lipotoxicity/ ketogenesis Flashcards

1
Q

when adipose tissue cannot keep up with TAG storage needs and a spill over of FFA into the blood occurs what happens?

A

lipotoxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

macrophages cause what type of response?

A

inflammatory response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

FFA entering non-adipose cells and stored as TAG is called?

A

ectopic fat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

when we have increased FFA in the blood what happens?

A

the liver takes them to get them out of the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

with prolonged TAG storage and Lipid droplet size increasing what happens to hepatocytes?

A

they start looking like adipocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what are the toxic lipids to the liver?

A
FFA
TAG, DAG
Lysophosphatidyl choline LPC 
Ceramides
Free Cholesterol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are some examples of causes of lipotoxicity in the liver?

A

Non-alcoholic fatty liver disease
Non-alcoholic steatohepatitis
inhibition of insulin receptors leading to insulin resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

low/no carb stimulates what?

A

ketogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

low/no carb stimulates B-oxidation which produces what?

A

acetyl CoA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

once acetyl CoA is increased where does it go?

A

some goes to krebs cycle

excess goes to ketogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

where does ketogenesis occur?

A

mitochondrial matrix

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what are the 3 ketone bodies we learned about?

A

acetone- exhaled by product
acetoacetate- functional
B-hydroxybutyrate- functional

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

functional ketones are transported from where to where?

A

liver in the blood to target tissues where it is converted back into acetyl CoA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are the 2 ketogenic amino acids?

A

Leucine
Lysine

Lindsay Lohan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

how does fat turn into acetyl CoA?

A

OHOT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

can acetyl CoA be turned into glucose?

A

no- pyruvate dehydrogenase is irreversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

the liver can _____ ketone bodies but it cannot _____ the ketone bodies

A

make; oxidize/consume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

how do we make HMG CoA in ketogenesis?

A

acetoacetyl CoA + H2O + acetyl CoA -> HMG CoA

HMG CoA synthase is the enzyme needed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what enzyme is needed to make HMG CoA in ketogenesis?

A

HMG CoA synthase

20
Q

what is the rate limiting step in the synthesis of ketone bodies?

A

HMG CoA synthase

21
Q

the cytosolic version of HMG CoA synthase is a part of what pathway?

A

cholesterol synthesis pathway

22
Q

cholesterol and ketones are made from the same materials BUT they are made under different conditions, what are the differences?

A

excessive fat burning in liver creates ketones

excessive sugar and insulin results in cholesterol

23
Q

what are the materials cholesterol and ketones have in common?

A

both start from acetyl CoA

both have HMG CoA as a precursor

24
Q

where does cholesterol synthesis happen?

25
what are the causes of high concentration of ketone bodies?
accelerated B-oxidation low carb starvation uncontrolled diabetes mellitus
26
what stimulates fat burning and inhibits liver glycolysis?
glucagon
27
glucagon also stimulates?
gluconeogenesis
28
what inhibits pyruvate dehydrogenase complex (prep step)?
acetyl CoA
29
during gluconeogenesis, oxaloacetate is stolen from where?
krebs cycle to make glucose
30
what does ketogenesis do to gluconeogenesis?
it stimulates it because gluconeogenesis makes glucose from pyruvate which is necessary when glucose levels in the body are low
31
in order to convert pyruvate into oxaloacetate, what enzyme do we need?
pyruvate carboxylase
32
what is the coenzyme needed to use pyruvate carboxylase?
biotin
33
in the mitochondria when we have increased FA oxidation and reduced OAA oxaloacetate what is the result?
an oversupply of acetyl CoA
34
when we have too much acetyl CoA what do we make?
ketone bodies
35
as our body produces ketone bodies, there is a shift in metabolism called?
ketosis
36
during ketosis what do we use for energy?
ketone bodies
37
as ketone bodies rise in the blood, what happens to gluconeogenesis?
it slows down resulting in less protein being consumed
38
what is it called when gluconeogenesis consumes less protein due to elevated ketone bodies?
protein sparing- ketogenesis is also protein sparing
39
during oxidation of ketones, acetoacetate and B-hydroxybutarate are transported in the blood to?
extrahepatic tissues
40
increased B-hydroxybutarate and acetoacetate in the blood lowers pH and leads to?
ketoacidosis | coma, death
41
increased ketones in blood and urine =
ketonemia | ketonuria
42
when can ketogenesis be dangerous?
starvation uncontrolled type 1 diabetes too extreme low carb diet/ prolonged
43
what are some conditions the ketogenic diet would be good for?
``` type 2 diabetes epilepsy cancer alzheimers parkinson's disease ```
44
what are the stimulators of ketogenesis?
glucagon decreased glucose increased AMP, ADP (decrease ATP) increased B-oxidation (increased acetyl CoA)
45
what are the inhibitors of ketogenesis?
increased ATP insulin increased glucose decreased acetyl CoA