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Fuel Metabolism > Lipid Metabolism > Flashcards

Lipid Metabolism Flashcards

1
Q

6 Major Classes of Lipids

A
  • Fatty acids
  • Triglycerides
  • Ketones
  • Cholesterols
  • Phospholipids
  • Sphingolipids
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2
Q

Structure of Major Lipids Classes

A
  • Fatty acids - building blocks
  • Triglycerides- glycerol + 3 FAs
  • Ketones- only 4 carbons so soluble - formed when FAs degrade - acetoacetate and beta-hydroxybutyrate
  • Cholesterols- has sterol nucleus (4 rings) with hydoxyl group and h8-C side chain; but most in body is cholesterol ester which is cholesterol + single FA chain
  • Phospholipids- glycerol backbone w/ 2 FA chains and 1 phosphoric acid chain
  • Sphingolipids - contain sphingosine derived from FA and serine (has 1 amino group and 2 hydroxyl groups)
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3
Q

Function of Major Lipid Classes

A
  • Fatty acids - metabolic fuel (esp for skeletal and heart muscle); building blocks/precursors for other lipids
  • Triglycerides- storage and transport form of FAs
  • Ketones- fuel for skeletal muscle, heart, kidney and brain
  • Cholesterols- in plasma membrane; makes steroids, vitamin D and bile acids
  • Phospholipids- membrane building block; signal transduction pathways; storage site for poly-unsaturated FAs
  • Sphingolipids - in membranes; surface antigens
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4
Q

How does the insulin:glucagon ration affect interconversion of lipids?

A
  • Dietary triglycerides –> triglycerides –> FAs –> acetyl CoA –> cholesterol or TCA cycle
  • Insulin = promotes synthesis of fatty acids and storage of lipids (shunt acetyl CoA to fatty acids and triglycerides instead of TCA cycle)
  • Glucagon = promotes mobilization and oxidation of lipids and synthesis of ketones (shunt FAs and tricglycerides to acetyl CoA)
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5
Q

Pancreatic Lipid Digestion Enzymes + Reactions (3)

A
  • Pancreatic lipase (TG–> FA + DG then acts on DG –> MG + FA) **requires colipase
  • Cholesterol Esterase (cholesterol esters –> cholesterol + FA)
  • Phospholipase A2 (phospholipid –> lysophospholipid + FA)
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6
Q

What is the primary emulsification agent and why?

A

bile salts!

- Converts fat globules to smaller and smaller droplets so that they are more easily attacked by enzymes (inc surface area)
- Works b/c bile salts are amphipathic (both hydrophilic and hydrophobic) and because low pKa of amino side chain
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7
Q

What are the key enzymes and reactions of dietary lipid repackaging?

A
  • 1- activate FAs via fatty acyl-CoA synthetases (FA + CoA + ATP –> fatty acyl CoA + AMP + PP)
  • 2- esterification rxns via fatty acyl CoA transferase for TGs and ACAT for cholesterol esters
    • MG + FA-CoA –> DG + FA-CoA –> TG
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8
Q

Effect of bile salt deficiency

A

.excrete lipid in feces because cannot emulsify and absorb (steatorrhea- lipids in feces - chalky or clay-colored)

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9
Q

Effect of colipase deficiency

A

severe weight loss because metabolic fuel lost in feces (needed for pancreatic lipase to work)

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10
Q

Effect of apoprotein B -48

A

.needed for chylomicron assembly so w/o it fat accumulates in intestinal cells and liver

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11
Q

Effect of fatty acyl CoA synthetase

A

cannot activate FAs once in intestinal cell …no fatty acyl CoA for esterfication reactions…cholesterol and MGs accumulate in intestine and there is a lack of cholesterol ester and TGs

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12
Q

Effects of Lipid Malabsorption (5)

A
  • Leads to inability to absorb fat-soluble vitamins
    • no Vit A - night blindness
    • no Vit D - osteoporosis
    • no Vit E - anemia
    • no Vit K - defective blood clotting
  • Also leads to inability to maintain weight
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13
Q

What happens if you have a diet rich in medium to small chain triglycerides?

