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Biochemistry I > Chapter 28: Ketogenesis and Ketone Bodies > Flashcards

Chapter 28: Ketogenesis and Ketone Bodies Flashcards

1
Q

Energy rich, ketone bodies that are water soluble derivatives of lipids

A
  • Acetoacetate
  • Acetone
  • B-hydroxybutyrate
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2
Q

Acetoacetate, acetone, and B-hydroxyutyrate are metabolic fuels that are

A
  • Exported from the liver when glucose and oxaloacetate supplies are low
  • During periods of starvation
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3
Q

After 3 days of starvation

A
  • 30% of the brain’s energy requirements are met by ketone body utilization
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4
Q

After 40 days of starvation

A
  • 70% of the brain’s energy requirements are met by ketone body utilization
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5
Q

Ketone bodies can be readily employed as a fuel for the brain since they are

A
  • Small

- Readily cross the blood brain barrier

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6
Q

Ketone bodies (mostly acetoacetic acid and B-hydroxybutyric acid) may also serve as metabolic fuel for

A
  • Skeletal muscle tissue during exercise

- Diabetes mellitus when glucose is poorly utilized

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7
Q

Ketogenesis

A
  • The production of ketone bodies by liver mitochondria
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8
Q

Ketogenesis serves to

A
  • Regenerate CoA

- Allows B-oxidation to continue

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9
Q

Small amounts of ketone bodies may also be produces in

A
  • The kidney
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10
Q

High rates of fatty acid oxidation in the kidney can generate large amounts of

A
  • Acetyl-SCoA
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11
Q

High levels of acetyl-SCoA can exceed the oxidative ability of the CAC, causing

A
  • The excess to enter ketogenesis
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12
Q

Ketogenesis is a metabolic pathway occurring in

A
  • Mitochondria of the hepatocyte
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13
Q

Ketogenesis converts excess acetyl-SCoA to

A
  • Acetoacetate

- B-hydroxybutyric acid

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14
Q

Metabolic sequence (steps) of ketogenesis

A
  1. B-ketothiolase
  2. HMG-SCoA synthase
  3. HMG-CoA lyase
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15
Q

B-ketothiolase catalyzes

A
  • Condensation of 2 molecules of acetyl-SCoA
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16
Q

Condensation of 2 acetyl-SCoA (by B-ketothiolase) forms

A
  • Acetoacetyl-SCoA

- H-SCoA

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17
Q

B-ketothiolase is working in/part of

A
  • Works in reverse direction

- Part of B-oxidation sequence

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18
Q

HMG-SCoA synthase is present solely in

A
  • Mitochondria of hepatocytes
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19
Q

HMG-SCoA synthase catalyzes

A
  • The combination of acetoacetyl-SCoA and acetyl-SCoA

- Rate limiting step of ketogenesis

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20
Q

The combination of acetoacetyl-SCoA and acetyl-SCoA (by HMG-SCoA synthase) forms

A
  • HMG-SCoA

- H-SCoA (which is required for B-oxidation)

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21
Q

The activity of HMG-SCoA synthase is increased with

A
  • Starvation

- Consumption of a high fat diet

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22
Q

HMG-CoA lyase

A
  • Cleaves HMG-CoA

- Generates acetoacetate and acetyl-SCoA

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23
Q

NAD-dependent B-hydroxybutyrate dehydrogenase can

A
  • Export acetoacetate from the liver

- Reduce acetoacetate to B-hydroxybutyrate

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24
Q

NAD-dependent B-hydroxybutyrate dehydrogenase is tightly bound to

A
  • The inner mitochondrial membrane
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25
Q

Acetoacetate can also be nonenzymically decarboxylated with the production of

A
  • Highly volatile acetone
  • CO2
  • Amount formed in healthy individuals is small
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26
Q

Acetoacetate accumulates in

A
  • Starvation

- Poorly controlled type I diabetes mellitus

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27
Q

When acetoacetate accumulates,

A
  • Acetone levels increase
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28
Q

Increased acetone levels cause the characteristic

A
  • Odor to breath of ketotic diabetic patients
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29
Q

The characteristic odor to breath of ketotic diabetic patients (due to increased acetone levels) is associated with the conditions of

A
  • Ketosis

- Ketonuria

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30
Q

Following synthesis in hepatic mitochondria, ketone bodies

A
  • Diffuse into the circulation

- Pass to peripheral tissues

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31
Q

Circulating ketone bodies in the peripheral tissues (heart, muscle, kidney cortex, and brain) may be

A
  • Oxidized for energy

- They are water-soluble fuels

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32
Q

Ketolysis

A
  • Oxidation of circulating ketone bodies for energy
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33
Q

