Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Biochemistry 2300 > Lectures 25/26: Lipid Metabolism > Flashcards

Lectures 25/26: Lipid Metabolism Flashcards

1
Q

Atherosclerosis

A

When normal lipid delivery systems are overwhelmed, lipoproteins end up in wrong spot
Lipids are deposited in arterial wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Lipoprotein particles

A

Water-insoluble fat is packaged into soluble lipoproteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Amphipathic

A

Phospholipid, cholesterol, apolipoproteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Hydrophobic

A

Triacylglycerols

Cholesteryl esters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Chylomicron

A

Mainly triglycerides
Density ~0.94
Proteins: apoB48, apoCII, poE
Transport triacylglycerols from intestine to adipose and other tissues
After TG are taken up, remaining chylomicron remnant is taken up by liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Very-Low-Density lipoproteins

A

Half triacylglycerol
Density ~0.94-1
Proteins: apoB48, apoCII, poE
Transport TG form the liver to the adipose and other tissues
TG are taken up, remaining lipoproteins are mainly cholesterol and are LDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Low-Density lipoproteins

A

Almost half cholesterol
Density ~1-1.063
Protein: apoB100
Peripheral tissue takes up to get cholesterol
LDL not taken up by peripheral tissue is cleared by the over
If LDL levels are too high, LDL can deposit cholesterol into arterial walls

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

High-Density lipoprotein

A

Mostly protein, 1/4 cholesterol
Proteins: apoA1, apoE
Transport cholesterol from tissues to liver
Cholesterol is excreted from liver
High HDL levers counteract the cholesterol deposition by LDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Lipid metabolism

A

Triacylglycerols contain fatty acids attached to a glycerol backbone
Fatty acids are broken down into acetyl-CoA, which feeds into the citric acid cycle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Triacylglycerol synthesis

A 
Glycerol-3-phosphate and fatty acyl CoA
Most in liver (VLDL secretion) and adipose tissue (storage)
Energy storage
TG is overflow pathway: excess nutrients
No feedback inhibition of TG synthesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Glycerol kinase

A

In liver

Phosphorylates glycerol to glycerol-3-phosphate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Glyceroneogenesis

A

Adipose tissue: they do not have glycerol kinase
Gluconeogenesis that stops at glycerol-3-phosphate: when glucose is not available, gluconeogenesis to DHAP, then DHAP is reduced to glycerol-3-phosphate
Cannot be active at the same time as glycolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Acyl CoA synthetase

A

Source for fatty acyl-CoA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Glycerol-3-phosphate

A

Precursor for TG and glycerophospholipids

Derived form glycolysis, or DHAP reduced during glycerneogenesis, or synthesized form glycerol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Mitochondrial dehydrogenase

A

Reduces DHAP to glycerol-3-phosphate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Fatty acid activation

A

Binding of fatty acids to CoA

Fatty acid + Co-ASH + ATP = Fatty acyl-CoA + AMP + ppi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Lipoprotein lipase

A

Hydrolyzes TG in capillaries before transport inside cell
Fatty acids are taken up by cells
Glycerol remains in blood stream: water soluble, taken up by liver
Adipose tissue: storage
Muscle: energy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Adipocyte

A

Adipose tissue
Takes up fatty acids
Activates with CoA
Fatty actyl-CoA are esterified with glycerol-3-phosphate to give triacylglycerides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Hydrolysis of triacylglycerols in adipose tissue

A

When body requires energy

Fatty acids and glycerol are secreted into the bloodstream

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Adipose triglyceride lipase (ATGL)

A

Catalyses lipolysis when energy stores are mobilized
Fatty acids excreted and bound to albumin, sent to muscle and liver
Glycerol sent to liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Hormone sensitive lipase

A

Catalyses lipolysis when energy stores are mobilized
Fatty acids excreted and bound to albumin, sent to muscle and liver
Glycerol sent to liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Glycerol

A

Used in liver: glycolysis or gluconeogenesis depending on hormones present
Can be made during chylomicron uptake into adipose tissue or during lipolysis in adipose tissue
Glycerol kinase synthesizes it into glycerol-3-phosphate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Glycerol-3-phosphate

