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Biochemistry Cardio > Fatty Acids > Flashcards

Fatty Acids Flashcards

1
Q

Components of a FA

A

Tail = hydrophobic/hydrocarbon chain

Head = terminal carboxylic acid
-forms ester bonds with OH groups on glycerol to form TGs

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2
Q

End product of FA beta-oxidation

A

Acetyl-CoA

—> can then make ketone bodies

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3
Q

Saturated vs. unsaturated

A

Saturated = 100% reduced (no 2x bonds)…solid at RT…more unhealthy

Unsaturated = 2x bonds…liquid at RT…

Saturated = higher melting temperature

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4
Q

Fluidity

A

Referring to phospholipids in cell membranes

If FA components are saturated = less fluidity in membrane

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5
Q

Alpha vs. beta vs. omega carbon

A

2 = alpha

In one naming system…

Carbob #1 = on carboxylic acid

Last (CH3) = omega

Double bonds (18:1 delta9) - means double bond starts on the 9th carbon

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6
Q

“-enoic” vs. “-anoic”

A
  • enoic = unsaturated

- anoic = saturated

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7
Q

Most common saturated FAs

A

Palmitic (palm oil and meat; C16:0)

Stearic (meat and cocoa butter; C18:0)

Diets rich in sat fats are increase risk for atherosclerosis, coronary heart disease, and stroke, and (-) effect on cholesterol profile

Recommended to limit to <7% of daily caloric intake

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8
Q

Common monosaturated FAs

A

Palmitoleic (C16:1; animal, veggie, and marine oils)

Oleic (C18:1, many oils…most abundant monosat in adipose tissue)

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9
Q

Common polyunsat FAss

A

Alpha-linolenic/ALA (18:3, omega-3, essential)

Linoleic (18:2, omega-6, essential)

Eicosapentaenoic/EPA (20:5, omega-3)

Docoahexaenoic/DHA (22:6, omega -3)

Arachidonic/ARA (20:4, omega-6)

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10
Q

Generally…

Animal sources =

Veggie sources =

A

Animal = sat and mono

Veggie = poly

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11
Q

Hydrogenating unsaturated FAs —> result?

A

Increase shelf life of food

Reduces cis bonds

INCREASES TRANS-BONDS = BAD for health (cardio risk)

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12
Q

Omega fats

A

Omega- 3 (ALA, EPA, DHA)
Omega - 6 (linoleic, ARA)

Important for growth and inflammatory response

DHA = essential or required nutrient in the brain and retina for optimal neuronal functions at all developmental stages

DHA + EPA = beneficial in the prevention and management of cardio disease and other chronic disorders

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13
Q

Competition between omega3 and 6 FAs

A

Use same synthesizing enzymes

In a typical western diet = 10x-30x omega 6 than 3

—> can have a loss of health benefits of omega-3s (recommended 1:1 to 4:1)

Best way to do this is through direct consumption (especially during preg and lactation)

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14
Q

Essential FAs

A

Cannot be made de novo…must be obtained in diet

Alpha-linoleic (18:3, omega3) = precursor to EPA and DHA

Linoleic (18:2) = precursor to ARA, which is the substrate for prostaglandin synthesis…in linoleic is low —> arachidonic acid becomes essential

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15
Q

16:0

A

Pamitic

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16
Q

18:0

A

Stearic

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17
Q

18:1

A

Oleic

18
Q

Alpha-linoleic

A

18:3, omega3

19
Q

Docosahexaenoic (DHA)

A

22:6, omega3

20
Q

Linoleic

A

18:2, omega 6

21
Q

Arachidonic (ARA)

A

20:4, omega6

22
Q

FA storage

A

Glycerol + 3FAs = TG

Ester bond b/w COOH (FA) and OH (glycerol)

Middle FA = usually unsaturated

TGs stored primarily as fat droplets in the cytosol of adipocytes (less hydrated, less heavy, smaller than glycogen)

23
Q

Main functions of TGs

A
  1. Long term energy storage in adipose and liver
  2. Physical organ cushion (e.g. kidney)
  3. Thermal insulation
  4. Transport of fat soluble vitamins
24
Q

Nonshivering thermogenesis

A

Brown adipose

Color because of abundance of mitochondrial cytochromes

More metabolically active than white adipose

thermogenin = protein that uncouples the e-chain from ATP synthesis and this makes non-shivering heat
—>important for new-borns to maintain body temp.

