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MCBM > Metabolic regulation > Flashcards

Metabolic regulation Flashcards

1
Q

glucose and intracellular ATP maintaine at ___mM to maintain homeostasis

A

5

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2
Q

Hexokinase is an ____which catalyze the same reaction although they have slightly different properties. Made from different genes with diff regulatory aspects.

A

isoenzyme

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3
Q

ATP, ADP and AMP bind to ___enzymes and change their activity level. They are examples of ____modifiers

A

regulatory; allosteric

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4
Q

Covalent modification is

A

phosphorolation

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5
Q

What is a futile pathway

A

ATP is hydrolyzed and nothing is gained when glycolyis and gluconeogenis is happening at the same time. So they are reciprocally regulated

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6
Q

Glucose gets into cell via ___

A

GLUT 4

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7
Q

GLUT 4 is ___dependent

A

insulin; otherwise sequestered internally in vesicles

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8
Q

What are 3 points of regulation for glycolysis

A
  1. Hexokinase
  2. Phosphofructokinase 1
  3. Pyruvate kinase
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9
Q

What are 3 points of regulation for gluconeogenesis

A
  1. Glucose 6-phosphatase
  2. Fructose-1, 6-bisphosphatase
  3. Pyruvate carboxylase + PEP carboxykinase
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10
Q

Glucokinase is liver specific____

A

isozyme; will forgoe glucose to make sure brain has enough.

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11
Q

Hexokinase 4 is sequestered in ____when glucose concentration is low.

A

nucleus. Cant encounter glucose and phosphorolate it so its kept in cell.

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12
Q

When glucose levels are ____ it binds to hexokinase 4 and releases it from the nucleus so it can start phosphorolating glucose so that it can be stored as glycogen

A

high

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13
Q

PFK 1 in glycolysis is an ____regulator

A

allosteric

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14
Q

High [ATP] and [citrate] allosterically signal that energy needs are met and inhibit:

A

PFK-1

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15
Q

High [ADP] and [AMP] allosterically signal need for ATP production and activate ____ and inhibit ___

A

PFK-1; FBPase-1

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16
Q

In the liver, the most important allosteric regulator of PFK-1 is _____ which is synthesized by _____

A

fructose, 2-6 bisphosphate; PFK-2

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17
Q

Glycogen stores in muscle can’t help maintain blood glucose levels bc it is never:

A

released. Doesn’t have glucose 6 phosphatase. Only uses glycogen for itself

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18
Q

Muscles have _____ receptors but no ____receptors; therefore it does not produce the enzymes for gluconeogenesis.

A

epinephrine; glucagon

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19
Q

What are the 3 principle hormones of fuel metabolixm

A
  1. insulin: fed
  2. glucagon: hungry
  3. epinephrine: terrified
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20
Q

Where does epinephrine come form

A

adrenal medulla; its actually a catacholamine

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21
Q

What is a phenol ring with two hydroxyl groups called

A

catecolamine. Derived directly from aa - tyrosine; have cell membrane associated receptors and trigger a second messenger

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22
Q

What is the classical second messenger

A

cyclic AMP

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23
Q

Where does glucagon come from

A

alpha cells of pancreas–>islets of Langerhaans

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24
Q

Pancreas has ___ and ___ functions

A

exocrine: digestive enzymes
endocrine: releases proteins into bloodstream so it can go throughout the body

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25
Q

Beta cells make

A

insulin

26
Q

Glucagon is a ____hormone

A

protein

27
Q

What are the targets of glucagon and epinephrine

A

Use cyclic amp signaling to change metabolic activity.

28
Q

What is a serpentine receptor

A

External ligand binding to receptor activates an intracellular GTP binding protein which regulates an enzyme that generates an intracellular second messenger. Go back and forth across cell membrane and when hormone binds it activates G protein

29
Q

What are the 5 proteins involved in epinephrine and glucagon signaling

A
  1. beta adrenergic receptor/glucagon receptor
  2. Gs protein
  3. adenylate cyclase
  4. protein kinase A
  5. cyclic nucletodie phosphodiesterase
30
Q
  1. Epeniphrine binds its specific receptor –>changes conformation of receptor site and G protein. When receptor binds it knocks off ___ and GTP associates. Alpha subunit loses affinity for its receptor and moves into cell membrane and binds to target enzyme: ______GDP falls off and GTP binds. Now has high affinity for target enzyme.
A

GDP; adenylate cyclase

31
Q

What is adenylate cyclase

A

the enzyme that converts ATP to cyclic AMP

32
Q

Protein Kinase A becomes activated by ____and changes metabolic activity of all of its protein targets by:

A

cyclic AMP; phosphorlation

33
Q

What are ways to self limit this process?

