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BCMB > Week 8 > Flashcards

Week 8 Flashcards

lipid metabolism

1
Q 
Fatty acids (FA) 
(function, synthesis, stimulator)
A

used as fuel in the body
Synthesized from glucose
Stimulated by insulin

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2
Q

Triacylglycerol (TAG)

Function, synthesis, transport/location

A

is the storage form of FA made in the liver.
Major dietary lipid
Travel in circulation as chylomicrons (dietary) or VLDL (endogenously synthesized)

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3
Q

How are Dietary Lipids digested?

A

Emulsified in small intestine by bile salts and Pancreatic lipase and colipase

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4
Q

Pancreatic lipase and colipase function

A

Hydrolyzes TAGs into free FAs and esterified glycerol

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5
Q

pancreatic esterases function

A

remove fatty acids from other compounds (cholesterols, etc)

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6
Q

What happens to Lipid/Bile micelles

A

Lipid portion is absorbed into the intestinal epithelial cells
(Chylomicrons)
Bile is resorbed in the ileum, to be re-used.

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7
Q

Do short and medium FA chains need bile?

A

No, they are absorbed directly into cells & will enter blood, transported by serum albumin

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8
Q

Synthesis of Chylomicrons

A
  1. Free FAs and 2-MG are re-formed into TAG in the intestinal smooth endoplasmic reticulum
  2. TAGs must be transported in lipoprotein particles due to insolubility
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9
Q

chylomicrons function

A

Transport of dietary fats

Newly released chylomicrons are called ‘nascent’

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10
Q

ApoE

A

ligand for membrane receptors on many cells (esp liver), allows entry into cell

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11
Q

ApoCII

A

activator of lipoprotein lipase (LPL)

Capillary endothelial cells, muscle and adipose tissues

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12
Q

chylomicron maturation

A

HDL in lymph and blood will transfer proteins to chylomicron, ‘maturing’ it

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13
Q

What tissues use oxidation of FA as a fuel source? And when?

A

primary fasting fuel source in cardiac, skeletal muscle, and liver

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14
Q

What tissues use the conversion of FAs to ketone bodies?

A

major fasting fuel source for brain, gut, etc.

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15
Q

Long Chain FAs are a predominant source of…

A

predominant source of oxidation for fuel during fasting states

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16
Q

Transport of Long Chain FAs

what releases them, how it travels through the blood, how it gets to the liver, and final destination when in the cell

A

Released from adipocytes by lipases
Travel in hydrophobic pocket of albumen through the blood
Transported into cell either via passive diffusion through bilayer or facilitated with fatty acid binding protein
Inside the cell, the FA is transported to mitochondria

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17
Q

Activation of Long Chain FAs

A

Must be activated by acyl-CoA before they can be oxidized

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18
Q

Acyl-Coa synthetase only activates…

A

long chain FAs, and is in ER, outer mitochondrial membrane, and peroxisome membrane

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19
Q

Very long chain synthase location

A

present in peroxisomes

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20
Q

medium chain synthetase location

A

present in mitochondrial matrix of liver and kidney cells.

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21
Q

Transport of Long Chain FA into MT

A

Carnatine serves as the transporter between outer and inner mitochondrial membranes

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22
Q

β-Oxidation

A

Sequentially cleaves the fatty acyl group into 2C acetyl-CoA units, starting with the carboxyl end attached to the CoA.
β carbon must be oxidized first

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23
Q

β-Oxidation: step 1

A

double bond formed between β and α carbons

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24
Q

β-Oxidation: step 2

A

water donates OH to β-carbon; and H to α-carbon

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25
Q

β-Oxidation: step 3

A

hydroxyl group of β carbon oxidized to a ketone

26
Q

β-Oxidation: step 4

A

bond between α and β carbons is cleaved by adding a coenzyme A (CoASH) to the βcarbon

27
Q

Energy Yield of β-Oxidation

A

1 mole of palmityl-CoA converted to 8 mole of acetyl CoA yields:
28 mole ATP

28
Q

Oxidation of Odd-Chain-Length FAs

A

Will undergo β oxidation rounds until there are 5 carbons left

29
Q

Oxidation of Medium-Chain FAs

A

Activated to acyl-CoA derivatives, then oxidized to acetyl CoA via β-oxidation spiral

30
Q

Medium-chain-length acyl-CoA synthetase has a broad range of…

A

specificity
Can bind drugs which are approx. same size
Salicylate (aspirin metabolism) and Valproate (anti epileptic)

31
Q

where are very long chain FAs oxidized?

A

exclusively in peroxisomes

32
Q

what tissues can not use FAs as fuel source?