A
  • medium and short chain FA (about 10 carbons or less) are released directly into portal blood where they are bound by albumin and transported directly to liver
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14
Q

Lipoprotein Properties

A
  • Chylomicrons - largest (why they enter lymph not circulation) - least dense; most lipid content
  • VLDL - next largest, least dense and most lipid
  • LDL - next least dense; next most lipid content; highest cholesterol content
  • HDL - smallest and highest density; about 50:50 lipid to protein content; next highest cholesterol content to LDL
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15
Q

What is the apoprotein content of each class of glycoproteins?

A
  • Chylomicrons- B C E
  • VLDL- B C E
  • IDL- B C E
  • LDL-B
  • HDL- A C E
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16
Q

What is the source of each class of glycoproteins?

A
  • Chylomicrons - intestine
  • VLDL - liver
  • IDL - from VLDL in plasma
  • LDL - from IDL in plasma
  • HDL - liver or intestine
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17
Q

What is the general function of each class of glycoproteins?

A
  • Chylomicrons - transport TGs to peripheral tissues
  • VLDL- transport TGs to peripheral tissues
  • IDL- transport TGs + LDL precursor
  • LDL - transport cholesterol to peripheral tissues
  • HDL- reservoir of apoproteins + brings cholesterol back to liver
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18
Q

Apoprotein Functions

A
  • Apo A- stim LCAT for reverse cholesterol transport by HDL
  • Apo B- binds/recognizes LDL receptors on cells
  • Apo C- activates LpL (lipoprotein lipase)
  • Apo E- binds/recognizes remnant receptors on liver (remnant recycling in liver)
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19
Q

LpL (function, location, regulation)

A
  • Function - degrades TGs –> FAs + glycerol (depletes chylomicrons, LDLs and IDLs of their TGs-> now call “remnant”) - So fatty acids can then be delivered to given cells
  • Location - in luminal wall of capillaries outside cell (esp in adipose, skeletal muscle and cardiac muscle)
  • Regulation -
    • All isozymes ACTIVATED by apo C-II
    • LpL in adipocytes specifically responds to insulin –> inc fat storage in adipose cells
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20
Q

Lipoprotein Lipase v Hepatic Lipase

A

both extracellular enzymes that hydrolyze

  • LpL - works on chylomicrons, LDLs and IDLs and have little affinity for IDLs because as they shrink, apo C-II is transferred back to HDLs
  • Hepactic Lipase- works on IDLs only (converts IDLs –> LDLs)
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21
Q

Steps of Reverse Transport of Cholesterol

A

1-Uptake of cholesterol by HDL (mediated by ABCA-1)

2-Esterification of HDL cholesterol by LCAT (stim by apo A)

3-Transfer of cholesterol ester from HDL to lipoprotein remnants

- Mediated by CETP or apo D
- "indirect path"
- These now full remnants cleared by liver

OR Transfer of HDL cholesterol esters to tissues via scavenger receptor B1

- HDL binds SRB1 receptors on liver or steroidogenic tissues 
- HDL not endocytosed (recycled)
- "direct path"
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22
Q

LDL receptors v remnant receptors

A
  • LDL receptors- on extra hepatic tissues (deliver cholesterol to them); also some on liver to get cholesterol from indirect path
    • Apo B binds LDL receptors
  • Remnant receptors-on liver; to recycle VLDL remnants (IDL)
    • Apo E binds remnant receptors
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23
Q

LDL receptors v scavenger receptors

A

LDL receptors- (75%) on extra hepatic tissues (deliver cholesterol to them); also some on liver to get cholesterol from indirect path
*Regulated by cholesterol concentration

