Lipid Metabolism Revision Flashcards

1
Q

lipoprotein lipase site and co factors required

A

vascular endothelium of extra hepatic tissue

requires apo c 11 and phospholipids

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2
Q

lipoprotein lipase vs HSL vs pancreatic lipase

A

lipoprotein lipase- break TAG in blood (from chylomicron) for uptake during feeding
HSL- break TAG during fasting that is stored in adipose tissue for oxidation
pancreatic lipase- break TAG in cavity of intestine for digestion during feeding

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3
Q

glycerol fate

A

can’t be utilized by adipose tissue due to deficiency of glycerol kinase so goes to liver and kidney

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4
Q

key enzyme of lipolysis

A

HSL helped by MAG

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5
Q

how do long chain fatty acids get to mitochondria

A

they from acyl coA which does in inner space of mitochondrial matrix then binds with carnitine to make acyl carnitine with CPT1 and goes to matrix by carnitine shuttle and in the matrix of the mitochondria, CPT2 separates acyl coA from the carnitine and the carnitine goes back to inner space.

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6
Q

each cycle of FA oxidation will release

A
acetyl coA (enters krebbs after)
formation of one FADH2 and one NADH
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7
Q

steps of beta oxidation

A

acyl coa – acyl CoA DH –> delta 2 trans enoyl coA –> beta hydroxyacyl coA –> b ketoacyl coA –> acetyl coA + new acyl coA (2 carbons less)

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8
Q

calculate # of acetyl coA
# of cycles
complete oxidation of FA

A
# of carbon / 2
# of acetyl coA - 1
7C-6
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9
Q

Importance of FA oxidation

A
  1. supply body with energy in starvation

2. formation of acetyl coA

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10
Q

malonyl coAA effect on b oxidation

A

produced during FA synthesis inhibits CPT 1

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11
Q

How is FADH2 released from peroxisomal oxidation regenerated?

A

by giving its H2 to H2O2 to from 2 H2O and it doesn’t go to ETC

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12
Q

refsum disease and symptoms

A
deficiency in a hydroxyls so accumulation of phytanic acid 
DBAP 
deafness
blindness
ataxia
polyneuropathy
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13
Q

two systems for fatty acid synthesis

A
  1. cytosolic de novo (lipogenesis)

2. microsomal system for elongation

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14
Q

acetyl coA for FA synthesis comes from

A

carbohydrate metabolism

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15
Q

site of cytosolic or de novo fatty acid synthesis vs microsomal

A

de novo: liver and lactating mammary gland and some in adipose tissue
microsomal: endoplasmic reticulum

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16
Q

how is acetyl coA produced from TCA go to cytosol for de novo synthesis and what happens to oxaloacetate

A

through citrate shuttle
oxaloacetate is then turned to malate then to pyruvate by Malik enzyme which can go back to mitochondria .
you can convert oxaloacetate straight to pyruvate if you don’t need NADPH+H

17
Q

FA synthesis enzymes

A

ACC- acetyl coA -> malonyl CoA

FAS- multi enzyme complex (7 enzymes and have acetyl carrier protein)

18
Q

product of FA synthesis

A

palmitic acid

19
Q

microsomal system differs from denote in 3 aspects

A
  1. can’t imitate, just elongate from 10-24
  2. enzymes are separate
  3. no ACP
20
Q

glycerol 3 phosphate in adipose tissue

A

no glycerokinase in adipose tissue (only liver and kidney) so produced by glucose by turning it into DHAB.

21
Q
tissue fat vs depot fat
site
function
composition
amount and effect on diet
A

tissue- every cell, enter in structural elements and not used for energy. made up of phospholipids, glycolipids and cholesterol. constant and not affected by diet.

depot fat- adipose tissue and for energy storage, TAG and increases by overeating and decreases by fasting

22
Q

tissue fat or depot fat?

which is rich in saturated and unsaturated fatty acids?

A

tissue fat- unsaturated fatty acids

depot fat- saturated fatty acids

23
Q

how are cyclic compounds formed?

A

from prostaglandin H synthase which has 2 activates: COX and peroxidase

24
Q

COX 1 vs COX 2

A

cox 1 - enzyme found in most tissues

cox 2- enzyme that is generated due to response to inflammation

25
Q

acrylic compounds: how are they formed and ex?

A

formed by action of lypoxygenase and leukotrienes and lipoxins

26
Q

functions of eicosonaoids

PGE2 and PGE2 alpha site and functions

A

both are in most tissues.
PGE2- vasodilation, muscle relaxation, relieves asthma. does antiflammatory reactions to protect body such as pain, fever, and vasodilation.

PGE2 alpha- vasoconstrictor, muscle contraction, causes bronchoconstriction, used in induction of labor

27
Q

PGI2 and TXA2 Site and function

A

PGI2- Endothelium of blood vessels
does vasodilation and inhibits

TXA2 - platelets
does vasoconstriction and activates lately aggregation

28
Q

leukotrienes and lipoxins site and functions

A

leukotries- platelet, mast cells, leukocytes
stimulate migration of neutrophils (chemotaxis) for polymorphonuclear infiltration in inflammatory reactions. It also does allergic reactions

lipoxins - arterial walls and anti inflammatory and decrease immune response

29
Q

steroidal anti inflammatory drugs inhibit: and ex

A

ex: hydrocortisone, prednisone, betamethasone
NO COX, NO LOX

phospholipase A2 so less availability of arachidonic acid

30
Q

non steroidal anti inflammatory drugs (NSAID) inhibit and ex

A

inhibit COX

aspirin: inhibit COX 1 more than COX 2 = bad
other: inhibit both equally such as ibuprofen and indomethacin

31
Q

singular

A

inhibits LOX so relieves bronchospasm and allergic reactions