A

Processed by glycerol-3-phosphate dehydrogenase to dihydroxyacetone phosphate: this can be used in glycolysis or gluconeogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Fatty acid oxidation

A

Breakdown of fatty acids in the mitochondrial matrix
Each reaction cycle removes 2 caron from the carboxyl end of the carbon chain
Also called beta-oxidation (broken at the beta end)
1NADH and 1 QH2
Regulated at transport step of fatty acids in mitochondria
Produces acetyl-CoA to enter TCA cycle
Requires oxygen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Step 1 of fatty acid oxidation: activation

A

Activated in cytosol through conjugation to CoA: CoASH

ATP hydrolyzed to AMP and pyrophosphate ppi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Step 2: import into mitochondria

A

Fatty acyl groups are transferred via carnitine

Carnitine deficiency slows down/prevents fatty acid oxidation

27
Q

Beta oxidation

A

Fatty acids degraded to acetyl-CoA
Cycle of 4 reactions, each cycle removes 2 carbons as acetyl-CoA from the carboxyl end of the fatty acid
Total energy yield: 35NADH and 17QH2=139 ATP

28
Q

Beta oxidation: first oxidation

A

Transfer of two electrons to FAD prosthetic group to form FADH2
Transfer of electrons from FADH2 to Q to form QH2
Saturated fatty acyl-coA is oxidized to 2,3-enoyl with C=C double bond
Catalyzed by a dehydrogenase

29
Q

Beta oxidation: hydration

A

Hydrates catalyzes the addition of water to the double bond

Hydroxy group formed

30
Q

Beta oxidation: second oxidation

A

Hydroxygroup oxidized to ketogroup
Electrons are transferred to NAD forming NADH
Catalyzed by a dehydrogenase

31
Q

Beta oxidation: cleavage, thiolysis

A

Catalyzed by thiolase
Release of acetyl CoA and an acyl-CoA chain that is 2 carbons shorter
Shortened acyl-CoA chain undergoes the next round of oxidation

32
Q

Oxidation of very long fatty chains

A

Oxidation in peroxisomes to medium-chain fatty acids which are then oxidized in mitochondria
Peroxisomal fatty acid oxidation does not yield ATP

33
Q

Adrenoleukodystrophy

A

Genetic defects in peroxisomal transports leads to build up of very long chain fatty acids

34
Q

Oxidation of unsaturated fatty acid

A

Additional enzyme are required to degrade the carbon chain around double bonds
Odd numbered double bonds require an isomerase
Even numbered bonds require dehydrogenase
Energy yield is lower than from saturated fatty acids

35
Q

Oxidation of odd chain fatty acids

A

Yields propionic acid, which is covered to succinyl CoA: glycogenic
After last beta oxidation, propionyl-CoA remains, carboxylation and isomeration yields succinyl-CoA
Some odd-chain fatty acids and propionic acid are generated by intestinal bacteria

36
Q

Vitamin B12 deficiency

A

Neurological damage because of accumulation of odd-chain fatty acids in neuronal membranes

37
Q

Fatty acid synthesis

A

In liver, adipose tissue, som other tissues
Synthesis from acetyl-coA, needs NADPH, systolic
Not identical to oxidation
Excess fatty acid synthesis can contribute to inappropriate fat accumulation

38
Q

Step 1 of fatty acid synthesis: transport

A

Transfer of acetyl-CoA into cytosol from mitochondria
Transports as citrate (costs ATP)
Citrate ligase cleave citrate to oxaloacetate and acetyl-CoA in cytoplasm
Cytosolic malic enzyme produces NADPH

39
Q

Step 2 of fatty acid synthesis: activation

A

Acetyl-CoA carboxylase catalyzes first committed step of fatty acid synthesis
Rate limiting step
Uses one ATP to make malonyl CoA

40
Q

Malonyl CoA

A

Inhibits carnitine palmitoyltransferase: import of fatty acids into mitochondria for oxidation

41
Q

Fatty acid synthase

A

Catalyzes the synthesis of saturated fatty acids up to 16 carbons long
540kD protein
To identical polypeptide sequences
Six active sites per polypeptide
Acts as tether and prosthetic group for acyl group of growing chain

