Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Cell Metabolism and Metabolic Control > Lipids > Flashcards

Lipids Flashcards

1
Q

Functions of lipids

A

Fuel/energy storage
Biological membranes
Intracellular messengers, cofactors and vitamins
PTMs

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

Lipid classes?

A

8 main, e.g. sterols, FAs etc

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

Why is glucose converted to fats for storage? Lipids vs glycogen stores?

A

We have almost an almost unlimited capacity for fat storage, unlike glycogen which is finite
Lipids - 80% stored energy, supply for about 12 weeks
Glycogen - 2500kJ, about 12 hours

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

FAs vs triglycerides?

A

FAs amphipathic, forming micelles (not great)

Esterified to TAGs - highly reduced, hydrophobic (unlike glycogen)

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

Synthesis of FAs

A

Begins with acCoA – malonyl CoA via ACC in cytosol

AcCoA first transferred to cytosol with citrate shuttle
FAS (FA synthase) builds up malonyl CoA into FA chain until it is 16C long = palmitate

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

Citrate shuttle

A

Returns oxaloacetate to mitochondrial matrix by conversion to malate with NADH and H
Oxaloacetate + acCoA in matrix = citrate
Critrate exported out and cleaved in cytosol to leave oxaloacetate and acCoA

Uses 2ATP

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

Types of FAS?

A

FASI - vertebrates and fungi, single polypeptide chain with multiple active sites forming homodimer
Chain is built up within the complex, sheltering hydrophobic intermediates from cytosol
More efficient - concentrated intermediates in complex passed between sites
Coordinated regulation of only one enzyme

FASII - plants and bacteria, separate enzymes
Diversion of FA intermediates allowed if needed in other pathways

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

FA synthesis end product and consumption?

A

Uses 1 ATP for malonyl-CoA production, and 2NADPH = energy expensive

Palmitate main product, extended by elongase enzymes in ER 
or desaturated (double bonded) by desaturase enzymes in ER
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Essential FAs?

A

Those mammals cannot produce e.g. linoleate, a-linoleate, needed from diet

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

FA synthesis regulation?

A

Max rate when metabolites and ATP are abundant
This is because when glycogen stores are saturated, excess glucose is converted to FA

ACC is main regulatory enzyme, controlled allosterically, by covalent mods, or by course control

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Control of ACC

A

Hormones - global control
Insulin (stimulates) through protein phosphatase 2A activation for dephos of ACC

Glucagon and adrenaline inhibit via PKA activation = phosphorylation = inactive ACC. They also suppress protein phosphatase 2A

Local control
Low ATP/high AMP = AMPK = phosphorylation

Binding of citrate (allosteric) promotes polymerisation to active filaments, even if phosphorylated globally

Binding of palmitoyl-CoA does opposite (dissociation to inactive dimers) through feedback inhibition

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

Regulation points of phospholipids/TAG synthesis?

A

GPAT, PAP, DGAT

HMG-CoA reductase

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

Fate of FAs?

A

Phospholipids or TAGs depending on physiological needs e.g. fed state, growth requirements

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

Synthesis of phospholipids/TAG

A

Common pathway from G3P, derived from DHAP in glycolysis

FAs esterified to CoA to make acyl-CoA with acyl-CoA synthase
Acyl chains transferred to -OH glycerol by acyl transferases eg GPAT

Esterification of 2 acyl chians to G3P = intermediate phosphatic acid for further processing to either phospholipids/TAG

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

Difference between acyl and acetyl?

A 
Acyl = chain tail region of FA
Acetyl = 2c addition by malonyl-CoA earlier
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

TAG production

A

PAP (phosphatid acid phosphatase) removes phosphate from phosphatic acid - diacylglycerol
DGAT adds 3rd acyl chain = TAG
Occurs on cytosolic face of ER and mc

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

TAG storage

A

Stored in dynamic lipid droplets in all cells, budding off from ER
Coated with perilipins
Associated with lipase enzymes for TAG breakdowns, lipase regulatory proteins and components for TAG synthesis
(if from adipose tissue)

Alternative storage if liver-synthesised; as lipoproteins in circulation

Mammary glands - secreted into milk

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

Brown adipose tissue?

A

Hibernating animals/newborns

Generates heat through oxidation of FAs in lipid droplets by mc that express thermogenin so no ATP is made

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

Regulation of TAG synthesis

A 
GPAT - first acyl transferase, fine control, inhibited by phosphorylation through PKA (glucagon/adrenaline): increasing FA oxidation
or AMPK (low ATP:AMP): decreasing glycogen and TAG synthesis

PAP - branchpoint of TAG vs phospholipids
Compartmentation; movement to ER membrane = active, contacting PA stimulted by high FA in cytoplasm (feedforward to prevent FA toxic build up)

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

Role of cholesterol?

A

Fluidity of membrane
Steroid hormone precursor
Cardiovascular disease
Diet and synthesises in liver (not in plants)

21
Q

Synthesis of cholesterol?