25
Q

Cholecytokinin (CCK)

A

Secreted from intestinal mucosa in response to presence of lipids

—> stimulates the gall bladder and pancreas to secrete their products

26
Q

Bile

A

Secreted by gall bladder in presence of CCK

27
Q

Enzymes secreted by pancrease

A

Pancreatic lipases

Stimulated by CCK

28
Q

Steps of FA and TG digestion

A
  1. Bile salts emulsify fats —> forming mixed MICELLES
  2. TGs are degraded by the lipases to form fFAs and 2-monacylgylcerol
  3. Lipid-soluble components (fat soluble vitamins etc) diffuse from the micelle into the mucosa of SI
  4. FFAs converted back to TG
  5. Mucosal cells package TGs, cholesterol and cholesteryl esters, phospholipids, and ApoB-48) into chylomicrons
29
Q

Chylomicrons

A

Apolipoprotein complex that transports dietary TGs to the peripheral cells

Outer layer = phospholipids, cholesterol, and apolipoproteins (polar groups face aqueous environment)

TGs = >80% of mass of cm

30
Q

Transport of TGs (in CM)

A
  1. CM is released into the lymphatic system
  2. Then into bloodstream for delivery to peripheral cells
  3. ApoC-II activates lipoprotein lipase
  4. Converts TGs —> fFAs and glycerol
  5. FFAs enter peripheral cells, where they are converted back to TGs for storage (adipose) or oxidized for energy (muscle)
31
Q

Steatorrhea

A

Increase in lipids (especially FSVs and essential FAs) in the feces

Caused by disturbance of lipid digestion and/or absorption

E.g. cystic fibrosis can cause thickness in SI secretions and disrupts digestion

Increasing short and medium FAs in the diet —> increase absorption rate of fat soluble vitamins and essential FAs

32
Q

Steps of synthesis of TGs

A
  1. Glycerol-3P (G3P) formed
  2. FA chain activated by Coenzyme A
  3. First FA chain attached to C1 position of G3P by an ACYL TRANSFERASE
  4. Process repeated to add a second carbon —> phosphatidic acid (PA)
  5. Phosphate removed from by PA phosphatase —> 1,2-diacylglycerol (DAG)
  6. Step 3 repeated to add third FA —> TGs
33
Q

Phosphatidic acid

A

Intermediate in TG synthesis (after second FA is added)

Can also be used in phospholipid synthesis

34
Q

Liver

Formation of G3P

A
  1. Reduction of DHAP
    — by G3P dehydrogenase (needs NADH)
    —intermediate from glycolysis
  2. Phosphorylating glycerol
    —by glycerol kinase (needs ATP)
35
Q

Adipose tissue

Forming G3P

A

Only express G3P dehydrogenase…so can only do that pathway to make G3P to start TG synthesis

Consequences for fasting state:

Hydrolyze TG —> fFAs and glycerol —> which cannot be used later in the well-fed state

Makes senses functionally because:

  1. Fasting state —> inhibit reverse reaction of glycerol —> G3P…therefore FAs must leave the cell to be used elsewhere in the body for energy … since TG synthesis has no backbone to add FAs to…
  2. G3P will be generated when there is sufficient DHAP (well-fed) —> when TG storage is desirable
36
Q

Glucagon/Epinephrine cascade to mobilize adipose TGs

A
  1. GPCR stimulated
  2. Elicit a cAMP-dependent 2nd messenger
  3. Stimulate PKA pathway
  4. Phosphorylates hormone sensitive lipase and perilipin (to allow lipase to access the TGs in the fat droplets)
37
Q

Albumin

A

Protein that binds to fFAs to transport them in blood

After they are released into blood from adipose after they are mobilized under glucagon/epi pathway

38
Q

Fate of fFAs that are not utilized by peripheral tissue after mobilized

A

Go to the liver —> repackaged into TGs

Exported to the perpheral cells or stored back in the adipocytes

39
Q

Fate of glycerol when TGs are broken down in adipose tissue

A

Go to liver

Fasting —> converted to glucose (gluconeogenesis)

Well fed —> G3P by glycerol kinase for TG syn

40
Q

Hormonal regulation during well fed state

A

High insulin

Stimulates synthesis and secretion of lipoprotein lipase

—> hydrolyzes circulating TGs in CMs
—> allows peripheral access to fFAs
Liver —> fFAs —> TGs —> exported to peripheral
Adipose —> fFAs —> TGs

Inhibits hydrolysis of preexisting TGs in adipose

41
Q

Lipoprotein lipase

Difference in response to insulin vs. glucagon/epinephrine

Skeletal Muscle and cardiac

A

More stimulated via glucagoon/epinephrine than by insulin

Makes sense because…

In a well fed state —> muscles can derive their energy from glucose and store than energy as glycogen…hydrolysis and utilization of fFAs for energy is less needed for skeletal muscles cells

Cardiac muscle
—> gets most of energy from TGs and will use both glucose and fFAs as energy sources for muscle contraction

42
Q

Hormonal regulation in fasting state

A

Low insulin/high glucagon

Muscle cells —> induce lipoprotein lipase to gain alternate fuel

Adipose —> stimulated to hydrolyzes TGs,

Liver —> produce glucose via gluconeo, use fFAs for energy, and also takes up fFAs in circulation —> TGs (to avoid too much fFAs in blood)

Biochemistry Cardio (13 decks)

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