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DEMS Unit 2 > Fats > Flashcards

Fats Flashcards

1
Q

De Novo Lipogenesis

A
  • fatty acid biosynthesis
  • occurs when glucose is in excess
  • acetyl CoA leaves mitochondria as citrate, then is converted back to acetyl CoA in cytosol
  • acetyl CoA-> malonyl CoA by acetyl CoA carboxylase
  • uses NADPH for energy
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2
Q

Acetyl CoA Carboxylase

A
  • rate limiting step in de novo lipogenesis (fatty acid biosynthesis)
  • inhibited by long chain fatty acids
  • activated by citrate
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3
Q

Fatty Acid Synthase

A

-puts together units of malonyl coA 2 at a time to form a fatty acid chain

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4
Q

Lipoprotein Lipase

A
  • takes triglyceride up into adipose tissue to be stored
  • degradation of TG stored in chylomicrons and VLDL
  • requires apoC-2 as cofactor
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5
Q

Fatty Acid Oxidation (Beta Oxidation)

A
  • during negative energy state
  • stored triglycerides are broken down by hormone sensitive lipase
  • taken up by liver and used as substrate in gluconeogenesis
  • converted to acyl carnitine to be transported into mitochondria in liver for oxidation
  • transported into mitochondria by carnitine palmitoyl transferase 1 (CPT1)
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6
Q

Hormone Sensitive Lipase

A
  • when insulin is low and counter regulatory hormones are high
  • breaks down stored triglycerides
  • degrades TG stored in adipocytes
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7
Q

Carnitine Palmitoyl Transferase 1 (CPT1)

A
  • transports actyl-carnitine into mitochondria in liver to be oxidized
  • rate limiting step
  • inhibited by malonyl coA
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8
Q

Ketogenesis

A
  • when insulin is very low and counter regulatory hormones are very high
  • during long term fasting
  • acetyl coA produced during beta oxidation in the liver can take alternative route to become a ketone body
  • occurs in mitochondria
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9
Q

HMG CoA Synthase

A

rate limiting step in ketogenesis

-synthesizes HMG CoA

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10
Q

Cholesterol Synthesis

A
  1. synthesized from acetyl CoA through formation of HMG CoA
  2. HMG CoA is converted to mevalonate
    - rate limiting step in HMG CoA reductase
  3. mevalonate converted to cholesterol
    - uses NADPH for energy
    - liver cell cytosol is major site of cholesterol synthesis
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11
Q

HMG CoA Reductase

A
  • rate limiting step in cholesterol synthesis
  • converts HMG CoA to mevalonate
  • regulation:
    1. transcriptional depression when HMG CoA is inc.
  • also SREBP upregulates transcrption
    2. translational regulation when cholesterol is inc.
    3. half life dec. when cholesterol inc.
    4. AMP kinase phosphorylates HMG CoA reductase, inactivating it
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12
Q

Glycerophospholipids

A
  • specialized lipid
  • glycerol backbone and PO4 group
  • make up bulk of membrane lipids
  • ex. phosphatidylcholine, phosphatidylserine, phosphatidylinositol
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13
Q

Sphingolipids: sphingomyelin

A
  • ceramide backbone
  • contains N atom
  • PO4 group with choline
  • major structural lipid in nerve tissue
  • precursor is ceramide made from fatty acid and serine
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14
Q

Glycosphingolipids

A
  • ceramide backbone

- sugar residues attached to head group

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15
Q

Leukotrienes and Prostaglandins/Thromboxanes

A
  • made from arachidonic acid
  • COX 1 and 2 are critical enzymes in this synthetic pathway
  • inhibited by NSAIDS
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16
Q

Lipoproteins- 3 Pathways

A
  • particles that contain apolipoproteins and lipids
  • how nonpolar lipids like cholesterols and triglycerides and phospholipids travel in blood
    1. dietary fat pathway (chylomicron)
    2. VLDL pathway
    3. HDL pathway
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17
Q

