Regulation of Metabolism Flashcards

1
Q

the 3 priorities (in order) for fuel utilizat

A
  1. maintain stable supply of substrates for the CNS and its functions….the brain has little ability to store energy.
    - in the well fed state = prefer glucose
    - in fasting state = can use ketone bodies
  2. maintain protein reserves
    - fasting state = metabolic pathways minimize utilization of proteins, and protein reserves are not regenerated either
    - well fed state = protein reserves will be replenished before glycogen reserves
  3. replenish the limited reserves of glycogen in both liver and muscle tissues
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2
Q

well fed state (general)

A

a. blood glucose levels are good enough for brain supply
b. glycogen is made and stored in muscle and liver cells (but not brain and fat cells)
c. fat is stored in adipose cells primarily
d. high insulin:glucagon ratio –> signals the body to make proteins, store glycogen, and store fat

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3
Q

fasting state (general)

A

a. glucose is moved from the glycogen stores
b. gluconeogenesis will be active
c. fat stores will be tapped –> moving TGs for energy
d. protein stores can be used

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4
Q

excitement state (general)

A

= adrenaline (epinephrine) rush –> catecholamine produced from phenylalanine and tyrosine in the adrenal gland

promotes rapid elevation of blood glucose levels and mobilization of fat stores

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5
Q

beta cells of the pancreatic islets

A

cells that produce insulin

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6
Q

which amino acid promotes insulin secretion

A

arginine

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7
Q

most potent stimulator of insulin secretion

A

high blood glucose

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8
Q

gastric hormones that promote insulin secretion

A

gastric inhibitory polypeptide

CCK

**these hormones are made after a meal - so can stimulate insulin secretion in anticipation of rising blood glucose levels

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9
Q

GLUT4

A

transporters that facilitate glucose entry into cells under high insulin levels

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10
Q

insulin effects (general)

A
  1. glucose uptake into cells (GLUT4)
  2. uptake of branched chain amino acids (Val, Leu, Iso)
  3. inhibition of protein degradation
  4. (+) glycogen synthesis (glycogen synthase)
  5. (-) gluconeogenesis
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11
Q

insulin and glucokinase (liver)

A

(+) glucokinase expression

increase liver uptake of glucose

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12
Q

glycogen phosphorylase and insulin

A

(-) activity

glycogen breakdown - which is not needed in a well fed state

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13
Q

glycolysis under high insulin

A

increased glycolysis (less gluconeogenesis at the same time)

(+) PFK-1 (via + PFK-2)

(+) pyruvate dehydrogenase complex

result = increase AcCoA production in liver and muscle

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14
Q

FA synthesis under high insulin

A

increased (liver)

(+) AcCoA carboxylase

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15
Q

TG synthesis under high insulin

A

increased (adipose tissue)

(+) lipoprotein lipase

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16
Q

pancreatic alpha cells

A

make glucagon

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17
Q

low levels of (?) stimulate glucagon release

A

plasma glucose

all amino acids (except branched chain) - especially arginine

18
Q

epinephrine –> insulin or glucagon?

A

glucagon secretion increased

19
Q

which organ is the major target for glucagon

A

liver

(+) glycogen breakdown –> (+) glycogen phosphorylase

(-) glycogen synthesis –> (-) glycogen synthase

(-) glycolysis –> (-) PFK-1

20
Q

glucagon and gluconeogenesis

A

stimulates it

amino acids –> glucose (+ FBPase-2)

glycerol –> glucose ( - pyruvate kinase)

OAA –> glucose (+ PEP carboxykinase)

21
Q

glucagon and FA mobilization

A

stimulates it

(+) TG lipase

22
Q

glucagon and ketogenesis

A

stimulates it

(+) AcCoA carboxylase

23
Q

effect of epinephrine in muscle

A

a. stimulates glycogen breakdown (inhibiting glycogen synthesis)

