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Kaiser-Lipids > Lipids > Flashcards

Lipids Flashcards

1
Q

What are the 5 classes of lipids

A
  1. Fatty Acids
  2. Neutral Glycerides
  3. Phospholipids
  4. Sphingolipids
  5. Cholesterol Derivaties
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2
Q

What is the general structure of fatty acids

A

R-COOH

R group is aliphatic

12-24 carbons long

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3
Q

Are double bonds on fatty acids usually cis or trans

A

Naturally there are cis.

separated by one methylene group.

CH3-(CH2)n-COOH

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4
Q

At higher temperatures are fatty acids solid like or fluid like?

Do double bonds increase or decrease the Tm?

A

Fluidlike. Unsaturated have lower melting points than satruated.

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5
Q

What are neutral glycerides?

A

Neutral glcerides are glycerol molecules esterfied to fatty acids. ex: if attached to three fatty acids it is a triglyceride

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6
Q

What are the three main components of a phosholipid structure

A

glycerol, 2 fatty acids, phosphate (phosphate can be attached to more things)

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7
Q

What is a sphingosine? What happened when it is added to a fatty acid

A

It is a long chain amino alcohol. When added to a fatty acid it becomes ceramide

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8
Q

What are two things that can be added to ceramide and create new types of sphingolipids?

A

If phosphatidylcholine is added it becomes a sphingomyelin

If a carbohydrate is added it becomes a glycospingolipid (ganglioside, globoside, cerebroside)

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9
Q

What are 4 functions of cholesterol?

A
  1. Bile salt precursor
  2. vitamin d prescursor
  3. membrane component
  4. steroid hormones
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10
Q

What component is used to make cholesterol

A

Acetyl Coa

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11
Q

What is a lipoprotein? What is its function

A

Lipid Transport

All plasma lipoproteins are spherical particles consisting of a disorganized core of triglycerides and cholesterol esters surrounded by a thin lipid monolayer of cholesterol and phospholipid. Apolipoproteins are embedded in the surface lipid shell, with their hydrophobic domains oriented toward the core and their hydrophilic domains oriented outward.

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12
Q

How are fatty acids transported

A

free fatty acids are NOT transported by lipoproteins but instead bind to albumin

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13
Q

What is chylomicron

A

A lipoprotein. the lightest and largest of all of them. It is made in the intestine and transports dietary triglycerides to peripheral cells and liver

They are made mostly of triacylglycerols with very little cholesterol, protein or phopholipid

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14
Q

What is the main apoprotein in chylomicron? What is th emechanism of lipid delivery?

A

B48, C E

Hydrolysis by lipoprotein lipase

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15
Q

VLDL

A

80 nm diameter. go form liver to circulation bringing mostly endogenously made triglyceride to cells for storage or use

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16
Q

What is the main protein of apoproteins? mechanism of lipid delivery

A

apoProtein: B100 C E

hydrolysis of lipoprotein lipase

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17
Q

LDLs

A

from intravascular metabolism of VLDLs. Transport cholesterol to perihperal cells

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18
Q

What is the apoprotein adn method of delivery for LDLs

A

B-100 and receptor mediated endoycytosis

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19
Q

HDLs

what apoprotein

A

smallest, most dense. made and secreted by the liver and small intesting. they transfer cholesterol to IDL and LDL

apoprotein A

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20
Q

What are the three kinds of gallstones

A
  1. CHolesterol dark greent o brown over 80% cholesterol
  2. Pigment stones: small and dark contain other parts of bile and less than 20% cholesterol
  3. Mized Stones: 20-80% cholesterol
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21
Q

What are the three main enzymes lipases for lipid digestion?

A
  1. Gastric Lipase in stomach
  2. Bile Salts in SI– emusilfies triaglycerides to smaller particles, reused mostly
  3. PTL lipase from the pancreas breaks them down to a MAG and fatty acid. then bile salts further break down in micelles
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22
Q

By what transport system to eneterocytes bring in lipids

A

enterocytes are inestinal mucoasa cells and they use the FATP4 transport system to bring in the fatty acids. within these cells they make chylomicrons

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23
Q

What does lipoprotein lipase do

A

LPL

it hydrolyzes chlyomicrons and VLDL from the bloodstream. it creates chylomicron remnants

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24
Q

what is steatorrhe

A

excess lipids in poop

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25
Q

Abetalipoproteinamia

A

apo- B-100 defect so that chylomicrons, vldl, ldl cannot be made. there is no long chain fatty acid absoprtion, gi symptoms, vitamin e cant be asorbed, cognitive problem

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26
Q

What are the disordders that could cause extreme chylomicron and triglyceride plasma levels

A

Apo 2-C definecy (protein on chylomicrons required for LPL), LPL defnicency, low LPL activity

