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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
Acetoacetate can also be nonenzymically decarboxylated with the production of
- Highly volatile acetone - CO2 - Amount formed in healthy individuals is small
26
Acetoacetate accumulates in
- Starvation | - Poorly controlled type I diabetes mellitus
27
When acetoacetate accumulates,
- Acetone levels increase
28
Increased acetone levels cause the characteristic
- Odor to breath of ketotic diabetic patients
29
The characteristic odor to breath of ketotic diabetic patients (due to increased acetone levels) is associated with the conditions of
- Ketosis | - Ketonuria
30
Following synthesis in hepatic mitochondria, ketone bodies
- Diffuse into the circulation | - Pass to peripheral tissues
31
Circulating ketone bodies in the peripheral tissues (heart, muscle, kidney cortex, and brain) may be
- Oxidized for energy | - They are water-soluble fuels
32
Ketolysis
- Oxidation of circulating ketone bodies for energy
33
Succinyl-CoA CoA transferase catalyzes
- Production of acetoacetyl-SCoA and succinate from succinyl-SCoA and acetoacetate - It is induced during periods of starvation
34
Before circulating, water-soluble ketone bodies can be utilized for fuel, they must be
- Activated by a mitochondrial acetoacetate | - Succinyl-CoA CoA transferase
35
Succinyl-CoA CoA transferase is found in
- Peripheral tissues only
36
The lack of succinly-CoA CoA transferase in the liver prevents
- Futile cycling of ketone bodies in the hepatocyte/liver
37
The cleavage of acetoacetyl-SCoA to 2 molecules of acetyl-SCoA (by B-ketothiolase) provides
- An abundant source of energy | - (Because acetyl-SCoA can enter CAC for oxidation)
38
Factors that affect ketogenesis
1. Substrate availability 2. Energy status 3. Endocrine factors 4. Diet 5. Uncontrolled diabetes mellitus
39
Under normal circumstances
- Ketogenesis in the liver is minimal | - Circulating level of ketone bodies is low
40
Elevated levels of acetoacetate and B-hydroxybutyrte may lead to
- A severe drop in blood pH | - Ketoacidosis
41
Ketogenesis is activated along with gluconeogenesis during
- Periods of fasting and starvation
42
The release of fatty acids from adipose tissue
- Increases the availability of pathway substrate (acetyl-SCoA)
43
Horomone-sensitive lipase of adipocytes is crucial to
- The availability of acetyl-SCoA (active during fasting/starvation)
44
If the demand for ATP is high,
- Acetyl-SCoA is likely to be further oxidized to CO2 in the CAC (instead of ketogenesis)
45
When demand for ATP is low (i.e. when ATP levels are high),
- CAC activity is inhibited (at the isocitrate dehydrogenase step) - Ketogenesis is favored
46
The rates of fatty acid oxidation and synthesis (and consequently acetyl-SCoA levels) are regulated by
- Glucagon and insulin levels
47
Glucagon inhibits
- Acetyl-SCoA carboxylase activity
48
Inhibition of acetyl-SCoA carboxylase activity by glucagon
- Reduces malonyl-SCoA levels - Inhibits glycolysis - Favors ketogenesis
49
Insulin increases the activity of
- Acetyl-SCoA carboxylase
50
Stimulation of acetyl-SCoA carboxylase activity by insulin
- Increases malonyl-SCoA levels - Inhibits carnitine shuttle - Inhibits fatty acid oxidation
51
Insulin also inhibits
- Hormone-sensitive lipase
52
Inhibition of hormone-sensitive lipase by insulin
- Reduces ketogenesis | - Favors fatty acid biosynthesis
53
During starvation,
- Ketone body production is increased | - Levels of acetoacetate and B-hydruxybutyrate rise
54
During the early stages of starvation, the elevated levels of ketone bodies can be used by
- Cardiac tissue - Skeletal muscle - Allows the brain to utilize glucose
55
In severe uncontrollable type I diabetes mellitus, the rate of lipolysis
- Is elevated - Produces acetyl-SCoA - Oxaloacetate levels are diminished
56
Production of acetyl-SCoA by elevated lipolysis rates occurs because
- Insulin is no longer inhibiting the hormone-sensitive lipase
57
Diminished levels of oxaloacetate by elevated lipolysis rates occurs because
- It is needed for gluconeogenesis
58
Acetyl-SCoA cannot enter the CAC, and therefore is used in
- The production of ketone bodies | - (Acetoacetate and B-hydroxybutyrate)
59
Strongly acidic ketone bodies (acetoacetate and B-hydroxybutyrate) are synthesized
