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BMS 100 Final > Lipids > Flashcards

Lipids Flashcards

1
Q

Bata oxidation:

A

once released from TGs via lipolysis, ffa’s can be broken down for energy via beta oxidation.

First step: activation of a fatty acid to a fatty acyl CoA.

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2
Q

Fatty acid activation (cytosol):

A

Uses one ATP molecule, but the equivalent of two ATPs worth of energy

-hydrolysis to AMP and PPi first, then PPi hydrolysis

-(1) & (2) together approx. twice the amount of energy as (3), but only 1 ATP was used

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3
Q

How do fatty acyl CoA’s get into the mitochondria?

A

Require a carnitine transport system that involves:
-an enzyme to transfer the fatty acyl from CoA to a carnitine carrier (transferase-cytosol)
-A translocator to move the acyl-carnitine across the inner membrane and move free carnitine out (translocate)
-an enzyme to transfer the fatty acyl from carnitine back to CoA (transferase-matrix)

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4
Q

Determine the # of acetyl CoA by:

A

dividing the # of carbons by two

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5
Q

Determine the # of cycles by:

A

subtracting 1 from the number of acetyl CoA
-this equals the # of NADH and FADH2.

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6
Q

Determine the energy from acetyl CoA via CAC:

A

For each acetyl CoA that goes through CAC, you make:
-3 NADH = 9 ATP
(1 NADH produces 3 ATP via ETC)

-1 FADH2 = 2 ATP
(1 FADH2 produces 2 ATP via ETC

-1 GTP
(equivalent to 1 ATP)

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7
Q

Subtract ____ ATP for fatty acid activation (making fatty acyl CoA)

A

2

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8
Q

To what is a fatty acid attached to become activated prior to beta oxidation? Does this process make or use energy? How much?

A

Before fatty acids can undergo β-oxidation, they must be activated by forming a thioester bond with coenzyme A (CoA). This process is catalyzed by acyl-CoA synthetases, enzymes that are present in both the cytosol and the mitochondria.

The amount of energy required to activate a fatty acid depends on the length of the fatty acid chain. For example, the activation of palmitoyl-CoA (16 carbons) requires 12.5 ATP molecules. This means that the activation of fatty acids is a relatively expensive process, but it is essential for the efficient breakdown of these molecules into energy.

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9
Q

What carrier is used to take a fatty acyl across the inner mitochondrial membrane?

A

The carnitine acylcarnitine translocase (CACT)

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10
Q

Calculate the energy yield from a 16:0 fatty acid, assuming that all acetyl CoA molecules also go through CAC:

A

Divide the number of C by 2 to get the number of acetyl CoA:
-16:0 produces 8 acetyl CoA
-Assuming the acetyl CoA goes into CAC, multiply by 12 to get the number of ATP (12)

Divide the number if C by 2 and (-) 1 to get the number of FADH2 & NADH:
-16:0 produces 7 FADH2 & 7 NADH
-FADH2 (multipluy by 2 to get number of ATP)
-NADH (multiply by 3 to get the number of ATP)

Add up all the ATP, and then subract 2 (because it took 2 ATP to attach the fatty acid to acetyl CoA to make the fatty acyl group that enters beta ox)

Total: 129 ATP

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11
Q

CAC makes:

A

3 NADH: 3*3=9 ATP

2 FADH2: 2*2=2 ATP

1 ATP (via GTP)

Total ATP for 1 acetyl CoA: 12

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12
Q

CAC= Kreb’s cycle:

A

TCA (tricarboxylic cycle):

Energy producing pathway found in mitochondria:
Indirect: NADH, FADH2
Direct: ATP (GTP)

Final common pathway for catabolism/oxidation of:
-glucose
-fatty acids
-amino acids

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13
Q

Creation of acetyl CoA after glycolysis:

A

Rxn occurs in the mitochondrial matrix

Exergonic and irreversible
Enzyme= pyruvate dehydrogenase complex

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14
Q

Once you haver acetyl CoA from glycolysis or beta oxidation, how does it enter CAC?

A

Acetyl-CoA, the product of either glycolysis or beta-oxidation, enters the citric acid cycle (CAC) through a reaction catalyzed by citrate synthase. Citrate synthase, located in the mitochondrial matrix, catalyzes the condensation of acetyl-CoA with oxaloacetate, a four-carbon compound, to form citrate, a six-carbon compound. This reaction is the first step in the CAC, and it is irreversible.

