetyl-CoA and free CoA
Enzyme: Thiolase
Out: 2 Acetyl-CoA

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30
Q

Energy yield of ketolysis

A

Resulting acetyl-CoA goes out to CAC and NADH goes to ETC

Beta-hydroxybutyrate = 21.5 ATP
Acetoacetate = 19 ATP
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31
Q

Fatty Acid Biosynthesis

A

Mostly liver; can occur in adipose
Synthesized in CYTOPLASM
Precursor is Acetyl-CoA—> needs shuttle to get across mitochondrial membrane
Occurs in response to HYPERgylcemic conditions and in response to INSULIN

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32
Q

Acetyl-CoA shuttle

A

1- acetyl-CoA+oxaloacetate=citrate (citrate synthase)
2- citrate leaves mitochondrial matrix to cytoplasm
3- citrate is cleaved = OAA + acetyl-CoA (ATP-citrate lyase)
4- OAA —> pyruvate (2 step process)
5- pyruvate is transported to mitochondrial matrix
6- pyruvate —> OAA in matrix (pyruvate carboxylase)

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33
Q

Formation of Malonyl-CoA (fatty acid biosynthesis)

A 
Primary regulatory step in fatty acid biosynthesis/rate-limiting
ACTIVATED = INSULIN
In: Acetyl-CoA and CO2 and ATP
Enzyme: acetyl-CoA carboxylase 
Out: malonyl-CoA and ADP
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34
Q

What is the effect of insulin and glucagon on acetyl-CoA carboxylase?

A

INSULIN = ACTIVATION

GLUCAGON = INHIBITION

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35
Q

Enzyme: Fatty Acid Synthase (FAS) in fatty acid biosynthesis

A

Is activated in hyperglycemic conditions where there is an increase of glucose uptake and excess carbohydrates get converted to fatty acids

Addition of 2 carbons from malonyl-CoA to carbonyl end of acyl receptors
Process turns NADPH to NADP+

Out: 16 carbon palmityl-CoA

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36
Q

What are the two essential fatty acids? Why are they essential?

A

Linoleic acid = omega-6
Alpha-linolenic acid = omega-3

The body cannot make fatty acids with CIS double bonds after position 9

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37
Q

Triacylglycerol Metabolism

A

Hepatocytes and intestinal epithelial cells
85% of total fuel stores for the body
Transported through blood via lipoproteins
Exported in chylomicrons and VLDL
adipose TAGs are released in response to FASTING

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38
Q

Triacylglycerol

A

Glycerol backbone

3 fatty acids linked via ester bonds

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39
Q

Fatty Acid Activation

A

In: TAG
Enzyme: acyl-CoA synthase
Out: fatty acyl-CoA

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40
Q

Glycerol 3-phosphate Production

A

1- reduction of glycolysis intermediate(dihydroxyacetone phosphate) by NADH

OR

2- phosphorylation of glycerol by ATP

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41
Q

Phosphatidic Acid Formation (lipogenesis 1/3)

A

In: G3P and 2 acetyl-CoA
Enzyme: acyl-CoA transferase
Out: phosphatidic Acid and 2 CoA

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42
Q

Diacylglycerol Formation (2/3 lipogenesis)

A

In: phosphatidic Acid and H2O
Enzyme: phosphohydralase
Out: 1,2-diacylglycerol and P

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43
Q

Formation of Triacylglycerol (3/3 lipogenesis)

A

In: 1,2-diacylglycerol and acetyl-CoA
Enzyme: acyl-CoA transferase
Out: triacylglycerol and CoA

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44
Q

What are the effects of insulin and glucagon on lipolysis?

A 
GLUCAGON = ACTIVATE 
INSULIN = INHIBIT
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45
Q

Triacylglycerol to Diacylglycerol ( 1/3 lipolysis)

A

REGULATORY STEP
In: triacylglycerol and H2O
Enzyme: triglyceride lipase/hormone-sensitive lipase —> acts on fatty acid at C-3
Out: diacylglcerol and free fatty acid

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46
Q

Diacylglycerol to Monoacylglycerol (2/3 lipolysis)

A

In: 1,2-Diacylglycerol and H2O
Enzyme: diglyceride lipase —> acts on C-1
Out: 2-monoacylglycerol and free fatty acid

47
Q

Monoacylglycerol to Glycerol (3/3 lipolysis)

A

In: 2-monoglycerol and H2O
Enzyme: monoglyceride lipase
Out: glycerol and free fatty acid

48
Q

Lipolysis Net Reaction

A

Triacylglycerol and 3 H2O —> Glycerol and 3 fatty acids

49
Q

What form is most dietary fat found in?

A

Triacylglycerols (TAGs)

50
Q

How much energy is conserved in a biologically useful form? What is it referred to as?

A

40% Chemical Power

51
Q

What are the activated precursors(3) that are used to build macromolecules?

A

UDP-glucose, fatty acyl-CoA, aminoacyl-tRNA

52
Q

What term is used to describe a metabolic pathway that produces energy and degrades macromolecules?

A

Catabolic

53
Q

What term is used to describe metabolic pathways that carry out the activation of precursors and the synthesis of macromolecules?