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27
Q

What is the emchanism of “fake fats”

A

These potential drugs cannot be absorbed because they are not recognized by the highly specific lipases. ex: Olestra

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28
Q

Potential targets for anti-obesity drugs

A
  1. fake fats

2 lipase inhibitors -orlistat

  1. target fatp4
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29
Q

Where does B oxidation occur

A

inner mt matrix

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30
Q

how do fatty acids get into the mitochondria

A

carnitine shuttle

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31
Q

what are the enzymes used by carnitine shuttle

A

there is carnitine palmitoyl 1 (CPT 1) on the mt membrane and CPT 2 on inner mt membrane. between the fattty acyl coa is temporarily esterfied to carnitine.

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32
Q

what is made at the end of every b oxidation round

A

2 carbon shorter fatty acyl coA, acteyl CoA, nadh, fadh2

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33
Q

What happens with odd chain FA degradation

A

end up with one 3 carbon: propinoyl coa which during a further series of reactions requiring biotin and vitamin b12 as coenzymes you get succinyl Coa

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34
Q

How many ATP are made in the oxidation of a saturated fatty acid

A

Ex: 12:0

5 FADH2= 10 ATP

5 NADH= 15 ATP

6 Acetyl CoA= 72 ATP

-2 ATP for aceyl Coa synthesis

total 95 ATP

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35
Q

Which two diseases did we learn associated with fatty acid degradation

A
  1. Zellweger
  2. Refsum
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36
Q

Zellweger SYndrome

A

No functional peroxisomes to break down fatty acids of certain size. affects cns and elsewhere. patients font live over a year. Shows peroxisomes responsible for breakdown of long fatty acids

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37
Q

Refsum Syndrome

A

Cant degrade 3 methyl branched fatty acids called phytanic acid. get a build up. change diet to exclude fat containing products from ruminant animals, high fat fish

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38
Q

What organ are ketone bodies made in

A

mitochondria of Liver (for use in the brain)

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39
Q

what are the three kinds of ketone bodies

A

3 hydroxybutyrate

acetone

acetoacetate

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40
Q

which molecule do ketone bodies make that cna feed into a cycle

A

they all make acetoacetate which can be turned into 2 acetyl coas which go to the tca cycle

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41
Q

What is the main regulation of ketone body formation

A

release fo fatty acids from adipose tissue (probably hormonally controlled)

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42
Q

What is physiological ketosis

A

late pregnancy, the neonatal period, high fat (low- carbohydrate) diets, starvation and severe exercise. Total blood ketone body levels are mildly elevated but extra-hepatic usage matches hepatic output reasonably well.

43
Q

what is pathological ketosis

A

there is no insluin so cells dont absorb glucose and no gluconeogenesis. leads to massive build up of ketone bodies

usually from insulin, sometimes alcohol

44
Q

What is hypoketoic hypoglycemia? cause, symptoms, treatment

A

symptom of startvation because of insuffiecient utlization of fatty acids as primary energy source

symptoms: muscle weakness, sleepiness, mood changes

treat thtough diet to keep blood glucose levels constantly ok

45
Q

What is the preferred energy source for the brain?

A

main fuel is glucose, can’t do beta oxidation so under fasting it is ketone bodies

46
Q

what is the preferred energy for muscle

A

glucose, ketone bodies and fatty acids. contains large glycogen stores. under resting conditions mostly beta oxidation, if glucose is used it is Cori Cycle

47
Q

preferred energy source for adipose tissue

A

glucose and fatty acids. glucose needed to make glycerol to combine with fatty acids to make triglycerides for storage.

48
Q

Kidney

A

GLucose, FAs, KBs

important site for gluconeogenesis

49
Q

liver energy source

A

alpha keto acids from amino acid degradation under normal conditions. under starvation uses beta oxidation. liver makes ost ketone bodies but cannot use them because of CoA transferase not being expressed. Doesn’t use glucose but makes it. when it does glycolysis it is just to make building blocks. Has glycogen storage.

50
Q

Heart muscle energy source

A

does not store glycogen-very little glucose- mostly aerobic

-gets energy from ketone bodies and FAs

51
Q

Where are fatty acids made

A

mostly in the liver but also adipose tissue

52
Q

Where is fatty acid synthesis

A

Cytosol

53
Q

How is acetyl coa brought to the cytosol for fatty acid synthesis

A

Regualted here at isocitrate dehdrogenase and citrate lyase

High levels of ATP stop isocitrate dehdro

High levels of ADP stop citrate lyase

54
Q

Are fatty acids made during starvation?