A
  1. G protein has inherent GTPase function: hydrolyze GTP, converts it to GDP which now has affinity for the receptor and its beta and gamma subunits. Moves back into its original position.
  2. cAMP doesnt hang around all day. Cyclic nucleotide phosphodiesterase hydrolizes cAMP and inactivates it
34
Q

cAMP phosphodiesterase is inhibited by:

A

caffeine and theophylline

35
Q

How is protein Kinase A activated; what does it catalyze

A

cAMP; catalyzes the phosphorylation of target proteins

36
Q

Insulin DOES NOT produce ____as a secondary messenger

A

cAMP

37
Q

What are C peptides indicative of

A

diagnostic tool that tells you if your body makes natural insulin and differentiates between Type 1 and Type 2 diabetes

38
Q

Which aa form disulfide bonds?

A

cysteine

39
Q

Insulin receptors come from:

A

receptor tyrosine kinases

“RTK”; cell signaling proliferation and growth

40
Q

3 aa that have hydroxyl groups:

A
  1. serine
  2. threonine
  3. tyrosine
41
Q

What do insulin receptors do

A

Auto phosphoralates its own tyrosine receptors that activates receptor and other targets.

42
Q

How does insulin signaling I occur

A
  1. Insulin binds to receptor and autophosphorolates on its own tyrosine residues
    2.
43
Q

Growth factors cause

A

cell proliferation

44
Q

Insulin is a potent ___factor that activates the ____pathway

A

growth; MAPK –> regulate transcription factors needed for cell division

45
Q

What is Ras

A

G protein; when GDP bound its inactive when GTP bound it activates Raf 1 Kinase that starts MAPK cascade that turns on genes for cell division.

46
Q

Ras is commonly _____in different cancers.

A

mutated. –>in GTPase domain; the part that is meant to turn off the singal. Cell keeps dividing

47
Q

IRS 1 can interact with

A

multiple targets.

48
Q

How does insulin signaling II occur

A

PKB activated by IRS1, which leads to phosphoprotein phosophatase 1 which takes phosophate group off that protein kinase A phosphorolates.

49
Q

What is the major modulator for PFK-1

A

Fructose 2,6 bisphosphate; allosterically increases PFK-1 affinity for F-6-P (fructose 6 phosphate); decreases PFK-1 affinity for ATP and citrate

50
Q

PFK-1 activation favors

A

glycolysis

51
Q

Active PFK-2, means there is a high amount of Fructose, 2-6 BP which activates ____ and favors___

A

PFK1; glycolysis

52
Q

If PFK-2 gets phosphorolated it becomes ___

A

inactivated; glycolysis would stop and gluconeogenesis would happen

53
Q

PFK-2 is a ____enzyme

A

bifunctional; also takes phosphate back off.

54
Q

What does pyruvate kinase do in glycolysis

A

Converts PEP to pyruvate and makes ATP; this is the first step thats irreversible in gluconeogenesis

55
Q

If ATP levels are high glycolysis:

A

slows down

56
Q

if ADP and AMP are high

A

we will need to make more ATP

57
Q

Liver has special isoenzyme of pyruvate kinase that is inactivated by_____. When blood glucose falls, ______is secreted. _____ levels increase. ____is activated. PFK-2 is phosphorolated and inactivated. _______ decreases; _____ activity decreases. Glycolysis slows down. Pyruvate kinase is _____ and inactivated.

A

PKA phosphorolation; glucagon; cAMP; PKA is activated; Fructose 2, 6 BP; PFK-1; phosphorolated.

58
Q

Gluconeogenesis is favored in the

A

liver

59
Q

pyruvate carboxylase is activated by

A

acetyl coA

60
Q

High levels of insulin blocks the transcription of

A

PEPCK; thus reducing gluconeogenesis.

MCBM (59 decks)

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