A

Anabolic

54
Q

Catabolism of precursors from lipids, carbohydrates, and proteins produces…?

A

Acetyl-CoA (to be used in the CAC)

55
Q

What are the high energy transferring molecules used in the CAC?

A

NADH and FADH2

56
Q

The CAC is an aerobic pathway. Where does the oxygen come from?

A

H2O

57
Q

What is the difference between citric acid and citrate?

A

citric acid is protonated

58
Q

What are the 8 intermediates of the CAC?

A

citrate and isocitrate(6C)
alpha-ketogluterate(5C)
succinate, furmate, malate, and oxaloacetate(4C)
succinyl-CoA (succinate+CoA)

59
Q

How many oxidation-reduction reactions are there in the CAC and what enzymes catalyze these?

A

4, dehydrogenases–> 3 convert NAD+ to NADH and 1 converts FAD to FADH2, two also participate in decarboxylation reactions producing CO2

60
Q

How much GTP is produced in the CAC?

A

1 GTP molecule

61
Q

Where in the cell is the Electron Transport Chain?

A

Mitochondrial Inner Membrane

62
Q

What molecules does the Electron Transport Chain/Respiratory Chain accept electrons from?

A

NADH and FADH2

63
Q

What makes up the ETC/Respiratory Chain?

A

four transmembrane complex and a small,mobile, hydrophobic non-protein electron carrier–Ubiquinone Q/coenzyme Q– and a peripheral protein–cytochrome C

64
Q

NADH donates 2 electrons to which complex?

A

Complex I

65
Q

FADH2 donates 2 electrons to which complex?

A

Complex II

66
Q

What happens after electrons are donated to Complex I and Complex II?

A

the electrons are transferred to coenzyme Q which is reduced to QH2–> QH2 will then transfer the electrons to Complex III

67
Q

What cytochromes are in Complex III?

A

cytochrome b and cytochrome c1–> sits on the cytoplasmic side of the inner membrane bridging Complex III and Complex IV

68
Q

What is the function of cytochrome C in the ETC?

A

It transfers electrons from Complex III to Complex IV

69
Q

Complex IV, also known as cytochrome oxidase, contains what two cytochromes and what other ion?

A

cytochrome a and cytochrome a3 and copper ions

70
Q

Describe how Complex IV transfers electrons.

A

Complex IV has an O2 binding site where it sequentially transfers electrons through the cytochromes to each oxygen atom (overall 2 protons and 2 electrons are added to each oxygen to make H2O

71
Q

How is some energy conserved as electrons are transferred from high energy molecules to low energy molecules?

A

Energy is conserved by the ETC complexes because they pump protons from the matrix to the cytoplasmic side of the inner membrane as they transfer electrons. This created concentration gradient and membrane potential captures about 40% of energy.

72
Q

What kind of molecule is Complex V?

A

An ATPase

73
Q

How does Complex V work?

A

it is driven by the proton gradient to drive ATP synthesis from ADP and P through a process called oxidative phosphorylation

74
Q

Why can cytochromes accept and donate electrons?

A

Heme prosthetic group–> interconverts between the oxidized (Fe3+) and reduced (Fe2+) states.

75
Q

How many heme groups does each cytochrome contain? What does this mean for electron transport?

A

1 cytochrome has 1 heme group so it can only transfer 1 electron at a time.

76
Q

What does aerobic capacity depend on?

A

density of mitochondria

77
Q

In what state MUST iron be in on a RBC for proper O2 binding and release?

A

Reduced/ ferrous/Fe2+

78
Q

Describe hemoglobin and myoglobin.

A

H- tetrameric, each subunit possess a heme, can carry up to 4 O2, RBC
M- monomeric, single heme group, the more aerobic the muscle, the higher the concentration of myoglobin

79
Q

Why do hemes absorb visible light?

A

due to the conjugated double bonds in the porphyrin ring to which the iron is bound

80
Q

How much ATP is formed via the oxidation of one Acetyl-CoA to 2 CO2?

A

10 ATP
3 NADH = 7.5 ATP
1 FADH2 = 1.5 ATP
1 per GTP

81
Q

PFK1 is allosterically regulated by the adenosine pool. What ACTIVATES PFK1?

A

ADP and AMP

82
Q

PFK1 is allosterically regulated by the adenosine pool. What INHIBITS PFK1?

A

ATP –> don’t need energy produced from glycolysis

83
Q

Effectors that inhibit enzyme activity are called?

A

negative effectors

84
Q

Effectors, that increase enzyme activity are called?

A

positive effectors

85
Q

Liver cells maintain a consistently high [ATP]. How does PFK1 overcome this?

A

Allosteric enzymes usually have MULTIPLE effector molecules. PFK1 has a second effector molecule, fructose 2,6-biphosphate that is produced in response to insulin binding and is degraded in response to glucagon binding.
HYPOglycemia= no F2,6BP is bound, ATP is bound, PFK1 is inhibited
HYPERglycemia= insulin binds to hepatocyte receptors, F2,6BP binds to allosteric site, overcomes ATP inhibition, PFK1 is activated

86
Q

Reversible phosphorylation, a form of covalent modification of enzymes, will occur on what amino acid side groups?