Succinyl-CoA CoA transferase catalyzes

A
  • Production of acetoacetyl-SCoA and succinate from succinyl-SCoA and acetoacetate
  • It is induced during periods of starvation
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34
Q

Before circulating, water-soluble ketone bodies can be utilized for fuel, they must be

A
  • Activated by a mitochondrial acetoacetate

- Succinyl-CoA CoA transferase

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35
Q

Succinyl-CoA CoA transferase is found in

A
  • Peripheral tissues only
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36
Q

The lack of succinly-CoA CoA transferase in the liver prevents

A
  • Futile cycling of ketone bodies in the hepatocyte/liver
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37
Q

The cleavage of acetoacetyl-SCoA to 2 molecules of acetyl-SCoA (by B-ketothiolase) provides

A
  • An abundant source of energy

- (Because acetyl-SCoA can enter CAC for oxidation)

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38
Q

Factors that affect ketogenesis

A
  1. Substrate availability
  2. Energy status
  3. Endocrine factors
  4. Diet
  5. Uncontrolled diabetes mellitus
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39
Q

Under normal circumstances

A
  • Ketogenesis in the liver is minimal

- Circulating level of ketone bodies is low

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40
Q

Elevated levels of acetoacetate and B-hydroxybutyrte may lead to

A
  • A severe drop in blood pH

- Ketoacidosis

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41
Q

Ketogenesis is activated along with gluconeogenesis during

A
  • Periods of fasting and starvation
42
Q

The release of fatty acids from adipose tissue

A
  • Increases the availability of pathway substrate (acetyl-SCoA)
43
Q

Horomone-sensitive lipase of adipocytes is crucial to

A
  • The availability of acetyl-SCoA (active during fasting/starvation)
44
Q

If the demand for ATP is high,

A
  • Acetyl-SCoA is likely to be further oxidized to CO2 in the CAC (instead of ketogenesis)
45
Q

When demand for ATP is low (i.e. when ATP levels are high),

A
  • CAC activity is inhibited (at the isocitrate dehydrogenase step)
  • Ketogenesis is favored
46
Q

The rates of fatty acid oxidation and synthesis (and consequently acetyl-SCoA levels) are regulated by

A
  • Glucagon and insulin levels
47
Q

Glucagon inhibits

A
  • Acetyl-SCoA carboxylase activity
48
Q

Inhibition of acetyl-SCoA carboxylase activity by glucagon

A
  • Reduces malonyl-SCoA levels
  • Inhibits glycolysis
  • Favors ketogenesis
49
Q

Insulin increases the activity of

A
  • Acetyl-SCoA carboxylase
50
Q

Stimulation of acetyl-SCoA carboxylase activity by insulin

A
  • Increases malonyl-SCoA levels
  • Inhibits carnitine shuttle
  • Inhibits fatty acid oxidation
51
Q

Insulin also inhibits

A
  • Hormone-sensitive lipase
52
Q

Inhibition of hormone-sensitive lipase by insulin

A
  • Reduces ketogenesis

- Favors fatty acid biosynthesis

53
Q

During starvation,

A
  • Ketone body production is increased

- Levels of acetoacetate and B-hydruxybutyrate rise

54
Q

During the early stages of starvation, the elevated levels of ketone bodies can be used by

A
  • Cardiac tissue
  • Skeletal muscle
  • Allows the brain to utilize glucose
55
Q

In severe uncontrollable type I diabetes mellitus, the rate of lipolysis

A
  • Is elevated
  • Produces acetyl-SCoA
  • Oxaloacetate levels are diminished
56
Q

Production of acetyl-SCoA by elevated lipolysis rates occurs because

A
  • Insulin is no longer inhibiting the hormone-sensitive lipase
57
Q

Diminished levels of oxaloacetate by elevated lipolysis rates occurs because

A
  • It is needed for gluconeogenesis
58
Q

Acetyl-SCoA cannot enter the CAC, and therefore is used in

A
  • The production of ketone bodies

- (Acetoacetate and B-hydroxybutyrate)

59
Q

Strongly acidic ketone bodies (acetoacetate and B-hydroxybutyrate) are synthesized

A
  • Faster than they can be utilized

- Leads to acidosis, nausea, vomiting, and abdominal pain

60
Q

Ketonemia

A
  • High levels of acetone found in the blood
61
Q

Ketonuria

A
  • High levels of acetone found in the urine
62
Q

Ketonemia and ketonuria can be detected

A
  • On the breath as a fruity odor
63
Q

Ketoacidosis

A
  • Life-threatening

- Complication of of poorly-controlled type I diabetes

64
Q

(Review) Ketone bodies are

A
  • Water soluble
  • Lipid-based fuels
  • Utilized by the brain/muscle during starvation
65
Q