  • Scavenger Receptors - (25%) low affinity for LDL but high affinity for oxidized LDL; located on macrophages
    • Not regulated by cellular concentration of cholesterol so as cholesterol accumulates macrophages –> foam cells (over time foam cells form atherogenic plaques)
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24
Q

2 Fates of IDLs

A
  • 1- Converted to LDL by hepatic lipase (return apo E back to HDL pool)
  • 2- Internalized by liver (apo E of IDL binds remnant receptors on liver)
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25
Q

Role of ABCA1

A

ABCA-1 mediates the transfer of unesterified cholesterol from cell to a lipid-poor HDL (nascent HDL)

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26
Q

ABCA1 Deficiency

A

**Deficiency in ABCA-1 –>deficiency in HDL –> dec cholesterol and inc TGs in blood –> yellow-orange enlarged tonsils (Tangier’s Disease)

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27
Q

What defect underlies familial hypercholesterolemia?

A
  • Also known as Type II hyperlipoproteinemia
  • Inherited defect in LDL receptor –> cannot get cholesterol into cell so high cholesterol levels in blood
  • Most common disease in lipid metabolism
28
Q

Cholesterol Structure

A
  • 4 ring nucleus + 8C side chain + hydroxyl group

- Cholesterol ester - hydroxyl becomes ester

29
Q

What is the primary substrate of cholesterol synthesis? Key Intermediates?

A

3 Acetyl CoA (primary substrate) —> HMG-CoA

HMG-CoA —> …2 isoprene units (5 carbons) —> squalene (30 carbons)–> cholesterol

30
Q

What is the rate-limiting step in cholesterol synthesis and how is it regulated?

A
  • Rate limiting step = HMG-COA Reductase

NADPH + HMG-CoA —> mevalonate + NADP+

  • Synthesis of enzyme repressed by cytosolic cholesterol
  • Diurnal variation (peaks 6 hrs after dark and min 6 hours after light)
  • Act by insulin and thyroid hormone
  • Deact by glucagon and cortisol
  • Modified via phosphorylation (deactivated when phosphorylated)
31
Q

How does liver contribute to cholesterol balance?

A
  • Receives it from diet via chylomicron remnants and from cells via reverse transport (HDL)
  • De novo synthesis
  • Repackages it and sends it off in VLDL
  • Converts it to bile acids (secreted or reabsorbed
32
Q

How would a genetic deficiency in apoprotein B cause hypercholesterolemia?

A

If deficiency in cell surface receptors for apoprotein B the cell would not be able to bind and endocytose the LDL and acquire cholesterol so cholesterol would stay in blood rather than enter peripheral tissues —> hypercholesterolemia

LDL receptors bind apoprotein B on LDL

33
Q

ACAT v LCAT

A
  • Both esterify cholesterol
  • ACAT is in extra hepatic cells for cholesterol storage
  • LCAT is w/ HDL helping w/ reverse transport of cholesterol
34
Q

Statins and Cholestyramine

A
  • Statins - drugs that inhibit the activity of HMG-CoA reductase to decrease cholesterol production
  • Cholestryamine- drug that binds to bile salts in the GI tract and are excreted in feces; prevents reabsorption of these bile acids so inc amount of cholesterol excreted from body
35
Q

Where is cholesterol converted to bile acids?

A

LIVER (cytoplasm?)

36
Q

What is the rate-limiting step in bile acid production?

A

Rate limiting step - cholesterol-7-alpha-hydroxylase (hydroxylation at B-7)

Inhibited by cholic acid (one of the major bile acids)

37
Q

Bile Acids v Bile Salts

A

Carboxyl group of bile acid side chain forms amide bond w/ glycine or taurine —> bile salts (AKA conjugated bile acids)

**Lower pKa of side chain

38
Q

Enterohepatic Circulation of Bile Acids

A
  • Only 5% of bile is excreted; rest is reabsorbed
  • Bile acids secreted from liver during digestion; then reabsorbed in lower small intestine; then released back into portal circulation (bound to albumin) —> liver
39
Q

What is the role of the citrate shuttle?