Dietary Fat Pathway (Chylomicron)

A
  • triglyceride rich particles take dietary fat to muscle/adipose tissue
  • made by GI tract from dietary fat
  • 10:1 :: triglyceride:cholesterol
  • contain apo B48, apoC2, apoE
  • triglycerides are broken down by lipoprotein lipase
  • not normally present in fasting serum
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18
Q

VLDL Pathway

A
  • pathway by which triglycerides derived from liver are delivered to muscle and adipose tissue
  • 5:1 :: triglyceride:cholesterol
  • contain apoB100
  • VLDL are metabolized by LPL to form LDL
  • most LDL particles are cleared by liver
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19
Q

HDL Pathway

A
  • transports cholesterol and other lipids from periphery to liver
  • reverse transport
  • protection against atherosclerosis
  • contains apoA1
  • ABC-A1 cassette facilitates transport of cholesterol from peripheral tissues to HDL
  • LCAT transfers fatty acid
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20
Q

Starting Material in Fatty Acid Biosynthesis? Where is it produced?

A
  • starting material: Acetyl CoA, produced in mitochondria in glycolysis
  • major sources: biosynthesis from small molecules, diet
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21
Q

Where does fatty acid biosynthesis occur?

A
  • occurs in cytosol

- occurs when dietary calories are in excess

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22
Q

What is rate limiting step in fatty acid biosynthesis?

A
  • formation of malonyl coA from acetyl coA by acetyl coA carboxylase
  • upregulated by citrate
  • inhibited by long chain gatty acyl coA
  • pathway inc. when insulin is inc.
  • pathway dec. when glucagon is inc.
  • inhibited by palmitoyl coA
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23
Q

What are final products of fatty acid biosynthesis? How do cells utilize these products?

A
  • product is palmitic acid (16:0)

- major component of cell membranes, storage form of metabolic energy, precursors for hormones

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24
Q

Fatty Acid Structure (Saturated vs Unsaturated)

A
  • hydrophobic hydrocarbon chain
  • hydrophilic carboxyl group
  • longer chain length is more insoluble in water
  • components of membrane lipids
  • saturated: always trans, no double bonds
  • unsaturated: cis, double bond, dec. melting temp
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25
Q

Fatty Acid Naming (2 Ways)

A
  1. ex. 20:4
    - numbered beginning with carboxyl carbon
    - # before colon indicates # of carbons in chain
    - #s listed after colon are position of double bond
    • numbered beginning with second carbon as a, b, ….
    • terminal methyl carbon is always w carbon
    • ex. w6= closest double bond to methyl group
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26
Q

Essential Fatty Acids

A
  • linoleic acid (w6)- precursor of arachidonic acid
  • linolenic acid (w3)
  • humans cannot make double bonds between carbon 9 and the w end of fatty acid
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27
Q

Fatty Acid Elongases

A
  • catalyzes the initial condensation step for elongation of saturated or polyunsaturated fatty acids
  • occurs in mitochondria
  • formation of double bond in fatty acid involves ER membrane
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28
Q

Triacylglycerol

A
  • synthesized from G3P and fatty acyl coA
  • fatty acid on carbon 1 is saturated, carbon 2 is unsaturated, and carbon 3 is either
  • major storage form of fatty acid
  • synthesized in liver
  • packaged with apo B100 to form VLDL for delivery to body
29
Q

Phosphatidylcholine

A
  • glycerophospholipid
  • along with PE is the most abundant phospholipid in body
  • main component in lung surfactant
  • serves as reservoir of choline
  • present in bile
30
Q

Phosphatidylinositol

A
  • glycerophospholipid
  • important in signal transduction (becomes IP3 and DAG)
  • reservoir for arachadonic acid which is used in PG synthesis
  • important in membrane protein anchoring
31
Q

Cholesterol Transport

A
  • not metabolized by oxidation, so can only be removed from body by excretion through bile acids
  • accumulation in blood vessels-> atherosclerosis
32
Q

Triglyceride

A

-accumulation in blood stream can cause pancreatitis and inc. risk for atherosclerosis

33
Q

Remnant Particles and Intermediate Density Lipoproteins (IDLs)

A
  • metabolic byproducts of metabolism of chylomicrons and VLDL
  • 1:1 :: triglyceride:cholesterol
  • atherogenic
34
Q

Low Density Lipoproteins (LDL)

A
  • produced from metabolism of VLDL
  • more cholesterol than triglycerides
  • very atherogenic
  • cleared from circulation by liver
35
Q

ABC-A1

A
  • facilitates transport of free cholesterol from peripheral tissues into HDL
  • mutation results in Tangiers Disease
36
Q

LCAT

A
  • catalyzes the formation of cholesterol esters in lipoproteins
  • LCAT is the enzyme that esterifies the free cholesterol on HDL to cholesterol ester and allows the maturation of HDL
  • deficiency in LCAT -> low levels of HDL cholesterol-> corneal opacities, renal insufficiency and hemolytic anemia
37
Q

CETP

A
  • plasma protein that facilitates the transport of cholesteryl esters and triglycerides between the lipoproteins
  • collects triglycerides from VLDL or LDL and exchanges them for cholesteryl esters from HDL, and vice versa
  • low levels of this protein-> high HDL levels and live longer than average
38
Q

Apolipoproteins

A
  1. can form structural backbone of lipoprotein particle, ex. apo B48, apoB100, apoA1
  2. enzymatic cofactors, ex. apoC2
  3. ligands for receptors, ex. apoB100, apoE
  4. clinically significant bc of association with atherosclerosis, ex. apo(a)
39
Q

Sources of Triglycerides

A
  • adipose tissue
  • muscle
  • palmitic acid
  • stearic acid
40
Q

Intramuscular Triglycerides

A
  • inc. training leads to inc. fat storage in muscle near mitochondria
  • also inc. in obesity
41
Q

Fuel Selection as Exercise Intensity Increases

A
  • begins with glucose as primary source
  • sustained low intensity exercise uses fat oxidation
  • inc. intensity uses glucose oxidation
  • very high intensity uses lactate production
42
Q

Adaptations with Training

A
  • inc. muscle mass
  • inc. mitochondrial content
  • inc. intramuscular glycogen and triglycerides
  • inc. rate of lypolysis, beta oxidation, and lactate clearance
  • inc. work capacity and shift to fat as preferred fuel
  • inc. lactate clearance
  • inc. VO2 max
  • better to be fat and fit and thin and unfit to dec. CVD mortality
43
Q

Exercise Recommendations

A
  • 2 hrs and 30 mins/week mod. intensity exercise
  • or 75 min/week vigorous aerobic activity
  • should do muscle strengthening activities that involve all major muscle groups 2 or more days per week
44
Q

Catecholamines

A
  • tightly control lipolysis

- bind to b-adrenergic and a2-adrenergic receptors on fat cell membrane-> inc. cAMP-> lipolysis

45
Q

Phospholipase

A

-breaks down phospholipids

46
Q

MCAD Deficiency (medium chain acyl coA dehydrogenase)

A
  • most common genetic cause of impaired fat oxidation
  • unable to complete beta-oxidation for medium chain fatty acids (C-6-C-10)
  • peripheral glucose utilization is increased
  • results in buildup of acids
  • failure to produce ketone bodies
47
Q

VLCAD Deficiency

A
  • similar to MCAD deficiency
  • defect in metabolism of fatty acids of longer chain length C-12-C-16)
  • milder sx and may appear later in life
  • develop muscle soreness or even rhabdomyolysis following exercise
48
Q

CPT-1 Deficiency

A
  • CPT-1 is required to carry fatty acids into the mitochondria where beta-oxidation takes place
  • defect in fat oxidation and develop fasting hypoglycemia with low ketone levels
  • present in infancy following viral illness
  • inc. free carnitine, low acyl-carnitine
  • inc. ammonia
  • tx: constant delivery of dietary carb to prevent hypoglycemia
49
Q

