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FoundSci Unit 4 > Lipid Synthesis > Flashcards

Lipid Synthesis Flashcards

1
Q

What are the functions of peroxisomes and what do they not produce?

A

Peroxisomes breakdown very long chain fatty acids through Beta oxidation until the chain length is 20 carbons

Also use alpha oxidation to degrade branched chain fatty acids (phytanic acid)

Synthesize fatty alcohols like plasmoglogens that are enriched in nervous, immune, and cardiovascular system

Peroxisomes do not produce ATP

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2
Q

What is different between perosiomal enzymes and mitochondrial equivalents?

A

Beta oxidation starts with an oxidase and produces hydrogen peroxide from FADH

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3
Q

What does it mean that peroxisomes do not produce ATP?

A

No citric acid cycle to oxidize acetyl-CoA

No electron transport chain to oxidize NADH

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4
Q

What is the main oxidase involved in Beta oxidation?

A

Acyl-CoA Oxidase

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5
Q

How do peroxisomes degrade phytanic acid?

A

Alpha Oxidation - Cells hvae no other mechanism to degrade branched fatty acids

Process that removes a one carbon fragment from the fatty acid and produces formyl-CoA instead of acetyl-CoA

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6
Q

What often causes peroxisome biogenesis disorders?

A

Mutations in PEX genes

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7
Q

How does a patient with Zellweger Syndrome present?

A

Mutation in PEX1 and is a peroxisome biogenesis disorder.

Patient presents with multiple developmental abnormalities, no peroxisomes in liver. Diagnosis includes accumulation of very long chain fatty acids in blood

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8
Q

How does a patient with Refsum disease present?

A

Alpha oxidation deficiency and is a peroxisomes biogenesis disorder.

Patient presents with multiple developmental abnormalities. Diagnosis includes accumulation of phytanic acid in blood.

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9
Q

What state does fatty acid synthesis occur in and where is synthesis most active?

A

Fatty acids are synthesized in the fed state.

Most active in the liver and adipose tissue

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10
Q

Where do fatty acid synthesis reactions occur?

A

In the cytoplasm

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11
Q

What is the significance of mitochondrial acetyl-CoA for fatty acid synthesis?

A

Fatty acid synthesis starts with acetyl-CoA

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12
Q

Synthesis of fatty acids repress ____

A

Fatty acid degradation

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13
Q

What are fatty acids converted to in the liver and adipose tissue?

A

Liver - Triacylglycerol (TAG)

Adipose - TAG droplet

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14
Q

Does the liver store fat?

A

No! But it makes a lot of it

If fat is found in the liver, it is pathological

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15
Q

What happens to fat made in the liver?

A

Fat is packed into lipoproteins and moved into circulation.

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16
Q

What happens to fat made in adipose tissue?

A

Stored!

Brown fat (thermogenic) and white fat (stores)

Adipose tissue is considered an endocrine organ

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17
Q

How does the body get ready to make fatty acids? (general)

A

Insulin stimulate glucose catabolism, which causes the mitochondria to fill with acetyl-CoA

The acetyl-CoA is exported from the mitochondria to the cytoplasm

Insulin activates the committed step of FA synthesis –> Acetyl-CoA carboxylase

18
Q

What are the 3 phases of fatty acid synthesis?

A
  1. Export of mitochondrial acetyl-CoA into the cytoplasm
  2. Committing acetyl-CoA to FA synthesis by carboxylation to malonyl-CoA
  3. Assembling a FA from acetyl-CoA and malonyl-CoA units
19
Q

How is acetyl-CoA exported from the mitochondria? First phase of FA synthesis

A

Tricarboxylic Acid Transporter

  1. Citrate formed from oxaloacetate and acetyl-CoA
  2. Citrate crosses the inner mitochondrial membrane into the cytosol through the TCA transporter
  3. ATP-citrate lyase cleaves citrate into its components; acetyl-CoA and oxaloacetate
  4. Acetyl-CoA used for FA synthesis
  5. Oxaloacetate is converted into pyruvate via malate dehydrogenase and malic enzyme which yields one molecule of NADPH
20
Q

Explain the second phase of FA synthesis which is committing acetyl-CoA to FA synthesis

A

Acetyl-CoA carboxylase converts acetyl-CoA to malonyl CoA (biotin dependent). This enzyme is active in the fed state.

Insulin activates Acetyl-CoA carboxylase through dephosphorylation

21
Q

What activates and inactivates acetyl-CoA carboxylase?

A

Activated by dephosphorylation by insulin in fed state

Inactivated during fasting by glucagon. Inactivated by epinephrine and inactive when energy is low (AMP)

22
Q

Explain the third phase of fatty acid synthesis where FA are synthesized from acetyl-CoA and malonyl-CoA

A

Fatty Acid Synthases assembles a 16 carbon fatty acid from acetyl-CoA and malonyl-CoA

Steps:

  1. Acetyl group transferred from acetyl-CoA to acyl-carrier protein site A on FA synthase
  2. Acetyl group moved from A site to a cysteine residue on C site
  3. Malonyl-group transferred from malonyl CoA to A site of FA synthase
  4. Acetyl group on C site moved to alpha carbon of malonyl group on A site and CO2 is released
  5. Keto group of Beta carbon is removed by 2 reductions and a dehydration reaction –> resulting saturated fatty acid moved back to C site
  6. Reactions 2-5 are repeated six times until FA on C site is 16 carbons long
  7. Palmitic acid released from enzyme
23
Q

Where does the NADPH for the reductions occurring in FA synthase come from?

A

Pentose Phosphate Pathway and Malic Enzyme Reaction

24
Q

What activates Fatty Acid Synthase? What is it’s overall reaction and main end product?

A

Insulin!

End product is 16-carbon saturated FA palmitic acid

Reaction
1 acetyl-CoA + 7 malonyl-CoA + 14 NADPH –> 1 palmitic acid + 7 CO2 + 14 NADP

25
Q

Where does elongation of fatty acids occur? What is the reaction?

A

Mostly at smooth endoplasmic reticulum

Similar to FA synthesis - Malonyl-CoA and 2 NADPH are substrates and CO2 is released

Elongation occurs at carboxyl end of molecule and elongation overall is important for membrane lipid synthesis

26
Q

Where does desaturation of fatty acids occur and what is the reaction?

A

Occurs at the endoplasmic reticulum.

Requires p450 monooxygenase system.

Different desaturases introduce doubel bonds at carbon 4, 5, 6, and 9. Consumes NADPH

27
Q

Combinations of elongation and desaturation reactions produce what?

A

Variety of polyunsaturated fatty acids

28
Q

How are triacylglycerols synthesized?

A

In order for FA to be transported or stored, fatty acids are esterified to glycerol

Glycerol comes from glycolysis via glycerol-P dehydrogenase from DHAP

Ester formation requires activation of fatty acid and this pathway produces intermediates for membrane lipids.

29
Q

What two processes of fatty acid metabolism need to be regulated?

A
  1. Synthesis and degradation of fatty acids - liver, adipose tissue, muscle. FAs synthesized during fed state and broken down in fasting state
  2. Mobilization and deposition of TAG - adipose tissue. Mobilization occurs during fasting
30
Q

What occurs if there is no repression of FA mobilization and degradation?

A

Hyperlipidemia, ketoanemia, ketoacidosis (Diabetes)

31
Q

What does insulin do in fed state that is important for FA metabolism?

A

Insulin stimulates key enzymes of glycolysis and produces acetyl-CoA and Glycerol-P

Insulin activates acetyl-CoA carboxylase via dephosphorylation through PP1

Insulin induces genes expression of acetyl-CoA carboxylase, FA synthase, malic anzyme, and glucose 6 phosphate dehydrogenase

32
Q

What occurs during fasting for FA metabolism?

A

Lack of insulin stimulation so you have decrease in acetyl-CoA carboxylase, FA synthase, malic enzyme, and G6PD

Glucagon signaling occurs through PKA - inactivate acetyl-CoA carboxylase

FA synthesis tied to low energy - AMPK inactivates acetyl-CoA carboxylase

33
Q

How are fatty acids transcriptional regulators of metabolism?

A

Fatty acids signal catabolic state and induce appropriate genes

FAs bind to transcription factor PPAR alpha (Peroxisome Proliferator Activator Receptor) which stimulates transcription of genes for beta oxidation and ketogenesis

34
Q

What is a target for lipid lowering drugs?

A

PPAR signaling

35
Q

How does fatty acid synthesis inhibit FA degradation?

A

FA synthesis produces malonyl-CoA which inhibits Carnitine-Palmitoyltransferase I (CPT I). This causes no uptake of FA into mitochondria

36
Q

How is FA mobilization regulated in adipose tissue during fasting?

A

Phosphorylation by PKA activates intracellular lipases, Adipose triglyceride lipase (ATGL) and Hormone Sensitive Lipase (HSL) to release fatty acids from adipose tissue.

PKA independent of glucagon since no glucagon receptors in adipose tissue.

37
Q

How is FA mobilization regulated in adipose tissue during fed state?

A

Fats retained in lipid droplets by insulin mediated inactivation of adipose triglyceride lipase (ATGL) and hormone sensitive lipase (HSL) through PP1

Insulin shuts down FA degradation in mitochondria and activates fatty acid synthesis via acetyl-CoA carboxylase

The resulting malonyl-CoA represses FA uptake unto mitochondria through CPT system - no beta oxidation of fatty acids

38
Q

How is FA mobilization regulated by cellular energy?

A

When cellular energy is low (high AMP), AMPK activates ATGL and HSL to release fatty acids from lipid droplets for beta oxidation

39
Q

What occurs when you have no insulin?

A

Hyperactive lipolysis and ketogenesis

40
Q

What can Niacin help with?

A

Niacin inhibits hormone sensitive lipase and TAG synthesis. Used to lower serum lipids and liver triglyceride synthesis. Also inhibits cholesterol synthesis

41
Q

What are the global effects of FA metabolism?

A

Mobilization of fats from adipose tissue provides way more FA than necessary (30-505 oxidized) and the rest goes back to adipose tissue.

FA metabolism starts slow and reduced glucose consumption gradually

FA metabolism changes respiratory quotient

RQ is CO2 eliminated/O2 consumed - fatty acid metabolism is 0.7 which mean it requires more O2 for complete oxidation

FoundSci Unit 4 (11 decks)

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