A
  • Acetyl CoA is made in mito but needed in cytoplasm for synthesis so…use citrate shuttle
    • Citrate from TCA cycle (made by citrate synthase) is sent across IMM —> cytoplasm then…
    • Citrate + ATP + CoASH —> acetyl CoA + OAA + ADP + P (via citrate lyase)
40
Q

What is the rate-limiting step in FA synthesis and how is it regulated?

A

acetyl CoA carboxylase

step that makes the malonyl CoA substrate

Acetyl CoA + HCO3- + ATP —> malonyl CoA

Requires biotin and ATP
Act by citrate
Inhibited by palmitoyl CoA
Inactivated by phosphorylation

41
Q

How does insulin affect FA synthesis?

A

Insulin promotes FA synthesis; activates PP1 which would remove P from acetyl CoA carboxylase

42
Q

What substrates are required for FA synthesis? How are they made?

A

Acetyl CoA (from citrate shuttle)

NADPH (pentose phosphate path OR OAA —> Malate–> Pyruvate + CO2 + NADPH via malate DH and malic enzyme)

Malonyl CoA (Acetyl CoA + HCO3- + ATP —> malonyl CoA via acetyl CoA carboxylase)

43
Q

Stoich of FA Synthesis

A

14H+ + acetyl CoA + 7 malonyl CoA + 14 NADPH —> palmitoyl CoA + 7CO2 + 7CoA + 14NADP+ + 7H2O

44
Q

Citrate Synthase

Citrate Lyase

Malate DH

Malic Enzyme

A

Makes citrate in TCA cycle

Citrate + CoASH –> acetyl CoA + OAA

OAA –> malate

Malate –> pyruvate + NADPH

45
Q

FAS Enzyme + 4 Core Reactions

A

4 core reactions of elongation

- Condensation -lose 1 C as CO2 -end w/ 4C product
- Reduction - use NADPH
- Dehydration -remove H20
- Reduction - use NADPH * **Then prime the 4C product and another malonyl CoA and REPEAT
46
Q

Role of ACP and what is its cofactor?

A

(acyl carrier protein)

thiol groups

primes the acetyl and malonyl groups (acts as scaffold for activating the acetyl CoA and malignly CoA)

47
Q

FA Synthesis in Liver v Mammary

A

In mammary gland, make decanoic acid instead of palm acid; only 10C chain so easier for baby to digest; does not need to be shuttled by chylomicron but can be sent directly into portal circulation

48
Q

How are FAs converted to TGs in adipose tissue?

A
  • Once FAs are taken into cell they are converted to fatty acyl CoA
  • Transfer FAs to C1 and C2 of glycerol-3-P then remove phosphate -> DG; then add another FA to 3-OH —> TG
49
Q

How is glucose involved in TG synthesis in adipose tissue?

A

Glucose is required to give you the G3P (glycerol-3-P) backbone glycolysis intermediate

50
Q

Phospholipid Structure

A

Glycerol backbone w/ 2 long chain FAs and 1 phosphoric acid

51
Q

5 Classes of Phospholipids

A
  • Phosphatidic acid
  • Serine
  • Ethanolamine
  • Choline
  • Inositol
52
Q

Phospholipid Functions

A
  • Structural component of membranes (lipid bilayer)
  • Enzyme activation
  • Second messenger signaling
  • Lung function - major component of surfactant
  • Detergent function in intestine and gall bladder - component of bile (too much phospholipids in bile —> gallstones)
53
Q

How are FAs mobilized from TGs in adipose tissues?

A
  • 3 Triacylglycerol Lipases- 3 enzymes that work together (inside cell)
    - ATGL (triacylglycerol —> FA + diacylglycerol)
    - HSL (diacylglycerol —> FA + monoacylglycerol)
    - MGL (monoacylglycerol —> FA + glycerol)
54
Q

What tissues use FAs as fuel? Which cannot and why?