42
Q

Acyl carrier protein

A

Fatty acid synthase

Binds and activates acyl groups similar to CoA

43
Q

Step 3 of fatty acid synthesis: elongation

A

Intermediates attach to carrier protein

Two carbons at a time

44
Q

Elongases

A

Makes fatty acids longer than C16 in ER or mitochondria
Addition of C2 units using acetyl CoA or malonyl CoA
4 step reaction
Requires 1NADH and 1NADPH

45
Q

Desaturases

A

Introduction of double bonds to fatty acids
Animals only have 4, 5, 6, and 9 denatures
No insertion of double bond beyond C9 counting carboxygroup
Denaturation coupled with elongation moves double bond down the chain

46
Q

delta4-desaturase

A

Double bond at 4 carbons from carboxyl group

47
Q

delta5-desaturase

A

Double bond at 5 carbons from carboxygroup

48
Q

Linoleum acid

A

Essential fatty acid
Animals cannot synthesize
delta12-desaturation: only in plants
Longer omega-6 and 3 fatty acids are made form linoleic and alpha-linolenic acid: essential

49
Q

Inhibition of fatty acid metabolism

A

From malonyl-CoA: to carinitine

From fatty acid: to acetyl-CoA carboxylase

50
Q

Ketone bodies

A

Synthesized by liver from acetyl-CoA when glucose is scarce and can be used as fuel by the brain
Metabolites: acetoacetate, 3-hydrobutyrate and acetone

51
Q

Ketogenesis

A

From acetyl-CoA in liver
Observed after several days of fasting, when fatty acids are far higher than carbohydrates, and in type 1 diabetes
Liver misses an enzyme of ketone catabolism, so it synthesizes but does not break down ketones

52
Q

Cholesterol synthesis

A

Synthesized from acetyl CoA
Requires NADPH and ATP
Dietary uptake and endogenous synthesis are balanced

53
Q

HMG CoA reductaste

A

Target of cholesterol-lowering drugs, statins

Convers HMG CoA to mevalonate

54
Q

Cholesterol

A

Incorporated into membrane, esterified for storage/packaging into VLDL, converted to bile acids and steroid hormones
Unesterified cholesterol can be cytotoxic: intercalates into membrane and disturbs their function
Cellular cholesterol levels must be tightly controlled

55
Q

Endocytosis of lipoproteins

A

Mediated by specific receptors that recognize the apolipoprotein

56
Q

LDL receptor

A

Located in all cells
Recognize ApoB, ApoE of LDL and VLDL remnants
Without protein part, lipoproteins are not taken up

57
Q

Efflux of cholesterol

A

Can be transferred to HDL to reduce cellular cholesterol content
Mediated by transmembrane protein ABCA1

58
Q

Cardiovascular Risk

A

Positive correlation with serum LDL, LDL/HDL ratio and serum cholesterol with cardiovascular risk
Negative correlation with serum HDL

59
Q

Nile red

A

Stains fat lesions red

High fat, high cholesterol diet leads to increase lesion area and occlusion of arterial lumen

60
Q

Chronic endothelial injury

A 
Hyperlipidemia
Hypertension
Hyperinsulinemia
Skiing
Hemodynamic factors
Toxins
Viruses
Immune reactions
61
Q

Atheroma formation

A

Initial changes in endothelial lining of artery
Monocytes adhere to endothelial cells
Infiltration of monocytes into intimate
Differentiation into macrophages
Causes: increased permeability for LDL, entry and retention of LFL into intimate, mild oxidation of LDL, uncontrolled uptake of LDL into macrophages and foam cell formation

62
Q

Unstable plaques

A

Smooth muscle cells migrate into intimate and proliferate
Further accumulation of lipids
Increased synthesis of extracellular matrix: hardening of artery
Beginning of cell death

63
Q

Plaque rupture

A 
Cell death: formation of necrotic core
Calcium deposition
Cholesterol crystal formation
Plaque instability 
Plaque rupture
64
Q

Lecithin-acyl CoA transferase (LCAT)

A

Activated by ApoA1
Esterifies cholesterol to cholesterol ester
Cholesterol ester forms hydrophobic core

Biochemistry 2300 (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions