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BIOL 3421 - molecular biochem > lipid degradation: fat digestion + mobilization > Flashcards

lipid degradation: fat digestion + mobilization Flashcards

1
Q

water soluble enzymes have a difficult time accessing fats for beta oxidation. how do we combat this?

A

the fats must be emulsified first

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2
Q

what does movement of fats through the blood require

A

requires associated water soluble proteins

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3
Q

stable C-C bonds require activation by ___ before oxidation

A

CoA

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4
Q

why is it called b-oxidation

A

CoA binds to the carboxyl at C1 first. This allows oxidation at C3, aka the b carbon

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5
Q

list 4 sources of fatty acids for b oxidation

A

fats in the diet, fats stored in cells as lipid droplets, fats synthesized in the liver from excess carbs that can be exported elsewhere, fats obtained by autophagy (recycled lipids from an organelle membrane)

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6
Q

humans in industrialized countries get __% of energy from dietary fats

A

40%

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7
Q

how does starvation affect autophagy in energy production

A

starvation can increase the use of autophagy

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8
Q

lipid droplets in adipocytes are full of ____ and ____

A

cholesteryl esters and TAGs

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9
Q

T or F: lipid droplets in adipocytes are surrounded by a phospholipid bilayer

A

false; they’re surrounded by a phospholipid monolayer

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10
Q

what are perilpins?

A

they’re proteins that cover the monolayer membrane of lipid droplets in adipocytes

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11
Q

function of perilipins?

A

they prevent lipid degradation (they protect the lipid droplets in adipocytes)

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12
Q

perilipins are bound to an accessory protein called ___

A

CGI

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13
Q

list two hormones that signal the need to bring TAGs out of storage and use them for energy

A

glucagon and epinephrine

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14
Q

why does glucagon serve as a signal to bring TAGs out of storage + use for energy

A

you’re hungry = need to access TAGs for energy

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15
Q

why does epinephrine serve as a signal to bring TAGs out of storage + use for energy

A

needed for adrenaline = require TAGs for energy

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16
Q

describe briefly what needs to happen to bring TAGs out of storage + use them for energy

A

hormone signals need to remove perilipin from the lipid droplet surface, and then TAGs need to be cleaved into free FAs to move through the bloodstream

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17
Q

describe the steps leading up to perilipin dissociation from CGI protein on lipid droplets

A

glucagon is involved in a GPCR/G protein signalling pathway, producing adenylyl cyclase, which in turn produces cAMP from ATP. cAMP stimulates PKA, which phosphorylates Hormone Sensitive Lipase (HSL) and perilipins. Phosphorylated perilipins dissociate from CGI protein

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18
Q

in the pathway of perilipin dissociation from CGI (to access TAGs for energy), what two things does PKA phosphorylate to release perilipin

A

Hormone Sensitive Lipase (HSL) and perilipin

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19
Q

in the pathway of perilipin dissociation from CGI (to access TAGs for energy), describe the steps that occur once perilipin is no longer bound to CGI

A

CGI activates ATGL, which converts TAGs into DAGs. Phosphorylated HSL-perilipin converts DAGs into MAGs. MGL converts MAGs to free FA + glycerol. Free FAs leave adipocyte and travel through the blood bound to serum albumin, and will enter target tissues by a FA transporter

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20
Q

in the pathway of perilipin dissociation from CGI (to access TAGs for energy), what is ATGL and what does it do

A

adipose TAG lipase. It converts TAGs to DAGs

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21
Q

in the pathway of perilipin dissociation from CGI (to access TAGs for energy), what converts DAGs to MAGs

A

phosphorylated HSL-perilipin

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22
Q

in the pathway of perilipin dissociation from CGI (to access TAGs for energy), what converts MAGs to FAs+glycerol

A

MGL: MAG lipase

23
Q

in the pathway of perilipin dissociation from CGI (to access TAGs for energy), why must free FAs travel through the blood bound to serum albumin

A

without the serum albumin, FA is too hydrophobic to be able to travel through the blood

24
Q

where is serum albumin produced

A

the liver

25
Q

how many fatty acids can one serum albumin bind to

A

7

26
Q

what target tissues does albumin bring FAs to

A

skeletal muscle, heart, kidney

27
Q

what happens to serum albumin when there is high blood glucose

A

it becomes glycated

28
Q

what is glycation

A

the non-enzymatic addition of reducing sugar products to amine groups on proteins and disrupts protein function + can contribute to tissue damage

29
Q

T or F: glycation involves enzymes to reduce sugar products to amine groups on proteins

A

false; no enzymes are required

30
Q

is glycation good or bad? explain

A

bad: if you have a lot of sugars in your blood and they start randomly sticking to stuff like serum albumin, the function of serum albumin will be disrupted

31
Q

list 4 diabetes symptoms that glycated albumin contributes to

A

retinopathies, renal disease, coronary heart disease, neuropathies

32
Q

glycerol only represents __% of the total energy stored in TAGs

A

5%

33
Q

after FAs and glycerol are released from lipid droplets, where does the glycerol go

A

to the liver

34
Q

list 2 things that can happen once glycerol from broken down lipid droplets is shipped to the liver

A
  1. it can be phosphorylated and oxidized to DHAP, which can be used for glycolysis or GNG
  2. it can be phosphorylated by glycerol kinase to make glycerol-3-phosphate for glycerophospholipid synthesis
35
Q

once glycerol from broken down lipid droplets is in target tissues, where does it need to go

A

the mitochondrial matrix

36
Q

in animals, where does FA oxidation take place

A

mitochondrial matrix

37
Q

T or F: FAs with 12C or less can cross the mitochondrial membrane unassisted

A

true

38
Q

T or F: FAs with 14C or more can cross the mitochondrial membrane unassisted

A

false; they require multiple enzymatic steps to enter the matrix

39
Q

what is the name of the steps required to get 14C+ FAs into the mito matrix in preparation for oxidation

A

the carnitine shuttle

40
Q

briefly list the 4 basic steps of the carnitine shuttle

A

FA is esterified to CoA, CoA is swapped for carnitine, FA-carnitine passes both mito membranes, carnitine is re-swapped for CoA

41
Q

describe step 1 of the carnitine shuttle

A

FA is converted to fatty acyl-CoA via acyl-CoA synthetases on the OMM. Costs 2 ATP equivalents

42
Q

how much ATP (if any) does step 1 of the carnitine shuttle cost

A

2

43
Q

describe step 2 of the carnitine shuttle starting with fatty acyl-COA

A

the CoA is exchanged via transesterification for a molecule of carnitine. The FA transiently attaches to the carnitine OH group, catalyzed by carnitine acyltransferase I in the OMM. Carnitine ester can now enter the IMS through large pores, then the matrix through a carnitine transporter on the IMM

44
Q

describe step 3 of the carnitine shuttle

A

fatty acyl group is transferred from carnitine back to CoA by carnitine acyl transferase II on the inner face of the IMM. Carnitine returns to the cytosol through the same transporter, and now we can do b-oxidation

45
Q

how/where is carnitine synthesized

A

synthesized from lysine in the liver/kidney/brain or obtained in the diet by red meat and dairy

46
Q

list 3 things that are associated with low carnitine levels

A

premature infants, diabetics, elderly

47
Q

list 4 things that carnitine supplements have been shown to reduce

A

hypertension, diabetic ketoacidosis, insulin resistance, cardiac arrhythmias

48
Q

what are the CoA and fatty acyl-CoA stores in the cytoplasm used for

A

FA biosynthesis and elongation

49
Q

what are the CoA and fatty acyl-CoA stores in the mito matrix used for

A

FA oxidative degradation

50
Q

what is the commitment step in FA oxidation

A

conversion of the fatty acyl-CoA to the carnitine ester

51
Q

why does malonyl-Co inhibit carnitine acyltransferase I

A

we use lots malonyl-CoA for FA synthesis, and it is committed to do so already, so there’s nothing else we can do with it, and synthesis and breakdown do NOT happen at the same time. The commitment step of synthesis inhibits the commitment step of degradation

52
Q

what would happen if you have a defective CGI protein

A

you cannot access DAGs

53
Q

Why would muscle weakness during prolonged exercise be a symptom of a carnitine acyltransferase deficiency?

A

during prolonged exercise, energy storage is from FAs (not glycogen anymore), so FAs are undergoing oxidation.

54
Q

Patients with a carnitine acyltransferase deficiency still can have some beta oxidation of fatty acids during exercise…how?

A

fatty acids that are long have to go through the whole pathway we covered, but smaller FAs don’t need to do that and can go right to the mitochondria

BIOL 3421 - molecular biochem (20 decks)

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