Statin Benefit Groups

A
  • clinical ASCVD: high intensity
  • LDL-C > 190 without secondary cause: high intensity
  • diabetes, age 40-75, LDL-C 70-189: mod or high intensity
  • no diabetes, age 40-75 yrs, LDLC 70-189 + 7.5% risk of CVD in next 10 years: mod intensity
50
Q

LDL-C Equation

A

-LDL-C = total cholesterol -(HDL-C + TG/5)

51
Q

Atherosclerotic Risk

A
  • age
  • male
  • african america
  • smoking
  • HTN
  • high total cholesterol
  • low HDL
  • diabetes
  • family hx
  • sedentary lifestyle
52
Q

Familial Hypercholesterolemia (FH)

A
  • most often defect in LDL receptor
  • dec. in LDL removal
  • autosomal dominant
  • premature death from atherosclerosis
  • sx: arcus cornealis (lipid deposits in cornea), xanthelasmas (lipid deposits on eyelid), tendinous xanthoma (Achilles big)
53
Q

Hypertriglyceridemia

A

-normal is

54
Q

Familial Chylomicronemia

A
  • LPL deficiency
  • APOC2 deficiency
  • GPIHBP1 deficiency
  • pancreatitis risk
  • no premature CHD
  • eruptive xanthoma
  • lipemia retinalis
55
Q

Familial Dysbetalipoproteinemia

A
  • broad beta disease
  • inc. triglycerides and/or inc. LDL
  • autosomal recessive
  • apoE2 rather then E3 or E4
  • inc. risk for CHD
  • dx: lipoprotein electrophoresis or apo E gentype
  • planar/palmer xanthomas on extensor surfaces
56
Q

Tangier Disease

A
  • altered ABCA-1 gene

- orange tonsils from accumulation of cholesterol

57
Q

LDL and BP Lowering Diets

A

-DASH, mediterranean

58
Q

HMG CoA Reductase Inhibitors

A
  • Statins
  • inhibit HGM CoA Reducatse
  • dec. hepatic pool of free cholesterol
  • inc. expression of LDL receptors on cell membranes
  • inc. catabolism of VLDL and LDL
  • dec. LDL concentration
  • with doubling of statin dose: LDL falls by 6%
  • side effectsL abnormal AST/ALT, myopathy, congitive impairment, new onset T2DM
59
Q

Intestinal Acting Cholesterol Agents

A
  • bile acid sequestrants: cholestyramine, colestipol, colesevelam
  • inhibition of cholesterol absorption: plant stanol esters and sterol esters
  • selective choesterol absorption inhibitors: ezetimibe (blocks cholesterol absorption at brush border)
60
Q

PCSK9 Inhibitors

A
  • monoclonal antibodies that restore LDL receptor function

- adverse: drug induced antibodies, allergy

61
Q

Management of Very High LDL

A

-max statin, ezetimibe, resin, fenofibrate, niacin

62
Q

Drugs Used to Lower Triglycerides

A
  • fibrates
  • omega 3 fatty acids
  • nicotinic acid
  • statins
63
Q

Niacin Contraindications

A
  • severe skin rash
  • liver disease
  • hyperuricemia/gout
  • peptic ulcer or IBD
  • impaired glucose tolerance
64
Q

How to raise HDL?

A
  • exercise (10%)
  • sustained weight loss
  • alcohol
  • smoking cessation
65
Q

Apo E Function

A
  • mediates remnant uptake

- on everything except LDL

66
Q

ApoA-1 Function

A
  • activates LCAT

- on HDL

67
Q

ApoC-2

A
  • lipoprotein lipase cofactor

- present in VLDL, chylomicrons, HDL

68
Q

ApoB-48

A
  • mediates chylomicron secretion

- present in chylomicrons

69
Q

ApoB-100

A
  • binds LDL receptor

- present in VLDL, IDL, LDL

DEMS Unit 2 (4 decks)

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