A

serine, threonine, and tyrosine –> all have an open OH group

87
Q

Where does the phosphate group come from in reversible phosphorylation?

A

ATP

88
Q

Describe the effect of covalent modification on glycogenesis in hepatocytes during hyper/hypoglycemic conditions.

A

Enzyme: glycogen synthase
Hyper: insulin, phosphatase, -OH form,GS is ACTIVE
Hypo: glucagon, kinase, -P form, GS is INACTIVE

89
Q

Describe the effect of covalent modification on glycogenolysis in hepatocytes during hyper/hypoglycemic conditions.

A

Enzyme: Phosphorylase
Hyper: insulin, -OH form, INACTIVE
Hypo: glucagon, -P form, ACTIVE

90
Q

What is genetic regulation?

A

cells can regulate the amount of enzyme present by altering their rates of degradation or synthesis

91
Q

Give two examples of genetic regulation in response to hyperglycemia (insulin)?

A

INDUCES glucokinase

REPRESSES glucose 6-phosphatase

92
Q

Give two examples of genetic regulation in response to hypoglycemia (glucagon)?

A

INDUCES glucose 6-phosphatase

REPRESSES glucokinase

93
Q

What metabolic processes will be active in a well-fed liver?

A

glycolysis, glycogenesis, pentose shunt, fatty acid synthesis, cholesterol synthesis, lipogenesis

94
Q

What metabolic processes will be active in a well-fed adipose?

A

glycolysis, pentose shunt, cholesterol synthesis, and to a lesser extent fatty acid synthesis–> most adipose TAGs are imported via VLDL and chylomicrons

95
Q

What metabolic processes will be active in a well-fed muscle cell?

A

glycogenesis–> can be anaerobic or aerobic based on presence of O2

96
Q

Insulin

A

released from beta cells in the pancreas
released in response to hyperglycemia
ANABOLIC hormone favoring biosynthesis

97
Q

Is glycolysis in the brain aerobic or anaerobic?

A

Anaerobic–> glucose is completely oxidized to CO2

98
Q

What is glucose converted into in RBCs?

A

lactate

99
Q

What metabolic processes will be active in a fasting liver cell?

A

glycogenolysis, gluconeogenesis, fatty acid oxidation

100
Q

What metabolic processes will be active in a fasting adipose cell?

A

lipolysis and fatty acid oxidation

101
Q

What metabolic processes will be active in a fasting muscle cell?

A

fatty acid oxidation, ketolysis, glycogenolysis–> fatty acids from adipose and ketone bodies from the liver are imported as fuel
NO GLUCAGON RECEPTORS

102
Q

Early Fasting State = glucagon>insulin–>sub-euglycemic

A

no food consumption for AT LEAST 4 hours, sufficient hepatic glycogen reserves, decrease in insulin release and increase in glucagon release

103
Q

Early Fasting State Liver

A

delivers enough glucose to the blood via glycogenolysis
gluconeogenesis produces a small amount of glucose since demand is minimal
ATP is produced by oxidizing fatty acids sent from adipose TAG reserves

104
Q

Early Fasting State Adipose

A

weak glucagon signal will stimulate lipolysis–> provides some fatty acids for tissues like the liver

105
Q

Early Fasting State Muscle

A

glycolysis continues to supply ATP, fatty acid oxidation can contribute to some energy production in more aerobic cells

106
Q

Early Fasting State Brain

A

glucose is main fuel source–> aerobic glycolysis, CAC, oxidative phosphorylation

107
Q

Early Fasting State RBC

A

glucose is ONLY fuel source, energy is produced via anaerobic glycolysis–> converted to lactate and exported

108
Q

Extended Fasting State

A

no food consumed for AT LEAST 2 days and NO hepatic glycogen reserves
hypoglycemia/glucagon»>insulin

109
Q

Extended Fasting State Liver

A

attempts to maintain glucose homeostasis via gluconeogenesis, no remaining glycogen stores
strong glucagon signal accelerates gluconeoenesis–> precursors consist mainly of amino acids(muscle) and glycerols and lactate(adipose), fatty acids from adipose(lipolysis) are used to make ATP and support ketogenesis releasing ketone bodies to be used as a fuel source

110
Q

Extended Fasting State Adipose

A

strong glucagon signal stimulates lipolysis providing large amounts of fatty acids and glycerol from TAG reserves

111
Q

Extended Fasting State Muscle

A

ketone bodies are main fuel source for aerobic ATP production, cortisol promotes proteolysis to generate amino acids that are sent to the liver as gluconeogenic precursors

112
Q

Extended Fasting State Brain

A

the brain uses both ketone bodies and glucose as fuel for ATP production–> by decreasing its need for glucose muscle protein is spared because the rate of hepatic gluconeogenesis is decreased

113
Q

Extended Fasting State RBC

A

glucose is used to make ATP via anaerobic glycolysis–> lactate–> reconverted to glucose by hepatic gluconeogenesis

Foundations (6 decks)

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