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Biochemistry 2 > E3 Lipotoxicity and Ketogenesis > Flashcards

E3 Lipotoxicity and Ketogenesis Flashcards

1
Q

define lipotoxicity.

A

adverse effects on glucose metabolism of excessive concentration of FFA in blood

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2
Q

what are the effects of excessive concentration of FFA in the blood?

A
  1. increased resistance of liver and muscle to insulin
  2. increased glucose production
  3. decreased in insulin production
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3
Q

when does lipotoxicity happen?

A

when adipose cannot keep up with TAG storage

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4
Q

in lipotoxicity, ______ will cause an inflammatory response.

A

macrophages

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5
Q

T/F. FFA’s enter non-adipose cells and store as TAG “ectopic fat”.

A

true

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6
Q

how does the liver respond to increased FFA in the blood?

A

the liver will take FFA to get them out of the blood

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7
Q

what will happen when there is an increased TAG storage/LD size during lipotoxicity?

A

hepatocytes start looking like adipocytes

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8
Q

when it comes to lipotoxicity and the liver, where are the FFAs coming from?

A

lipolysis of adipocyte TAG and de novo synthesis of FA in the liver

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9
Q

what are some toxic lipids?

A

FFA, TAG, DAG, lysophosphatidyl choline (LPC), ceramides, free cholesterol

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10
Q

T/F. stimulation of insulin receptors leads to insulin resistance.

A

false; inhibition

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11
Q

what are two conditions that can occur with lipotoxicity and the liver?

A

Non-Alcoholic Fatty Liver Disease (NAFLD)

Non-Alcoholic Steatohepatitis (NASH)

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12
Q

match the intramuscular triglyceride levels and insulin sensitivity to the population.

A. normal population
B. athletes
C. obese individuals

  1. low IMTG
  2. high IMTG
  3. greater insulin sensitivity
  4. moderate insulin sensitivity
  5. low insulin sensitivity
A

A. 1 and 4
B. 2 and 3
C. 2 and 5

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13
Q

T/F. Ketone bodies will be produced when there is a substantial amount of carbohydrates.

A

false; low/no carbs

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14
Q

what is the primary substrate from b-oxidation in which ketone bodies are produced from?

A

acetyl CoA

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15
Q

ketone bodies are converted back to acetyl CoA at target tissues to enter which cycle?

A

citric acid cycle

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16
Q

what is the tissue and cell location of ketogenesis?

A

liver, mitochondrial matrix

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17
Q

T/F. the liver only produces ketone bodies, therefore it does not use them.

A

true

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18
Q

T/F. the brain prefers fructose, therefore, it cannot adapt to ketone use during starvation or lack of glucose.

A

false; brain prefers glucose, therefore, it can adapt to ketone

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19
Q

during ketogenesis, low/no carb will be a stimulator. does that increase or decrease b-oxidation?

20
Q

an increased rate of FA oxidation will lead to an increase of acetyl CoA. where will some of the acetyl CoA go to? where will the excess go?

A

some- Krebs cycle

excess- ketogenesis

21
Q

what are the three ketone bodies produced during ketogenesis?

A

acetone
acetoacetate
b-hydroxybutyrate

22
Q

which ketone bodies are the functional ketone bodies?

A

acetoacetate

b-hydroxybutyrate

23
Q

which ketone bodies are transported from the liver to target tissue where they are converted back to acetyl-CoA?

A

functional ketone bodies (acetoacetate and b-hydroxybutyrate)

24
Q

what are the ketogenic amino acids?

A

leucine and lysine

25
Q

what amino acids are both ketogenic and glucogenic?

A 
phenylalanine
isoleucine
tryptophan
tyrosine
threonine
26
Q

ketogenesis starts with how many acetyl CoA?

27
Q

acetyl CoA becomes acetoacetyl CoA via thiolase. acetoacetyl CoA becomes HMG-CoA via what enzyme?