A

2 AcCoA + AcCoA = HMG-CoA on ER cytosolic leaflet

HMG-CoA reductase catalyses = mevalonate
Several steps = cholesterol

22
Q

Fine control regulation of HMG-CoA reductase

A

Phosphorylation, short term
PKA, AMPK = inactive
Protein phosphatase = active

Responds to energy levels - low = inactive because process is energy expensive

23
Q

Course control of HMG-CoA reductase

A

TF family SREBP
High cholesterol = SREBP on ER membrane, inactive
Low = cleavage of TF domain, migration to nucleus

Sensed by SACP and Insig, which bind sterols and oxysterol when their conc is high = binding to SREBP = retention at ER

Insig degraded when not binding sterols, SCAP and SREBP binding = golgi secretion where TF domain is cleaved

24
Q

Role of TAGs

A 
Store of metabolic fuel
Membrane expansion
Sterol provision
Toxicity protection - sequestration of unesterified amphipathic FAs to prevent unwanted membrane interactions
Signalling
25
Adipocytes?
Main storage of lipid droplets | Produce hormones e.g. lectin to regulate appetite/hunger in response to lipid droplet size
26
Why are TAGs good energy stores?
Carry more energy per carbon (more oxidation allowed), and non-polar so bind less water e.g. than glycogen Good for long term - released more slowly
27
TAG breakdown
By lipases TAG - DAG - MAG - glycerol (can enter glycolysis for some energy) FAs released = beta oxidation for majority of energy
28
Lipases in TAG breakdown?
Hormone sensitive lipases (HSL); first two Adipose triglyceride (ATGL) for first step Monoacylglycerol (ATGL) for last step
29
Regulation of TAG breakdown
Hormone-triggered Glucagon/ adrenaline bind GPCR = adenylyl cyclase activated = PKA activation = first HSL and perilipin (recruits HSL) phosphorylated for activation.
30
Perilipin in breakdown?
Coats the lipid droplets - conformational change from phosphorylation allows HSL to enter, increasing lipolysis by over 50 fold (HSL alone = 2/3 fold)
31
ATGL in lipolysis? Regulation?
HSL knock-out mice show this is key factor, main element acting in first step Found in adipose tissue: transcription inhibited by insulin, induced by fasting Fine control - activated by regulatory protein CGI-58 and phosphorylation by AMPK
32
Coordinated regulation of lipolysis?
Glucagon - perilipin phosph, CGI dissociates to form CGI-58 Recruits ATGL to surface for step 1 HSL recruitment and phosph = step 2 MGL = final stage
33
Inhibition of lipolysis?
Insulin, fine control Phosphatase enzymes reverse phos Phosphodiesterase (PDE) blocks cAMP activation of PKA
34
Processing of dietary FAs?
Emulsification in small intestine by bile salts = micelles TAGs partly digested in small intestine = MAGs MAGS -- intestinal mucosa epithelial cells -- TAGs Form chylomicrons with cholesterols, secreted to lymph -- blood -- tissues
35
Chylomicrons
Packaging of hydrophobic TAGs for transport Core = lipids Surface = phospholipids/apolipoprotins for targeting
36
Apolipoprotein C-II
ApoCII binds lipoprotein lipase on capillary surfaces in muscle/adipose
37
Lipoprotein lipase
Extracellular, hydrolyses TAG = FAs and glycerol Activated by ApoCII binding Secreted by target cells
38
Lipoprotein classes
Chylomicrons - least dense, most TAG. Dietary lipid from intestine VLDL TAG and cholesterol ester Endogenous lipid from liver LDL Cholesterol and chol esters (VLDLs minus TAG) Uses ApoB-100 HDL Protein Conversion of cholsterol in LDL/VLDL to esters Various apolipoproteins
39
Interconversion of lipoproteins?
High dietary FAs = chylomicron remnants into liver = VLDLs, broken down by lipase = free FAs VLDL remnants = LDL, cholesterol enters liver etc
40
LPL (lipoprotein lipase) regulation
Course control as extracellular Inversely regulated in response to TAG needs in adipose (storage) or muscle (energy) Fasting -- muscle isoform upregulated --- breakdown of FAs by oxidation and vice versa Expression controls where lipoproteins are used
41
LDL metabolism and regulation
Different mechanism - bind a ApoB-100 to cell-surface receptor Taken up in clathrin-coated pits, enter endosomes Receptor back to cell surface LDL digested in lysosomes LDL receptor regulation transcriptionally with SREBP
42
FA transport?
Longer chains - shorter ones can diffuse FAT/CD36 = receptor FATP1-6 = transporter protein FABPpm = binding protein
43
Regulation of CD36?
Stored in vesicles (compartmentation) - released to membrane by insulin/AMPK
44
Carnitine shuttle?
Transport of FAs into mitochondria, as inner mc membrane is impermeable to >12c FAs acyl-CoA -- acyl transferred to carnitine by acyltransferase 1 in outer membrane, Transporter in inner membrane exchanged this for carnitine acyltransferase 2 in matrix returns acyl group to CoA
45
FA oxidation in mc matrix
FA chain oxidised to give 2c acetyl-CoA, NADH and FADH2 (sequential, 4 reactions in each) acCoA oxidised to CO2 in CAC, also giving NADH and FADH2 ATP generated from ADH and FADH2 in electron transport chain
46
Alternative FA oxidation?
Long or branched FA breakdown happens in peroxisomes | FA chains with odd carbon numbers have added 3 reactions at the end
47
Regulation of FA oxidation
Derivation of FA from TAGs Uptake of FA - proteins like CD38, FATP1-6, FABPpm Carnitine shuttle
48
Regulation of carnitine shuttle
Component 1, CAT1 - catalyses acyl group transfer to carnitine Catalytic domain inhibited by malonyl-CoA (first intermediate in FA synthesis, to inversely regulate FA synthesis and oxidation) Tied in to ACC, reglating FA synthesis - glucagon = ACC inactivation = less malonyl CoA = FA uptake and breakdown

Cell Metabolism and Metabolic Control (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions