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Metabolism > Fats III- Lipogenesis and Lipid Transport > Flashcards

Fats III- Lipogenesis and Lipid Transport Flashcards

1
Q

What is the function of chylomicrons?

A
  • Carry ingested fats to peripheral tissues
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2
Q

What type of fats fo very low-density lipoproteins carry?

A

Only endogenously synthesised fats

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3
Q

Where are lipoproteins secreted to following digestion?

A
  • Lymph

- Then blood

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4
Q

What happens to excess dietary carbohydrate?

A
  • Undergoes insulin-stimulated lipogenesis
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5
Q

What can glucose be converted to to produce triglycerides?

A
  • Fatty acids
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6
Q

Where are packaged triglycerides secreted from?

A
  • Packaged into VLDLs

- Secreted from liver

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7
Q

What enzyme is expressed in response to insulin for triglyceride digestion?

A

Lipoprotein lipase (LPL_

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8
Q

What does the enzyme lipoprotein lipase (LPL_ do?

A
  • Attaches to capillary endothelial cells

- Digests triglycerides from chylomicrons and VLDLs releasing fatty acids

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9
Q

What are fatty acids taken up by after being digested by LPL?

A
  • Adipose tissue and restored to triglycerides

- Muscle and other tissue to be oxidised and to produce carbon dioxide, water and ATP

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10
Q

What is lipogenesis?

A
  • A process that converts excess dietary carbohydrates into fat for storage as a source of long-term energy
  • Lipogenesis occurs in response to high glucose (and insulin) levels after a meal
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11
Q

What enzyme in the TCA cycle is inhibited by ATP and NADH and what is the consequence of this?

A
  • Isocitrate dehydrogenase

- Mitochondrial accumulation of citrate

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12
Q

How does a high carbohydrate diet affect the levels of isocitrate dehydrogenase?

A
  • While resting results in low use ATP
  • Increase in TCA cycle and intermediates
  • Increase in ATP
  • Leads to the inhibition of isocitrate dehydrogenase
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13
Q

What happens to accumulated citrate from the TCA cycle?

A
  • Exported from mitochondria to cytosol for fatty acid synthesis
  • Triglycerides packaged into VLDLs
  • Exported to adipose tissue
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14
Q

What is the starting substrate for endogenously synthesised triglycerides?

A
  • Citrates
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15
Q

Want enzyme converts citrate to acetyl CoA in lipogenesis?

A
  • ATP citrate lyase
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16
Q

What are the conversion steps from citrate to triglyceride?

A
  • Citrate
  • Acetyl CoA
  • Malonyl CoA
  • Fatty acids
  • Triglycerides
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17
Q

What enzyme carboxylates acetyl CoA to malonyl CoA?

A
  • Acetyl CoA carboxylase
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18
Q

What enzyme condenses malonyl CoA and acetyl CoA to create nascent fatty acid?

A
  • Cytosolic fatty acid synthase (FAS)
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19
Q

How is the fatty chain elongated in lipogenesis?

A
  • Subsequent condensation, dehydration and reduction reactions
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20
Q

How is glycerol produced to form triglycerides in lipogenesis?

A
  • 3 fatty acids esterified to form glycerol
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21
Q

What is the rate-limiting and regulating step in lipogenesis?

A
  • Carboxylation of acetyl CoA to Malonyl CoA by acetyl CoA carboxylase (ACC)
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22
Q

What is ACC enzyme activated and inactivated by?

A
  • Activated by insulin and citrate

- Inactivated by glucagon and adrenalin

23
Q

The availability of what substances promotes lipogenesis?

A
  • Malonyl CoA

- NADPH (from pentose phosphate pathway)

24
Q

What molecule acts as an inhibitor of carnitine palmitoyltransferase (CPT-1) therefore of the carnitine shuttle system?

A
  • Malonyl CoA
25
Q

What is the benefit of Malonyl CoA inhibiting the carnitine shuffle?

A
  • Prevents futile degradation of fatty acids after a meal when there is plenty of glucose available for energy provision
  • Promotes export of fatty acids from liver (packaged in VLDLs) to adipose tissue
26
Q

Why are fats and cholesterol packaged with proteins (lipoproteins)?

A
  • They cannot dissolve in the bloodstream
27
Q

What are liver-synthesised lipoproteins packaged with?

A
  • Other lipids and apolipoproteins to form VLDLs
28
Q

What is the function of low density lipoproteins?

A
  • Carry cholesterol from the liver to the body (hence raises cholesterol levels)
29
Q

What is the function of high density lipoproteins?

