B2.043 Metabolism and its Regulation Pt. 2 Flashcards

1
Q

how can metabolic plasticity be altered?

A

suppressed by over consumption of food

lost in type 1 diabetes

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2
Q

what mechanisms maintain caloric homeostasis in the fed state?

A

glycogenesis
glycolysis
lipogenesis

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3
Q

what mechanism maintain caloric homeostasis in the fasted state?

A
glycogenolysis
gluconeogenesis
lipolysis
fatty acid oxidation
ketogenesis
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4
Q

what are the 4 primary mechanisms for switching between fed and starved states?

A

substrate supply
allosteric effectors
covalent modification
induction repression of enzymes

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5
Q

what substrate is necessary for glycogenesis and lipogensis?

A

dietary glucose

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6
Q

what substrate is required for ketone body synthesis by the liver?

A

high serum fatty acid concentration

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7
Q

what substrates must be available for protein synthesis?

A

all 20 AAs

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8
Q

when can the brain use ketone bodies?

A

when blood concentration is high

about 48 hours starved

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9
Q

what are the 3 primary substrates involved in allosterically affecting the fed state?

A

glucose
fructose 2,6-P2
Malonyl-CoA

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10
Q

what enzymes does glucose allosterically affect?

A

inhibits glycogen phosphorylase
stimulates glycogen synthase
stimulates glucokinase

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11
Q

what enzymes does fructose 2,6-P2 allosterically affect?

A

inhibits fructose 1,6 bisphosphatase

stimulates phosphofructo-1-kinase (PFK1)

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12
Q

what enzyme does malonyl-CoA allosterically affect?

A

inhibits carnitine palmitoyl coA transferase 1 (CPT1)

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13
Q

what is CPT1?

A

rate limiting enzyme in oxidation of fatty acids

inhibited in fed state bc don’t want fats you just made to be broken down immediately

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14
Q

what substrate is required to transport long chain fatty acids into the mitochondrial matrix space?

A

carnitine

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15
Q

where does fatty acid oxidation occur?

A

mitochondrial matrix space

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16
Q

what are the 2 primary substrates involved in allosterically regulating the fasted state?

A

long chain acyl coA

acetyl coA

17
Q

what enzyme does long chain acyl CoA allosterically affect?

A

inhibits acetyl CoA carboxylase to prevent fat production

18
Q

what enzymes does acetyl CoA allosterically affect?

A

inhibits pyruvate dehydrogenase (makes pyruvate)

stimulates pyruvate carboxylase (makes oxaloacetate and eventually glucose)

19
Q

what is the primary covalent modification that affects switching between fed and starved states?

A

phosphorylation
nonphosphorylated = fed
phosphorylated = starved

20
Q

high insulin
low glucagon
low cAMP
low PKA activity

A

fed state

21
Q

low insulin
high glucagon
high cAMP
high PKA

A

starved state

22
Q

what are the rate limiting enzymes impacted by induction-repression pathways in the fed state?

A

glucokinase- glycolysis
G6P dehydrogenase -pentose phosphate
acetyl-CoA carboxylase- fatty acid synthesis

23
Q

in the well fed state, what enzyme accounts for 10% of total liver enzymes?

A

fatty acid synthase

24
Q

what transcription factors does insulin act on?

A

inhibits forkhead transcription factor

stimulates SREBP-1

25
Q

what transcription factor does glucagon act on?

A

CREB

26
Q

what are the 2 rate limiting enzymes impacted by induction-repression pathways in the fed state?

A
glucose 6 phosphatase
PEP carboxykinase (only subject to regulation by transcription)
27
Q

what is hexokinase 4?

A

glucokinase

glucose sensor in the liver

28
Q

what makes glucokinase different from the other hexokinases?

A

higher Km

allows glucokinase to sense and respond immediately to the glucose concentration in the blood

29
Q

what is fructose 2,6-bisphosphate?

A

master regulator of glycolysis and gluconeogenesis in the liver
promotes glycolysis
inhibits gluconeogenesis

30
Q

how is fructose 2,6-bisphosphate made?

A

made from fructose 6-phosphate by a kinase
converted back to fructose 6-phosphate by a phosphatase
kinase and phosphatase located on same bifunctional enzyme

31
Q

how is the F2,6P2 bifunctional enzyme regulated?

A

phosphorylation
phosphorylated = active phosphatase
nonphosphorylated = active kinase

32
Q

can you synthesize glucose from fatty acids with even numbers of carbon atoms?

A

no

33
Q

why cant you synthesize glucose from fatty acids with even numbers of carbons?

A
  1. no pathway exists for conversion of acetyl-CoA to glucose

2. the acetyl group of acetyl-CoA is completely oxidized to CO2 and water by the citric acid cycle

34
Q

can we synthesize glucose from fat?

A

fat= triacylglycerol
one glycerol and 3 fatty acids
glycerol can be converted to glucose, fatty acids cannot

35
Q

what is anaplerosis?

A

enzyme catalyzed reaction that results in net synthesis of a citric acid cycle intermediate

36
Q

which compound is recycled into the citric acid cycle to allow for continuous operation?

A

oxaloacetate

37
Q

what are 2 examples of anaplerotic pathways?

A

pyruvate + ATP +Co2 yields OAA + ADP +P

glutamate +NAD+ yields alpha-ketoglutarate + NADH + NH4+

38
Q

what are compounds called that are metabolized via an anaplerotic pathway?

A

glucogenic

39
Q

what are compounds called that are metabolized via acetyl-CoA?

A

ketogenic