Lipids & Lipid Catabolism Flashcards

1
Q

Most fatty acids are __ to __ carbons in length.

A

16; 18

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2
Q

Most fatty acids have an [even/odd] number of carbons.

A

even

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3
Q

The majority of fatty acids in plants and animals are ______.

A

unsaturated (Often polyunsaturated/PUFAs)

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4
Q

The first double bond is usually between carbon __ and carbon __.

A

9; 10

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5
Q

In PUFAs, are double bonds conjugated or not?

A

Not conjugated

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6
Q

Fatty acid double bonds are almost always [cis/trans], giving them a rigid __º bend.

A

cis; 30

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7
Q

Melting point [increases/decreases] with chain length and [increases/decreases] with unsaturation/double bonds.

A

increases; decreases

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8
Q

The oxidation of fatty acids to ___ and ___ is highly [endergonic/exergonic].

A

CO2; H2O; exergonic

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9
Q

What is the chemical formula for fatty acids?

A

CH3(CH2)nCOOH

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10
Q

What’s the difference between saturated and unsaturated fatty acids?

A

Saturated: No double bonds
Unsaturated: Contains at least one double bond

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11
Q

Where is the alpha carbon in a fatty acid?

A

Next to C1, the carboxylate carbon

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12
Q

For PUFAs, C1 is assigned to the _____ _____ _____, and it’s also designated __.

A

terminal methyl carbon, omega (ω)

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13
Q

Cis double bonds restricts _____ and causes a _____ in the hydrocarbon tail.

A

rotation; bend

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14
Q

Saturated fatty acids pack into ______ ______.

A

crystalline arrays

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15
Q

Glycerol and fatty acids are esterified to generate a _______.

A

triacylglycerol/triglycerides

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16
Q

What are the two advantages that triglycerides (as storage forms of energy) have over polysaccharides?

A
  1. More reduced than carbohydrates, so contain 2x as much energy per gram
  2. Since hydrophobic, don’t need to carry the weight of water necessary for hydration
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17
Q

Trans fats make oils ____ at room temperature.

A

solid

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18
Q

Why are trans fats bad for you?

A
  1. Increased risk of heart disease
  2. Increases LDL (bad) cholesterol
  3. Lowers HDL (good) cholesterol
19
Q

Trans fatty acids are _____, making their melting points [higher/lower] than those with cis bonds.

A

linear; higher

20
Q

Lipid bilayers are amphipathic. What does this mean?

A

They have both polar/hydrophilic and non-polar/hydrophobic regions.

21
Q

What model is used to illustrate membrane structure? What does it look like?

A

Fluid mosaic model

Integral proteins float in this sea of lipid.
Proteins and lipids are free to move laterally in the plane of the bilayer.
(Movement from one leaflet of the bilayer to the other is restricted)

22
Q

Why do lipid bilayers form?

A

Each lipid molecule has a very hydrophobic tail, which forces surrounding H2O molecules to become highly ordered.

This goes against the second law of thermodynamics, which says that the entropy of an isolated system not in equilibrium will tend to increase over time (become more random).

23
Q

Clusters of lipid molecules and micelles increase entropy. Why?

A

Only lipid portions at the edge of the cluster force the ordering of water. Fewer H2O molecules are ordered.

All hydrophobic groups are concealed from water in micelles.

24
Q

Steroid hormones are [slow/fast]-acting, and they effect gene expression by doing what?

A

slow; activating nuclear receptors

25
Q

Some lipids are fast acting and bind to what?

A

Membrane receptors

26
Q

Cyclooxygenase (COX) converts arachidonic acid to what?

A

C20 eicosanoids
(Ex. Prostaglandins, thromboxanes, and leukotrienes)

27
Q

What do nonsteroidal anti-inflammatory drugs (NSAIDs) like aspirin and ibuprofen do?

A

They block the formation of prostagladins and thromboxanes from arachidonate by inhibiting the enzyme cyclooxygenase (COX)

28
Q

Aspirin is a [covalent/noncovalent], _____ inhibitor.

Ibuprofen is a [covalent/noncovalent], _____ inhibitor.

A

covalent; suicide

noncovalent; competitive

29
Q

Why are omega-3 fatty acids healthy?

A

They’re converted to arachidonic acids more slowly than omega-6 fatty acids, increasing the omega-3/omega-6 ratio and reducing inflammation

30
Q

Fats provide __ times the metabolic energy of an equal weight of hydrated glycogen.

A

6

31
Q

The rate of lipid digestion depends on what?

A

The surface area of the interface

32
Q

Triacylglycerols are degraded into free fatty acids and glycerol by what?

A

Lipases

33
Q

What do pancreatic lipases do?

A

Catalyze the sequential hydrolysis of triacylglycerols at their 1 and 3 positions, generating two free fatty acids and a 2-monoglyceride

34
Q

Phospholipids are also degraded by what? How?

A

Pancreatic phospholipase A2 cleaves C2 fatty acid to yield lysophospholipids, which are detergents that emulsify fats

35
Q

What are the three steps of free fatty acid catabolism?

A

Activation: Conversion of a fatty acid to a fatty acyl-CoA by fatty acyl-CoA synthetase

Transportation: The transport of fatty acyl-CoA across the mitochondria inner membranes through carnitine acyltransferases

Fatty acid beta oxidation: Sequential removal of 2-carbon units by oxidation at beta-position of the fatty acyl-CoA molecule

36
Q

What are the three stages of fatty acid oxidation?

A

Stage 1: Fatty acid is oxidized to acetyl-CoA (beta-oxidation)

Stage 2: Acetyl groups oxidized to CO2 via the citric acid cycle

Stage 3: Electrons derived from the oxidations of stages 1 and 2 pass to O2 via the respiratory chain, providing the energy for ATP synthesis by oxidative phosphorylation

37
Q

Most fatty acids consumed are unsaturated. How are they metabolized?

A

Oxidation requires an additional isomerase to reposition the double bond, converting the cis isomer to a trans isomer, an intermediate in beta oxidation.

38
Q

What happens to acetyl-CoA in ketogenesis?

A

It’s converted to acetoacetate or beta-hydroxybutyrate

39
Q

Name the three ketone bodies

A

Acetoacetate, beta-hydroxybutyrate, and acetone

40
Q

Normally, ketone body formation is [high/low].

A

low

41
Q

When does acetyl-CoA accumulate?

A

During starvation or untreated diabetes

42
Q

Ketone body formation occurs where?

A

The matrix of the liver mitochondria

43
Q

Why is acetyl-CoA converted to ketone bodies in the liver and not metabolized through the TCA cycle during starvation?

A
  1. Oxaloacetate is limiting
  2. Mito NADH levels are high from beta-oxidation, which shuts down some enzymes