A

No. Even though there is acetyl CoA and ATP there is no glucose intake so there are low levels of oxaloacetate in the liver so there can be no FA synthesis. Instead ketone bodies are made

55
Q

What is the overall reaction to make Palmitate?

how many acetyl Coa, NADPH, H, ATP

A

requires 8 acetyl Coa (from amino acids, glucose); 14 NADPH, 14 H, 7 ATP

creates a 16:0 Fatty acid

56
Q

What is the first and most important step of fatty acid synthesis in the cytosol? Does it require any cofactors

A

Acetyl CoA Carboxylase

forms Malonyl CoA

it is the rate limiting, committed step. Requires ATP, Biotin

inhibited by AMPK, increased by Citrate, decreased by palmitoyl CoA

57
Q

Fatty Acid Synthase

What is its structure? How does it attach to intermediates?

A

It carries out the rest of fatty acid synthesis after acetyl coa carboxylase. It is adimer with two identical multifunctional polypeptides. Has a domain that is homologous to ACP

ACP is Acyl Carrier Protein in E. COli (has vitamin component) that attaches to the intermediates of fatty acid synthesis

58
Q

How does alcohol affect the liver

A

It leads to an accumulation of NADH in the mitochondria which inhibits isocitrate dehydrogenase and leads to less glucose synthese

59
Q

Where does chain elongation occur for fatty acid synthesis

A

At the SER Membrane. ELongation starts after 16B palmitate made.

60
Q

DUring elongation how many carbons are added at a time? What is the donor and what is the acceptor

A

2 carbons. Acyl CoA is the donor and the acceptor is Malonyl CoA

uses multiple enzymes unlike first 16C

61
Q

How are unsaturated fatty acids made and where

A

They are made on ER membrane by desaturases. It is direct oxidative desaturation

62
Q

Where on the chain can humans add double bonds

A

omega 9, omega 6 omega 5. so we cannot saturate beyond carbon C

omega 6 and 3 are essential fatty acids.

63
Q

Which enzyme inactivates carboxylase for FA synthesis

A

AMP activated protein kinase (AMPK)

It phophorylates carboxylase. AMPK is upregulated by AMP, down by ATP (allosterically)

64
Q

Which enzymes activates carboxylase for FA synthesis? What regulates it?

A

Protein Phosphatase 2A (PP2A)

it removes the phophate group activating the enzyme. It is increased by insulin, decreased by glucagon/epi

65
Q

What are all the way fatty acids syntheis is regulated

A

AMPK

PP2A

Citrate Lyase

Isocitrate Dehydrogenase

66
Q

What happens to fatty acids during fasting, high fat diet, diabetes and high epi

A

Increased fatty acid oxidation and decreased fatty acid synthesis.

67
Q

How are Lipogenic enzymes regulated

A

They all have similar promoter regions so expression is controlled easier

68
Q

what are lipogenic enzymes

A

All the enzymes in FA synthesis.

acetyl coa carboxylase, FA synthase, citrate lyase, malic enzyme, DH of PPP (to make NADPH)

These are all increased in the long term by high CH diet, linsulin

decreased by: high fat/low CH diet, fasting

Short term are more affected allosteric or covalent modification

69
Q

How do levels of Malonyl CoA effect CPT

A

inversely. when it is why there is less cpt so there is less beta oxiadtion

70
Q

How do these things affect the levels of Acetyl CoA carboxylase?

  1. AMPK
  2. PP2A
  3. Citrate
  4. Palmitoyl CoA
A
  1. inactivates it by phophorylation (increased by AMP, decreased by ATP)
  2. activates it by dephophsylation (increased from insulin, decreased by glucagon/epi)
  3. Increased by citrate
  4. decreased by palmitoyl coA
71
Q

How much does the number of adipose tissue change throughout a lifetime

A

generally set by teen years. unless extreme what changes it the cell volume

72
Q

What happens in adipose tissue in a fed state (high insulin)

A

Glucose is converted into glycerol-P and acetylcoA which is made into fatty acids and combined to make triglycerides.

Chylomicrons and VLDL also feed into the fatty acids

73
Q

What happens in a fasting state in adipose tissue

A

Triglycerides are converted to FA and glycerol by Hormone senstive lipase

-Lipolysis

74
Q

How is hormone sensitive lipase controlled

A

when cAMP is made adenylate cyclase it binds to PKA activating it. When it is active it can ativate HSL by phosphoylation

75
Q

How does insulin effect fatty acid release from adipose tissue

A

Insulin increaes PDE (phosphodiesterase) which facilitates the reaction turning cAMP into AMP so that HSL is never activated.

76
Q

Leptin

A

Made by adipocytes so it is a adipokine. It decreaes hunger and increases caloric expenditure.