**the glucose released STAYS IN THE MUSCLE CELL and used for energy production

24
Q

glucose 6 phosphatase

liver vs. muscle

A

muscle does not have glucose6-phosphatase

therefore…the glucose created by breaking down glycogen CANNOT leave the cell

in the liver…glucose-6P –> glucose –> secreted

25
Q

epinephrine effect in liver

A

a. (+) glycogen breakdown and gluconeogenesis
b. (+) FA mobilization from adipose tissue
c. (+) glucagon (-) insulin
d. increase delivery of O2 to tissues, including increasing heart rate, bp, and dilation of the respiratory passages (physiology)

26
Q

the 2 enzymes that are allosterically regulated in glycogen metabolism

A
  1. glycogen phosphorylase (breakdown)

2. glycogen synthase

27
Q

glycogen metabolism regulation in liver

A

things that inhibit breakdown (glycogen –> glucose1P)

  • glucose
  • ATP
  • glucose6P

things that stimulate synthesis
- glucose 6P

28
Q

glycogen metabolism regulation in muscle

A

inhibit breakdown (glycogen –> glucose1P)

  • glucose-6P
  • ATP

stimulate breakdown

  • Ca2+ (released during muscle contraction)
  • AMP (low energy state)

stimulate synthesis
- Glucose-6P

29
Q

Ca2+ and glycogen metabolism

A

Ca2+ released from SER during muscle contraction –> need energy –> (+) glycogen breakdown

binds to calmodulin subunit of glycogen phosphorylase kinase and can activate the enzyme even in the absence of phosphorylation (which will then activate glycogen phosphorylase)

30
Q

Hexokinase I, II

A

first step of glycolysis in muscle (not liver)

low Km for glucose and readily phosphorylates its substrate

feedback inhibition by the product of the reaction (G6P)

31
Q

Hexokinase IV (glucokinase)

A

first step in glycolysis in liver (not muscle)

high Km for glucose, and sequestered in the nucleus of the hepatocyte at lower glucose concentration

NOT inhibited by G6P like in muscle

traps glucose in the cell for storage as glycogen or FAs

32
Q

PFK-1

A

glycolysis (F-6P –> F-1,6BP)

stimulated by AMP and F-2,6-BP

inhibited by H+, ATP, citrate

33
Q

F-2,6-BP

A

made/degraded by the bifunctional enzyme PFK-2/FBPase-2 respectively

stimulates PFK-1 and glycolysis

therefore (+) PFK-2 activity –> (+) PFK-1

34
Q

F-1,6-BPase-1

A

gluconeogenesis enzyme (F-1,6-BP –> F-6P)

stimulated by citrate

inhibited by AMP and F-2,6-BP

35
Q

pyruvate kinase

A

glycolysis (PEP –> pyruvate)

stimulated by :
- F-1,6-BP

inhibited by:

  • ATP
  • alanine (most common aa precursor for gluconeo)
36
Q

pyruvate carboxylase

A

gluconeogenesis (pyruvate –> OAA)

stimulated by AcCoA (suggest low CAC intermediates and need more OAA)

inhibited by ADP

37
Q

phosphoenolpyruvate carboxykinase (PEPCK)

A

gluconeogenesis (OAA –> PEP)

inhibited by ADP

38
Q

oxidative phase in PPP is used to generate what

A

reducing power in the form of NADPH

39
Q

rate limiting step in oxidative PPP

A

glucose-6-phosphate dehydrogenase (1st rxn)

NADPH = product and it allosterically inhibits the enzyme

40
Q

end product of oxidative PPP

A

ribose-5P = used for forming nucleotides

if cell has enough ribose5P –> excess redirected down non-oxidative phaes

41
Q

end products of non oxidative PPP

A

useful glycolytic intermediates (G6P, F6P, Glyceraldehyde 3P)

42
Q

epimerase in nonoxidative phaes

A

first reaction

ribose-5P –> xylulose-5P

which activates a protein phosphatase that activates PFK-2 –> increase F-2,6,BP –> increaes glycolysis