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week 9 > Muscle Cell Metabolism > Flashcards

Muscle Cell Metabolism Flashcards

1
Q

How is ATP utilized in muscle and name 3 ATPases

A

Na+/K+ ATPase Ca+2 ATPase Myosin ATPase

also through anabolic rxns

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2
Q

how do the different muscle types use fuel preference and regulation

A

Cardiac- FA, lactate and glucose skeletal- glucose, FA, ketone bodies, some AA (branch chain) smooth- requires less ATP

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3
Q

what are the two main fuel sources for skeletal muscle and how do they change at rest versus with exercise

A

glucose and FA

FA preferred at rest (except after feeding) and then with extensive exercise after oxygen is availble again it switches back to this

glucose (CHO) utilization increases with exercise intensity and can result in aerobic and anerobic metabolism

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4
Q

What are the possible sources for glucose in skeletal muscle

A

food, glycogen in liver or muscle

  • muscle glycogen stays in muscle - glycogen in the liver can come from food or be made in liver
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5
Q

what are different ways that glucose can be metabolized by skeletal muscle

A

glycolysis, glycogen synthesis or PPP

Once it is phosphorylated by hexokinase (glucokinase in liver) it is trapped in cell. It can then goes to glycolysis, glycogen synthesis or PPP

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6
Q

what 2 general phases make up glycolysis

A

hexos: energy used

trios phase: energy produced and reducing power produced

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7
Q

Differentiate the two paths of glycolysis and when one is prefered

A

then goes on depending on availability of oxygen:

oxygen available: ETC –> NAD+ regenerated, Co2 and H20 produced, 32 ATP

anaerobic: NAD+ regenrated only 2 ATP

- begining of exercise before blood reaches muscle, extrenous exercise when no Oxygen is availble, fast twitch fibers

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8
Q

what are the glut receptors on skeletal muscle

A

glut4

insulin sensitive tyrosine kinase receptors that are upregulated to the cell surface to allow glucose into skeletal muscle

  • exercise can upregulate glut 4 to cell surface
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9
Q

What is the function of hexokinase in glycolysis

what inhibits it

A

converts glucose to glucose- 6- phosphate

the phosphorylation traps it in the cell

low Km

negative feedback –>Inhibited by product - glucose 6-phosphate

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10
Q

What is the function of Phosphofructokinase-1 in glycolysis

what activates it

what inhibits it

A

converts fructose 6- phosphate to fructose 1-6 bisphosphate

*feed forward mechanism during exercise to stim pyruvate kinase

▪Activated by AMP and Fructose-2,6-bisphosphate

▪Inhibited by ATP and Citrate

ATP levels pretty steady but AMP levels change largely

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11
Q

What is the function of Pyruvate kinase in glycolysis

and how is it regulated

what activates it

what inhibits it

A

converts phosphoenol pyruvate to pyruvate

▪Activated by Fructose 1, 6-bisphosphate

▪Inhibited by ATP

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12
Q

what is glucogenolysis

what is the substrate

where does it occur

A

the process by which stored glucose (glycogenesis) is released.

stored in muscle and liver, only liver glycogen contributes to blood glucose levels

substrate: glycogen
occur: cytosol

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13
Q

how does osmotic pressure impact glycogenolysis

A

osmotic pressure can inhibit glycogen storage

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14
Q

what enzyme catalyzes the release of glucose from glycogen

what enzyme catalyzes the release of free glucose

A

glycogen phorphylase

glucosidase removes the branching

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15
Q

what is phosphorolysis

how does a mutation in one of the muscle specific phosphorylases result in pathogenesis

A

breaks down glycosidic bonds

McArdle disease- cant break down glycogen, exercise induce muscle pain and cramps, can see myoglobin and CK in blood (dark urine). can occur as an adult or in childhood.

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16
Q

regulation of glycogenolysis (Glycogen phosphorylase specifically)

A

stimulation: Ca and hormones (epi), AMP
inhibition: ATP and glucose-6-phosphate

Ca and epinephrine can activate a kinase to dephosphorylate the phosphorylase converting it to its active form. Whereas AMP increases its active form

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17
Q

deficiencies in what result in an inability to store glycogen in muscle

A

mutation in glycogenin-1 ( muscle specific isoform)

see depletion of glycogen in Pts

cardiac probs, exercise intolerance

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18
Q

where does glycogenesis

A

cytosol

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19
Q

what is Glycogenin

A

protein that autoglycosylates to form glycogen core to which glycogen synthase adds to. Glycogen cannot be synthesized without a glycogen core

