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Bloc E - GI & Metabolism > Feb9 M1-Lipid Metabolism 1 > Flashcards

Feb9 M1-Lipid Metabolism 1 Flashcards

1
Q

lipids general definition + example

A

organic compound insoluble in water

FAs only have carboxyl, otherwise no polarity

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2
Q

lipids in cell membrane

A

phospholipids, cholesterol, fatty acids

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3
Q

lipids one fct in plasma membrane

A

allow motility and movement of transmembrane receptors

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4
Q

lipids role in brain and adipose tissue

A

brain: insulation for electrical transmission (change in electrical charge across plasma membranes)
adipose tissue: insulation, retain heat

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5
Q

what happens to TGs until absorbed + other source of lipids

A

digested by pancreatic enzymes to make 2-monoacyl-glycerol and fatty acids
(can also synthesize lipids in the body)

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6
Q

what happens to 2-monoacyl-glycerol and fatty acids in intestinal cells

A

resynthesized in TGs and secreted in lymphatics in chylomicrons (lipid rich) then go to blood and to liver

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7
Q

what liver does to chylomicrons

A

hydrozyles them, gets TGs again and secretes them in blood as VLDL

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8
Q

(IMPORTANT) starting molecule for FA synthesis and 1st rx and enzyme

A

acetyl-CoA (2 Cs)

1. add carboxyl group to make malonyl-CoA (3 C) by malonyl-CoA carboxylase

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9
Q

2nd rx to make FAs

A

1 (acetyl-CoA or growing FA chain) +

1 malonyl-CoA + 1 NADH = FA longer by 2 C + CO2 + NAD+ + water

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10
Q

rate limiting enzyme in FA synthesis

A

acetyl-CoA carboxylase

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11
Q

positive regulators of acetyl-CoA carboxylase (2)

A
  • protein phosphatase (insulin cascade, protein phosphatase is phosphorylated, now active, it removes a P from ACC and ACC is active)
  • citrate (a metabolite of TCA cycle so lot of eat shows we have enough nutrients)
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12
Q

negative regulators of ACC (acetyl-CoA carboxylase)

A
  • glucagon
  • E (activates PKA, prot kinase A, which will phosph ACC)
  • high AMP. (sensed by AMP kinase which will phosph ACC)
  • palmitoyl-CoA (end product of the whole thing)
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13
Q

malonyl-CoA important role

A

lowers FA mitochondrial uptake and degradation to make energy (don’t want to do that when synthesizing lipids)

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14
Q

what enzyme takes care of the synthesis of palmitate (16C) + charact

A

FA synthetase (FAS). massive enzyme. homodimer with 2 multifunctional (multireaction) chambers

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15
Q

substrates needed for palmitate synthesis by FAS

A

NADH (many), 1 acetyl CoA, 7 malonyl CoA (cycle of 7 rxs repeated for each malonyl-CoA added

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16
Q

4 things we can do with palmitate

A
  1. extend it (some enzymes can make it 18C or even more but less common)
  2. desaturate it (desaturases can work on carbons 4,5,6,9 starting from carboxyl)
  3. store it
  4. add it or add its derivatives to complex fatty acids
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17
Q

why some fatty acids are essential

A

can’t synthesize fatty acids with double bonds other than on carbon 4,5,6,9 so need some exogenous FAs

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18
Q

functions of essential FAs (that we can’t synthesize)

A

positive effects on cholesterol synthesis and metabolism

19
Q

what storing palmitate means

A

make it TGs by adding this FA to glycerol (make triacylglycerol, synonym of TG)

20
Q

step 1 in storing palmitate

A

glycerol phosphate (glycerol with P in C3) + palmitate give glycerol P with palmitate on C1 (done by acyltransferase)

21
Q

step 2 in storing palmitate

A

add palmitate on C2 of the glycerol (get DAG phosphate, glycerol with palmitate on C1,2 and P on C3)
(done by acyltransferase)

22
Q

step 3 in storing palmitate

A

DAG phosphate (also called phosphatidic acid) has its P removed by a phosphatase to make DAG (important signaling molecule)

23
Q

step 4 in storing palmitate

A

DAG (signaling molecule) has FA (palmitate) added to C3 by acyltransferase

24
Q

what happens in the liver with TGs made from palmitate

A

exported in VLDL (apoB), goes to adipose tissue, TGs broken into FFAs and glycerol

25
Q

complex FAs that we can make palmitate into

A

can make it phospholipid or glycolipid

26
Q

phospholipid composition

A

glycerol with 1 FA chain on C2 + one carbon with phosphate + important moiety added for membrane fluidity and structure (bc has neg charge)

27
Q

glycolipid composition

A

glycerol with N-FA chain on middle C, FA on a side C and carbohydrate on other side carbon

28
Q

platelet-activating factor composition

A

glycerol with P + moiety on a side C, acetyl group on middle C, saturated FA on last C

29
Q

platelet-activating factor function

A

when released, binds receptor on platelets and affects coagulation and clotting properties

30
Q

enzyme family that cleaves phospholipids and how the enzymes in the family differ

A

phospholipases A1, A2, C or D. depending on where they cleave the carbons of the glycerol backbone

31
Q

phospholipase 2: why important component of venoms and why is toxic

A
  1. cleaves a substrate to release arachidonic acid (highly inflammatory molecule)
  2. toxicity to cells by binding a specific receptor
32
Q

sphingomyelins composition

A

sphingosine molecule with N-FA on 2nd carbon (all that forms ceramide) and then moiety (like choline) added on 3rd carbon

33
Q

sphingosine def

A

glycerol with saturated FA on 1st C

34
Q

sphingomyelins function

A

highly present in CNS. role in electrical activity of neurons

35
Q

Niemann-Pick disease pathophgy

A

sphingomyelinase deficiency. can’t cleave phosphochlorine off the ceramide (of sphingomyelin) and sphingomyelin accumulates

36
Q

why sphingomyelinase deficiency is a problem

A

sphingomyelin is constantly turned over (broken down and synthesized)

37
Q

hallmarks of Niemann-Pick disease

A
  • enlarged liver and spleen filled with lipids
  • mental retardation and neurodegen
  • death in early childhood (type A)
38
Q

what gives the glycolipids different properties

A

the different sugars attached on them

39
Q

ganglioside GM2 structure

A

ceramide (glycerol backbone C1 = FA, C2 = N-FA) with glucose, galactose, and galactosamine molecules

40
Q

main problems and symptoms seen in lipids metabolism defects

A

CNS, neuro, seizures, degeneration

41
Q

Tay-Sachs disease cause

A

defect in beta hexosaminadase A resulting in accumulation of ganglioside GM2

42
Q

2 regions of high Tay-Sachs prevalence in Quebec + how it differs

A

Saguenay Lac Saint-Jean region and Ashkenazi Jews. mutation is diff in the two groups

43
Q

2 Tay-Sachs regions within French Canadian population + how they differ

A
  1. Saguenay Lac Saint-Jean
  2. Bas Saint-Laurent and péninsule du Gaspé
    * two different mutations

Bloc E - GI & Metabolism (58 decks)

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