Long term effects

77
Q

Ghrelin

A

made by the stomach it increases appetite

changes frequently (with every meal)

short and long term effects

78
Q

Bile Salts

A

In mice increase brown adipose tissue activity, and prevents diet induced obesity and insulin depndent diabetes

they think in humans it incerases energy expenditure. maybe by creating heat

79
Q

Phophoplipid degradation

A

Done by phopholipases. they are all specific to a different part of the phopholipid. Phopholipase C cleaves between glycreol and phophate

80
Q

Where are sphingolipids degraded

A

in the lysosome

81
Q

what causes tay-sachs disease

A

deficiency in enzyme to breakdown gangliosides ( a type of sphinoglipid with a carb attached to a ceramide).

leads to neurodegeneration, blindness, weakenss, seizures and red macula

82
Q

What causes gangliosidosis

A

accumulation of gangiosides. neuro problems, red macula, big liver spleen, skeletal deformitites

83
Q

What is Sandhoff disease

A

Accumulation of globosides

-similar to tay sachs but also visceral involvement

84
Q

What is Fabry disease?

A

x linked globoside accumulation. rashes, kidney/heart failure, burning pain in extremeties

-enzyme replacement therapy available

85
Q

What is Gaucher diseae

A

glucocerebroside accumulation

-most common lysosomal disease

big spleen liver, sometimes cns, osteoperosis

ERT avaialble

86
Q

Niemann Pick (A +B)

A

accumulation of sphingomyelin

big liver spleen, neurodegenreative course, cherry red macula

87
Q

Metachromatic Leukodystrophy

A

sulfatide accumulation

-cognitive problems, demylination, nerves stain

88
Q

Krabbe Disease

A

Galactocerebroside accumulation. mental/motor deteriation. blindness/deafness, no myelin

89
Q

What is Farber disease

A

ceramide accumulation

-joint dformity

90
Q

What are all of the sphingolipidosis diseases

A

tay sachs

farber

gaucher

krabbe

fabry

niemann pick

gangliosidosis

sandhoff

metachromatic leukodystrophy

91
Q

What things can go through the bilayer? partially? not at all?

A

ok: gases, small uncharged polar molecules

Patiral: water, urea

No: large uncharged polar ions, charged polar molecules, ions

92
Q

What is the difference between and early and late endosome

A

Early is right after endocytosis and has the same pH as the blood. a late endosome has a pH drop because of proton pumps. It combines with primary lysosome to form secondary lysosome

93
Q

What happens with the iron receptor

A

Transferring the receptor, is still on in the endosome but is released with the pH drop and the receptor is returned to the surface

94
Q

what are the 4 functions of cholesterol

A

membrane component. precursor of bile salt, vitamin d and steroid hormones

  • it can be made into a lot of different things
  • enzyme definicies all lead to problems
95
Q

is plasma cholesterol realted to death rate

A

yes

96
Q

How much cholesterol is made per day in the body? what is it made from? how is it degraded

A

0.5 g/day in diet, .5 g/day from cytoplasmic synthesis

it is made form acetyl coA

no degradation pathway-they are excereted as bile salts

97
Q

what is the most important enzyme in cholesterol synthesis. where is it

A

HMG-CoA Reducatase in the ER

-drugs target this enzyme

98
Q

What is presented by cells that take up LDL

A

An LDL receptor. Do it by endocytosis. Receptor is recycled. Cholesterol is either stored or incorporated.

LDL receptor binds to Apo B

99
Q

What is familial hypercholesterolemia

A

disorder ohigh-LDL cholesterol levels, mustation in receptor or apoB100. It is autosomal dominant

can be caused by:

no receptr

receptor not properly localized

low affinity for apo9 on reveptor (change in binding domain)

ldl recpeptor does not accumualte in coated pits (mutation in cytoplasmic domain)

100
Q

What are cholesterol levels for heterozygous patients

A

happens to 1/500. blood cholesterol is over 300 mg/dl. The LDL levels are over 220 mg/dl

if untreated 85% have MIs before age of 60

give them statins

101
Q

what happens with homozygrous FH patients

A

10^-6 frequency. blood cholesterol is 500-1200 mg/dl. MI before 30 if untreated. have to dialysis like treatment to remove LDL

-essential HMGcoA reductase is always 100% on.

102
Q

What is SREBP

A

Sterol regulatory element binding protein

-a transcription factor for both LDL receptor and HMG coA reductase. It binds to to SRE on gene.

It is anchored to ER until is cleaved by protease and can go to nucleas. The protease is inhibited by cholesterol

103
Q

What are target levels for

  1. total cholesterol
  2. LDL
  3. HDL
  4. Triglycerides
A
  1. Under 200
  2. Under 160
  3. Greater than 45
  4. Under 150
104
Q

What happens to LDL if it has been in the bloodstream for a long time

A

They get oxidized. And get cleared out by macrophages. These accumualte in foam cells which can cause plaques

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