A

HMG-CoA synthase

28
Q

T/F. HMG-CoA becomes acetoacetate (fKB), which splits and becomes acetone (KB) and b-hydroxybutyrate (fKB).

29
Q

what is the key regulatory enzyme for ketogenesis?

A

mitochondrial HMG-CoA synthase

30
Q

T/F. Acetone is produced in large amounts in healthy people.

A

false; small amounts

31
Q

in diabetes, an increase in _______ will lead to an increase of acetone.

A

acetoacetate

32
Q

T/F. there are two versions of HMG-CoA synthase.

A

true; mitochondrial and cytosolic

33
Q

since mitochondrial HMG-CoA synthase is the rate limiting step in ketogenesis, is the cytosolic version also the rate limiting in cholesterol synthesis?

34
Q

matching.
A. location: mitochondrial matrix
B. location: cytosol
C. HMG-CoA is the rate limiting step
D. Stimulated by low carbohydrate
E. Stimulated by high carb/insulin response
F. Stimulated by excessive fatty acid degradation

  1. ketogenesis
  2. cholesterol synthesis
A 
A. 1
B. 2
C. 1
D. 1
E. 2
F. 1
35
Q

under normal conditions in ketogenesis, are there low or high levels of serum ketone bodies?

A

low levels

36
Q

under normal conditions in ketogenesis, what conditions can cause low levels of serum ketone bodies to rise?

A

starvation
very low card diet
uncontrolled (type 1) diabetes mellitus

37
Q

put the process in order.

  1. acetyl CoA goes to CAC and ketogenesis
  2. citric acid cycle slows, ketogenesis is accelerated
  3. GNG is also stimulated but relies on proteins, and steals OAA from CAC
  4. increased FA oxidation producing a lot of acetyl CoA
A

4, 1, 3, 2,

38
Q

T/F. when we have increased concentration of ketone bodies being produced from the liver, this reduces our need for glucose. therefore, GNG slows the need to use protein or steal OAA making it protein sparing.

39
Q

can the rise of ketone bodies in the blood become a problem? if so, what is that problem?

A

yes, rise of b-hydroxybutyrate and acetoacetate in the blood drops the pH, leading to ketoacidosis, which can lead to coma or death

40
Q

matching the type of diabetes to the details.

A. non-insulin dependent
B. insulin dependent
C. stimulates lipolysis, FFA in plasma, ketone body production
D. high insulin response
E. stimulates liver glycolysis, FA synthesis, cholesterol synthesis
F. low insulin response
G. can lead to ketoacidosis
H. does not normally lead to ketoacidosis

  1. type 1
  2. type 2
A 
A. 2
B. 1
C. 1
D. 2
E. 2
F. 1
G. 1
H. 2
41
Q

T/F. the ketogenic diet is based on moderate fat and low carb and protein.

A

false; high fat, low carb, moderate protein

42
Q

what is the primary energy source in a ketogenic diet?

A

ketone bodies

43
Q

why was a ketogenic diet originally developed for?

44
Q

how do ketone bodies affect GABA and glutamate?

A

KB inhibit glutamate decarboxylase
lowering glutamate (excitatory)
increasing conversion to GABA (inhibitory)

45
Q

a ketogenic diet may lead to high GABA levels, why is this bad?

A

inhibits sodium and calcium channels, what are needed for neuronal excitation

46
Q

the ketogenic diet is now being proposed to help with what other conditions?

A

cancer, alzheimer’s, parkinson’s

47
Q

ketogenic diet matching.

A. glucagon 
B. insulin
C. high ATP/energy
D. low glucose
E. high AMP/ADP 
F. low acetyl CoA
G. high acetyl CoA 
H. high beta oxidation
  1. stimulator
  2. inhibitor
A 
A. 1
B. 2
C. 2
D. 1
E. 1
F. 2
G. 1
H. 1

Biochemistry 2 (14 decks)

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