A

mainly used by liver, muscle, heart and kidney (IN MITO) but ALL tissues can use FAs as fuel except…

- Brain- FAs cannot cross blood brain barrier
- RBCs- no mito
55
Q

What 2 proteins have high affinity for free FA?

A
  • Albumin- when in blood- bound noncovalently

- FABP- intracellular (once FA is in cell it binds FABP then is converted to fatty acyl CoA)

56
Q

Carnitine Shuttle

A
  • Carnitine Shuttle
    • Used to get fatty acyl CoA across IMM
    • OUTSIDE MATRIX- CAT I or CPT I (fatty acyl CoA + carnitine —> CoA + fatty acyl-carnitine)
    • Then fatty acyl-carnitine crosses IMM
    • INSIDE MATRIX- CAT II or CPT II (Fatty acyl-carnitine + CoA —> Fatty acyl-CoA + carnitine)
    • Translocase replaces carnitine to outside matrix
57
Q

How much ATP is made from full oxidation of palmitic acid?

A

129!

7 (3 ATP/NADH) = 21
7(2 ATP/FADH2) = 14
8 (12 ATP/acetyl CoA) = 96 …=131
- If you include complete oxidation of palm acid (so had to turn palm acid into palm CoA) then that cost 2 ATP so …=129

58
Q

Carnitine Deficiency + Causes

A
  • Carnitine Def- cannot get fatty acyl CoA into mito matrix so no FA oxidation (**same thing happens if CTP-I deficiency)
  • Can be caused by certain drugs that are low molecular weigh organic acids and form acyl carnitines that are excreted from body
59
Q

Peroxisome Oxidation v Mito Oxidation

A
  • Used for very long chain FAs and branched chain FAs
  • Very Long Chains…
    • Uses isozymes of mito oxidation
    • Less energy yield than mito oxidation b/c FADH2 made in first step is regenerated by O2 to form hydrogen peroxide so it does not go on to make ATP
  • Branched Chains…
    • Cannot undergo beta oxidation b/c beta carbon has methyl group branch; hydroxylation at alpha group instead
      • Uses alpha-hydroxylase
60
Q

Refsum’s Disease

A

Genetic def in alpha hydroxylase so cannot oxidize branched chain FAs

- retinitis pigmentosa, hearing loss, peripheral neuropathy, ataxia
- Limit diet - no dairy, beef, lamb (phytanic acid)
61
Q

Zellweger Syndrome

A
  • absence of peroxisomes —> accumulation of very long chain FAs and branched chain FAs
    • Fatal by age 2; brain kidney and liver damage
62
Q

What is the most prevalent lysosomal storage disorder? How is it treated?

A
  • Gaucher’s Disease - sphingolipid disorder (usually in membranes and myelin of neurons)
  • Treated w/ enzyme replacement (recombinant glucocerebrosidase) but very expensive
63
Q

Ketone Synthesis

A
  • IN LIVER MITO
  • 2 acetyl CoA —> acetoacetyl-CoA —> HMG CoA —> acetoacetate beta-hydroxybuterate
  • Thiolase, HMG-CoA Synthase, HMG-CoA Lyase
64
Q

Ketone Oxidation

A
  • Oxidation
    • ONLY IN NON-LIVER TISSUES MITO
    • beta-hydroxybutyrase -> acetoacetate + succinyl CoA —> acetoacetyl-CoA —> 2 acetyl CoA
    • BetaHOB dehydrogenase, SCOT, thiolase
65
Q

How/when are ketones used?

A

Provide fuel for muscles and brain during starvation (prevents you from breaking down protein in your muscle)

  • Stim by dec in insulin/glucagon ratio (so during fasting/starvation)
  • *or in people w/ diabetes (no insulin)

Fuel Metabolism (6 decks)

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