- Faster than they can be utilized | - Leads to acidosis, nausea, vomiting, and abdominal pain
60
Ketonemia
- High levels of acetone found in the blood
61
Ketonuria
- High levels of acetone found in the urine
62
Ketonemia and ketonuria can be detected
- On the breath as a fruity odor
63
Ketoacidosis
- Life-threatening | - Complication of of poorly-controlled type I diabetes
64
(Review) Ketone bodies are
- Water soluble - Lipid-based fuels - Utilized by the brain/muscle during starvation
65
(Review) Acetoacetic acid and B-hydroxybutyric acid are produced in a physiological process from
- 3 molecules of acetyl-SCoA
66
(Review) HMG-SCoA synthase is
- The rate limiting step in ketogenesis
67
(Review) The rate of ketogenesis is increased
- During periods of starvation | - In uncontrolled/untreated type I diabetes mellitus
68
(Review) Pathway flux is regulated by
- Substrate availability - Energy status - Endocrine factors - Diet - Diabetic status
69
(Review) Ketoacidosis is
- A life-threatening complication of poorly-controlled type I diabetes
70
Ketoacidosis is a cimplication of type I diabetes, but
- NOT type II diabetes
71
In type I diabetes
- Patient is unable to produce insulin | - Autoimmune problem
72
In type II diabetes
- Patient can produce (and often overproduces) insulin | - Body does not respond to insulin
73
Ketoacidosis is seen much more prevalently in
- Type I diabetes
74
Organic acids
- Water soluble derivatives of lipids
75
Acetoacetate and 3-hydroxybutyrate
- Not really ketones themselves, but are ketone bodies | - Can be made by the body
76
Acetyl-CoA produced from FA mobilization during fasting inhibits/activates
- Inhibits PDH | - Activates pyruvate decarboxylase
77
OAA used in gluconeogenesis and acetyl-CoA is also used in
- Ketogenesis
78
Acetoacetate may be spontaneously
- Converted to acetone (released on breath and thus not available) - Reduced to 3-HB by HBDH during ketogenesis
79
PDH converts pyruvate to
- Acetyl-CoA (also in the mitochondrial matrix)
80
During periods of starvation, B-oxidation is also occurring in the inner mitochondrial membrane and produces
- Acetyl-CoA
81
Energy from B-oxidation drives
- Gluconeogenesis (also during periods of starvation)
82
Acetoacetate is converted to B-hydroxybutyrate by
- B-hydroxybutyrate dehydrogenase | - NADH-dependent
83
Ketone bodies in circulation are a means for
- 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
Acetoacetyl-SCoA is converted to acetyl-SCoA, which
- Enters the CAC | - Produces ATP
85
Succinyl-CoA CoA transfease is NOT found in
- The liver mitochondria where ketone bodies are produced
86
Succinyl-CoA CoA transfease is induced
- During periods of starvation
87
In the periphery, acetoacetate (ketone bodies) are utilized as fuel when
- Insulin/glucagon ratio is low (starving state)
88
Extrahepatic tissues that utilize acetone (ketone bodies) as fuel during the starving state
- Skeletal muscle - Heart - Renal cortex
89
Significant utilization by brain druing starvation
Fatty acids cannot cross BBB
90
Ketogenesis is interrelated with
- Lipid, CHO, and amino acid metabolism in liver
91
During high rates of FA oxidation
- Large amounts of acetyl-SCoA are produced
92
Production of acetyl-SCoA during high rates of FA oxidation
- Exceeds the ability of CAC | - Ketogenesis is favored
93
Substrate availability (regulation)
- Release of FA and formation of acetyl-SCoA during starvation (i.e. when carbohydrate is not available)
94
Energy status
- Dictates the fate of acetyl-SCoA
95
Ketogenesis is stimulated by glucagon since
- Acetyl-SCoA carboxylase is inhibited | - Hormone-sensitive lipase is activated
96
Ketogenesis is inhibited by insulin since
- In the fed state, hormone-sensitive lipase is inhibited | - Acetyl-SCoA carboxylase is activated
97
Cortisol and catecholamines
- Increase ketogenesis
98
Glucose sparing
- Ketone bodies serve as fuel during starvation (insulin is low) - Particularly by brain
99
Hormone-sensitive lipase is inhibited by
- Insulin
100
In type I diabetes, insulin production
- Is low | - No insulin means HSL activity is unregulated
101
In extreme ketosis, blood ketone levels may reach
- 90mg/dL | - (Normal is 3mg/dL)

Biochemistry I (34 decks)

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