(Review) Acetoacetic acid and B-hydroxybutyric acid are produced in a physiological process from

A
  • 3 molecules of acetyl-SCoA
66
Q

(Review) HMG-SCoA synthase is

A
  • The rate limiting step in ketogenesis
67
Q

(Review) The rate of ketogenesis is increased

A
  • During periods of starvation

- In uncontrolled/untreated type I diabetes mellitus

68
Q

(Review) Pathway flux is regulated by

A
  • Substrate availability
  • Energy status
  • Endocrine factors
  • Diet
  • Diabetic status
69
Q

(Review) Ketoacidosis is

A
  • A life-threatening complication of poorly-controlled type I diabetes
70
Q

Ketoacidosis is a cimplication of type I diabetes, but

A
  • NOT type II diabetes
71
Q

In type I diabetes

A
  • Patient is unable to produce insulin

- Autoimmune problem

72
Q

In type II diabetes

A
  • Patient can produce (and often overproduces) insulin

- Body does not respond to insulin

73
Q

Ketoacidosis is seen much more prevalently in

A
  • Type I diabetes
74
Q

Organic acids

A
  • Water soluble derivatives of lipids
75
Q

Acetoacetate and 3-hydroxybutyrate

A
  • Not really ketones themselves, but are ketone bodies

- Can be made by the body

76
Q

Acetyl-CoA produced from FA mobilization during fasting inhibits/activates

A
  • Inhibits PDH

- Activates pyruvate decarboxylase

77
Q

OAA used in gluconeogenesis and acetyl-CoA is also used in

A
  • Ketogenesis
78
Q

Acetoacetate may be spontaneously

A
  • Converted to acetone (released on breath and thus not available)
  • Reduced to 3-HB by HBDH during ketogenesis
79
Q

PDH converts pyruvate to

A
  • Acetyl-CoA (also in the mitochondrial matrix)
80
Q

During periods of starvation, B-oxidation is also occurring in the inner mitochondrial membrane and produces

A
  • Acetyl-CoA
81
Q

Energy from B-oxidation drives

A
  • Gluconeogenesis (also during periods of starvation)
82
Q

Acetoacetate is converted to B-hydroxybutyrate by

A
  • B-hydroxybutyrate dehydrogenase

- NADH-dependent

83
Q

Ketone bodies in circulation are a means for

A
  • Transporting lipid in a water-soluble form
  • Do not require albumin for transport in blood
  • Do not require lipoproteins for transport in the blood
84
Q

Acetoacetyl-SCoA is converted to acetyl-SCoA, which

A
  • Enters the CAC

- Produces ATP

85
Q

Succinyl-CoA CoA transfease is NOT found in

A
  • The liver mitochondria where ketone bodies are produced
86
Q

Succinyl-CoA CoA transfease is induced

A
  • During periods of starvation
87
Q

In the periphery, acetoacetate (ketone bodies) are utilized as fuel when

A
  • Insulin/glucagon ratio is low (starving state)
88
Q

Extrahepatic tissues that utilize acetone (ketone bodies) as fuel during the starving state

A
  • Skeletal muscle
  • Heart
  • Renal cortex
89
Q

Significant utilization by brain druing starvation

A

Fatty acids cannot cross BBB

90
Q

Ketogenesis is interrelated with

A
  • Lipid, CHO, and amino acid metabolism in liver
91
Q

During high rates of FA oxidation

A
  • Large amounts of acetyl-SCoA are produced
92
Q

Production of acetyl-SCoA during high rates of FA oxidation

A
  • Exceeds the ability of CAC

- Ketogenesis is favored

93
Q

Substrate availability (regulation)

A
  • Release of FA and formation of acetyl-SCoA during starvation (i.e. when carbohydrate is not available)
94
Q

Energy status

A
  • Dictates the fate of acetyl-SCoA
95
Q

Ketogenesis is stimulated by glucagon since

A
  • Acetyl-SCoA carboxylase is inhibited

- Hormone-sensitive lipase is activated

96
Q

Ketogenesis is inhibited by insulin since

A
  • In the fed state, hormone-sensitive lipase is inhibited

- Acetyl-SCoA carboxylase is activated

97
Q

Cortisol and catecholamines

A
  • Increase ketogenesis
98
Q

Glucose sparing

A
  • Ketone bodies serve as fuel during starvation (insulin is low)
  • Particularly by brain
99
Q

Hormone-sensitive lipase is inhibited by

A
  • Insulin
100
Q

In type I diabetes, insulin production

A
  • Is low

- No insulin means HSL activity is unregulated

101
Q

In extreme ketosis, blood ketone levels may reach

A
  • 90mg/dL

- (Normal is 3mg/dL)

Biochemistry I (34 decks)

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