A
  • Carries excess cholesterol back to the liver for disposal (lowers blood cholesterols)
30
Q

Order lipoproteins from lowest density to highest

A
  • Chylomicron, VLDL, IDL, LDL and HDL
31
Q

What are VLDLs composed of and where are they assembled?

A
  • Triglycerides, cholesterol and apolipoprotein B100

- Hepatocytes

32
Q

What happens to VLDLs after they have been assembled?

A
  • Particles exocytosed and acquire other apolipoproteins (CII, E) from HDL particles to mature
33
Q

What substances facilitate progressive offloading of fatty acid and glycerol cargo from VLDL to produce IDL?

A
  • CII

- Lipoprotein lipase (LPL)

34
Q

What does IDL do?

A
  • Continues to offload fatty acids and glycerol to epithelial cells and HDLs to form LDL
35
Q

How much of plasma cholesterol is in LDL?

A
  • 70%
36
Q

What does LDL apo bind to?

A
  • Endothelial LDL receptors

- Entire particles are endocytosed

37
Q

What happens to LDLs within a cell?

A
  • Fuse with lysosomes and are dismantles, releasing cholesterol
38
Q

What happens to cholesterol once it is offloaded into a cell?

A
  • Not immediately used for structural or synthetic purposes

- May be esterified with fatty acids by acyl-COA cholesterol transferase (ACAT)

39
Q

Describe HDLs, where are they assembled?

A
  • Small and most dense

- Assembled in liver and intestine from apoproteins and phospholipids

40
Q

What is the most abundant apolipoprotein in HDLs, and what does it contain?

A
  • APO-A1

- Contains CII that is transferred to chylomicrons and VLDLs to aid activation of LPL

41
Q

What is the function of ApoE?

A
  • Transferred to aid receptor-mediated endocytosis
42
Q

What is the function of HDL?

A
  • Takes up extra cellular cholesterol from peripheral tissue and transport through bloodstream to liver as cholesterol esters for bile excretion
43
Q

What happens to excess cellular cholesterol?

A
  • It can be packaged into HDLs when its hydrophilic hydroxyl group at C3 is shielded by a fatty acid
  • Esterification by ACAT results in them
44
Q

What happens to excess intracellular cholesterol?

A
  • Pumped out of cells by ATP-binding cassette transporter 1 (ABCA1)
  • Esterification can occur within HDL by actions of lecithin cholesterol acyl transferase (LCAT)
45
Q

What occurs when there are high levels of cholesterol in the bloodstream?

A
  • Hardening and narrowing of arteries
  • Atherosclerosis
  • High levels of LDL- particles will form deposits in walls of arteries
46
Q

What is the consequence of accumulation of fat within arterial wall?

A
  • Development of plaques
  • Restrict blood flow
  • Coronary arteries could be blocked- CHD
47
Q

What deficiencies could lead to hypercholesterolemia?

A
  • An enzyme- e.g. LPL
  • Apoprotein- e.g. B100, CII, E)
  • Receptor (e.g. LDLR)
48
Q

What is the consequence of a LDLRAP1 mutation for genetic dyslipidaemias?

A
  • Gene encoring an adaptor protein that assists efficient endocytosis of receptor-bound LDL particles
  • Mutations cause an autosomal recessive form of familial hypercholesterolemia
49
Q

What is the consequence of an APOB gene mutation as an example of a genetic dyslipidaemia?

A
  • Makes two versions of apolipoprotein B11
  • Mutations can reduce LDL clearance
  • Severe childhood hypocholesterolaemia if both copies mutated
  • Increased risk of mid-life heart disease with one affected copy
50
Q

What is the consequence of PCSK9 protein mutation as a genetic dyslipidaemia?

A
  • Protein that breaks down LDL receptors before they reach cell surface
  • More cholesterol can remain in the blood stream
  • Autosomal recessive inheritance of gain-of-function mutations in this gene reduce number of LDL and therefore increase blood cholesterol
51
Q

What substances inhibit endogenous synthesis of cholesterol and how?

A
  • Statins and intracellular cholesterol

- Inhibition of HMG-CoA reductase

52
Q

What is the consequence of reduced intracellular cholesterol?

A
  • Enhances transcription of LDL receptor and increases amount of cholesterol intake from LDLs
53
Q

What is the purpose of up regulation of LDL receptors?

A
  • Key physiological mechanism that lowers blood cholesterol

- Main way statins exert a therapeutic effect

Metabolism (9 decks)

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