A

RBCs (no mitochondria!)
Adipocytes
Brain

33
Q

Ketone bodies function

A

serve as major source of energy in these tissues

34
Q

where are ketone bodies synthesized? released? what is it converted into?

A

Synthesized in liver from acetyl CoA (generated in β-oxidation)
Released into the blood as ketone bodies – re-converted to acetyl CoA in tissues for TCA cycle

35
Q

Ketogenic diets

A

High protein, low carb diets are considered ‘ketogenic’

High amounts of ketogenic amino acids

36
Q

How is Ketogenesis regulated?

A

inhibited by insulin and feeding

activated by fasting and increases in cAMP and lipolysis

37
Q

Skeletal muscle preferences for Fuel Sources

A

Skeletal muscle will preferentially use FAs over glucose as fuel as FA concentration increases in blood

38
Q

FA Synthesis

what stimulates it, location, precursor, products

A

Stimulated when excess calories are ingested.
Occurs primarily in the liver, process begins with glycolysis, citrate from glycolysis moves to cytosol and reforms acetyl CoA. Acetyl CoA is converted to malonyl CoA.

39
Q

What is FA Synthase Complex? What does it create?

A

Large enzyme complex, many subunits. Creates 16 C long chain called palmitate

40
Q

Activation and conversion of Palmitate

A

Activated to Palmitoyl CoA

Converted to TAG in the liver

41
Q

De-saturation of Fatty Acyl CoA

location, molecular requirements, restrictions

A

Occurs in endoplasmic reticulum

Requires NADH, O2, and cytochrome b5

Some cannot be synthesized, so must be obtained from diet
Omega 3 fatty acids (ω 3 FA) and Omega 6 fatty acids (ω 6 FA)

42
Q

Synthesis of TAG and VLDL

A

Occurs in the liver and adipose tissue using G3P from glycerol or DHAP

43
Q

Lipoprotein lipase (LPL)

A

Delivers of VLDL TAGs. Cleaves TAG into FA and glycerol

44
Q

Km of muscle LPL

A

Has a low Km. Allows it access to fuel source even when levels are low

45
Q

Km of adipose LPL

A

Has a high Km. Will only work in fed state (storage)

46
Q

Fasting – Adipocytes Release FA

A

When insulin is low, adipocytes will break down their stores of TAGs into FAs and glycerol
Hormone sensitive lipase

47
Q

Glycerophospholipids and Sphingolipids are lipids that aren’t used for fuel. What other functions do they have?

A 
Cell membranes (phosphatidyl choline, etc)
Signaling molecules (PIP2, arachidonic acid, etc)
Myelin sheath (sphingomyelin)
48
Q

Synthesis of Glycerolipids

A

Glycerol 3-P + 2 activated FAs form phosphatidic acid
Hydrophilic head-groups are added to third carbon of the glycerol
Polar uncharged OR charged

49
Q

Degradation of Glycerophospholipids

A

Phospholipases in cell membrane or lysosomes degrade glycerophospholipids

50
Q

Cholesterol synthesis: Part 1

A

Synthesis of mevalonate from acetyl-CoA

Committed and rate limiting step

51
Q

Cholesterol synthesis: Part 2

A

3 phosphates are added to mevalonate to activate it
Forms activated isoprenes (5 carbons)
isomers

52
Q

Cholesterol synthesis: Part 3

A

Six of these activated isoprenes are condensed to eventually form Squalene

53
Q

Cholesterol synthesis: Part 4

A

Forming ring structures from the squalene

54
Q

VLDLs transport

A

Transport endogenous fats

Liver to peripheral (muscle, adipose)

55
Q

IDLs transport

A

Remnants of VLDLs not taken up by the liver

Still contain some TAGs and cholesterol

56
Q

LDLs transport

A

low density lipids
After some TAGs removed from IDL (usually to liver)

Rich in cholesterol

Deliver to liver (~60%)

Deliver to adrenocortex, gonads, etc (steroid synthesis)

57
Q

HDL and Reverse Cholesterol Transport

A

Maturing HDLs are picking up cholesterol of tissues

To prevent it from diffusing back to the tissues, LCAT within the HDL will convert it to a cholesterol ester, thus trapping it inside the HDL

HDL will then deposit the excess cholesterol back to the liver

58
Q

Cholesterol ester transfer protein (CETP)

A

mediates the swapping of TAGs with cholesterol esters between VLDLs and HLDs

59
Q

Apoproteins function

A

serve as receptor ligands/directing to specific tissues

60
Q

maturation of HDLs

A

Accumulate phospholipids and cholesterol from vascular endothelial lining

Fills the empty inner core of the nascent HDL, becomes more round = mature HDL

BCMB (8 decks)

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