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20
Q
A
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21
Q
A
22
Q
A
23
Q

what is the role of phosphoglucomutase

A

turns glucose 6 phosphate into glucose 1 phosphate

24
Q

what is the role of pyrophosphorylase

A

converts glucose 1- phosphate to UDP-glucose

25
Q

what is the function of transferases

synthases

A

add branches

add glucose to non reducing ends

if there is a protein core then the UDP glucose can be used

26
Q

How is glycolysis and glycogenolysis regulated to ensure both dont occur simultaneously while both are in the cytosol

A

Glycogen synthase and phosphorylase are reciprocally regulated by covalent modifications

phosphorylation inhibits glycogen synthase ( resulting in glycogen formation, active in dephosphorylated form)

but activates glycogen phosphorylase (resulting in degredation, active in phosphorylated form)

27
Q

what form of FAs can move inside of the cell

what is required for transportation of fatty acids

location

A

activated form is required- attached to acyl CoA

carnitine

matrix of mitochondria ( transported into inner mitochondria after turned into acylcarnitine) –> fatty acyl CoA regenerated and then B-oxidation begins

28
Q

what is produced in B oxidation

A

for each round you shorten by 2 C units, most oxygation occurs at B carbon

final: NADH and FADH2 or QH2

29
Q

what controls the release of FA from adipose

A

hormones

30
Q

what regulates B oxidation

A

energy levels/ stores

rate of NADH and QH2 oxidation

31
Q

***What inhibits fatty acyl CoA movement to site of oxidation (matrix)

A

Malonyl CoA

important in FA synthesis in cytosol but inhibits carnitine transferase (CPT-1) in matrix of mitochondria

32
Q

what enzymes are important at what stages

A

thiolytic –> cleave to CoA

different classes of acyl CoA dehydrogenases act on diff size FAs

long 12-20 carbons

med 6-12 carbons

short 2-4 carbons

33
Q

what will a mutation in acyl CoA dehydrogenases result in

A

accumulation of fatty acyl carnitine

hypoglycemia, hyperketonia (hyperketonemia??) under prolonged fasting

34
Q

what process yeilds the highest amount of ATP

A

FA- B oxidation

20% increase from the 32 ATP produced in aerobic

35
Q

is oxygen a substrate for the TCA cycle

A

no but TCA cycle is linked to ECA

36
Q

what would defeciencies TCA cycle catabolism result in ( specifcally in the pyruvate dehydrogenase complex that involves 5 coenzymes)

A

lactic acidosis and neurological deficiets

mutation in pyruvate dehydrogenase is called leigh syndrome

  • if affinity for cofactor is decreased then could supplement
37
Q

where does conversion of acetyl coA take place

A

mitochondria matrix face of inner membrane

38
Q

what activates the pyruvate dehydrogenase complex

A

activation

  • Ca
  • dephoshorylation
  • ADP
  • pyruvate

downregulated

  • acetyl coa when available from other sources
  • NADH
39
Q

what is the significance of oxaloacetate

what does deficiency result in

how is it regulated by acetly CoA

A

important to replenish intermediates in TCA cycle

▪Def. result in lactic acidosis and neurological dysfunction

allosterically activated by acetyl CoA–>

increase flux through citirix acid cycle

requires biotin

40
Q

what are the different ways that acetly coA could be formed

A

produced from fatty acid oxidation, pyruvate, ketone bodies, several amino acids and acetate

41
Q

what is the location of the TCA cycle

A

mitochondiral matrix with exception of one complex which is in inner membrane

42
Q

what are the 2 stages of the TCA cycle

A

Loss of CO2

Regeneration of oxaloacetate

43
Q

what pathway does thiamine def impact

A

TCA, result in lactic acidosis and neurological dsyfunction

44
Q

how is the TCA cycle regulated

A

phosphylation state of ATP

redox state of NAD+

Ca will increase TCA by stimulating enzymes in cycle

45
Q

what aspects of TCA anabolism is important for AA synthesis

A

oxaloacetate and a-ketaglutarate (brain)

46
Q

what aspects of TCA anabolism is important for FA synthesis

A

citrate

47
Q

What aspects of TCA anabolism is important for gluconeogeesis- malate

What aspects of TCA anabolism is important for heme synthesis - succinyl CoA

A

malate

48
Q

What aspects of TCA anabolism is important for heme synthesis

A

succinyl CoA

49
Q

where is the ETC cycle at how does it charge the location it resides

A

inner mitochondria membrane (exception of cyt c in inner membrane space)

creates - inside and + charge outside

50
Q

what are the 5 ETC complexes

A

majoi

51
Q
A

week 9 (6 decks)

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