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biochem 2 ex. 2 > lipotoxicity/ ketogenesis > Flashcards

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

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2
Q

macrophages cause what type of response?

A

inflammatory response

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3
Q

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

A

ectopic fat

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4
Q

when we have increased FFA in the blood what happens?

A

the liver takes them to get them out of the blood

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5
Q

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

A

they start looking like adipocytes

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6
Q

what are the toxic lipids to the liver?

A 
FFA
TAG, DAG
Lysophosphatidyl choline LPC 
Ceramides
Free Cholesterol
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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

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8
Q

low/no carb stimulates what?

A

ketogenesis

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9
Q

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

A

acetyl CoA

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10
Q

once acetyl CoA is increased where does it go?

A

some goes to krebs cycle

excess goes to ketogenesis

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11
Q

where does ketogenesis occur?

A

mitochondrial matrix

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12
Q

what are the 3 ketone bodies we learned about?

A

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

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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

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14
Q

what are the 2 ketogenic amino acids?

A

Leucine
Lysine

Lindsay Lohan

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15
Q

how does fat turn into acetyl CoA?

A

OHOT

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16
Q

can acetyl CoA be turned into glucose?

A

no- pyruvate dehydrogenase is irreversible

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17
Q

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

A

make; oxidize/consume

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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

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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?

A

cytosol

25
Q

what are the causes of high concentration of ketone bodies?

A

accelerated B-oxidation
low carb
starvation
uncontrolled diabetes mellitus

26
Q

what stimulates fat burning and inhibits liver glycolysis?

A

glucagon

27
Q

glucagon also stimulates?

A

gluconeogenesis

28
Q

what inhibits pyruvate dehydrogenase complex (prep step)?

A

acetyl CoA

29
Q

during gluconeogenesis, oxaloacetate is stolen from where?

A

krebs cycle to make glucose

30
Q

what does ketogenesis do to gluconeogenesis?

A

it stimulates it because gluconeogenesis makes glucose from pyruvate which is necessary when glucose levels in the body are low

31
Q

in order to convert pyruvate into oxaloacetate, what enzyme do we need?

A

pyruvate carboxylase

32
Q

what is the coenzyme needed to use pyruvate carboxylase?

A

biotin

33
Q

in the mitochondria when we have increased FA oxidation and reduced OAA oxaloacetate what is the result?

A

an oversupply of acetyl CoA

34
Q

when we have too much acetyl CoA what do we make?

A

ketone bodies

35
Q

as our body produces ketone bodies, there is a shift in metabolism called?

A

ketosis

36
Q

during ketosis what do we use for energy?

A

ketone bodies

37
Q

as ketone bodies rise in the blood, what happens to gluconeogenesis?

A

it slows down resulting in less protein being consumed

38
Q

what is it called when gluconeogenesis consumes less protein due to elevated ketone bodies?

A

protein sparing- ketogenesis is also protein sparing

39
Q

during oxidation of ketones, acetoacetate and B-hydroxybutarate are transported in the blood to?

A

extrahepatic tissues

40
Q

increased B-hydroxybutarate and acetoacetate in the blood lowers pH and leads to?

A

ketoacidosis

coma, death

41
Q

increased ketones in blood and urine =

A

ketonemia

ketonuria

42
Q

when can ketogenesis be dangerous?

A

starvation
uncontrolled type 1 diabetes
too extreme low carb diet/ prolonged

43
Q

what are some conditions the ketogenic diet would be good for?

A 
type 2 diabetes
epilepsy 
cancer
alzheimers
parkinson's disease
44
Q

what are the stimulators of ketogenesis?

A

glucagon
decreased glucose
increased AMP, ADP (decrease ATP)
increased B-oxidation (increased acetyl CoA)

45
Q

what are the inhibitors of ketogenesis?

A

increased ATP
insulin
increased glucose
decreased acetyl CoA

biochem 2 ex. 2 (8 decks)

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