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15
Q

Acetyl CoA and oxaloacetate combine to make _______

A

Citrate:
Enzyme: citrate synthase
CoA helps transfer the acetyl group to oxaloacetate:
-citrate is the first molecule of CAC

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16
Q

Both glycolysis and beta ox ultimately connect to CAC via what molecule?

A

Acetyl CoA

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17
Q

What preparatory step (substrate(s), enzyme and product(s)) is needed to connect glycolysis to CAC? Does it make or use indirect energy?

A

The preparatory step that connects glycolysis to the citric acid cycle (CAC) is the pyruvate dehydrogenase complex (PDH complex).

Produces indirect energy.

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18
Q

What is the first reaction of CAC (substrate(s), enzyme, product(s))?

A

The first reaction of the citric acid cycle (CAC), also known as the Krebs cycle, is the condensation of acetyl-CoA with oxaloacetate to form citrate.

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19
Q

How do amino acids feed into CAC?

A

Deamination and transamination

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20
Q

Aspartate =>

A

oxaloacetate

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21
Q

Glutamate =>

A

alpha ketoglutarate

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22
Q

Alanine =>

A

Pyruvate

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23
Q

Aspartate =>

A

fumarate
(this conversion is also important in the urea cycle)

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24
Q

Overall CAC reaction:

A
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25
Q

Catabolism of what 3 types of molecules can feed into CAC?

A

carbohydrates, fats, and proteins

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26
Q

What is the overall energy yield from 1 round of CAC?

A

6 ATP

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27
Q

Beta ox of saturated, even-numbers fatty acids:

A

Each round produces:
1FADH2 (from B2) and 1 NADH (from B3)

Acetyl CoA

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28
Q

What about unsaturated and/or odd-numbered fatty acid chains?

A
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29
Q

Enzymes names for saturated vs. unsaturated?

A

there are some minor differences in the way these enzymes function with unsaturated fatty acids, as they must first undergo hydration before they can be further metabolized.

30
Q

For each double bond, how many fewer ATP produced?

A

This is because the hydration of double bonds requires an additional enzyme, enoyl-CoA hydratase, which consumes one ATP molecule per reaction.

31
Q

Beta ox: Odd numbered:

A

Last round of beta ox produces 1 acetyl CoA and 1 propionyl CoA.

Propionyl CoA uses up 1 ATP to enter CAC:
-enters at succinyl CoA step, by passing the production of 2 NADH

32
Q

How many ATP less does a propionyl CoA make compared to an acetyl CoA?

A

Propionyl CoA makes about 1 ATP less compared to acetyl CoA.

33
Q

MCAD deficiency:

A

Deficiency of the first enzyme of beta oxidation (medium chain acyl dehydrogenase)

34
Q

Which three of the following will result from an MCAD deficiency? why?

A. High concentration of fatty acids
B. Low concentration of fatty acids
C. Hyperglycemia
D. Hypoglycemia
E. Hyperketonuria
F. Hypoketonuria

A

A. High concentration of fatty acids
C. Hyperglycemia
E. Hyperketonuria

35
Q

MCAD deficiency: What is happening with GNG?

A

Low oxaloacetate, so less GNG

Used up: combines with acetyl CoA to enter CAC to make energy

36
Q

MCAD deficiency:

A

can lead to coma and death if untreated, but once identified can be successfully treated with diet:
-Identified by newborn screening
Diet:
-frequent feeding: infants present as very lethargic, may need to wake for feedings
-Diet high in carbs and protein, low in fat

37
Q

Peroxisomal beta oxidation:

A

used to shorten very long chain fatty acids (VLCFA) into medium and long chain fatty acids.
-No carnitine transport required
(a transport protein brings the fatty acyl CoA’s across the single membrane)
-The shortened fatty acids are then further degraded in the mitochondria as per usual

38
Q

Major difference to mitochondrial beta oxidation:

A

Does not result in energy production
Remember: ETC is only in mitochondria

39
Q

CAC prep step:

A

pyruvate dehydrogenase complex allows pyruvate from glycolysis to enter CAC via acetyl CoA

Involves 3 enzymes:
-E1, E2, E3

4 coenzymes:
TPP (from B1), CoA (from B5), lipoamide (lipid coenzyme), NAD+ (from B3), FAD (from B2)

40
Q

E1:

A

uses TPP (from B1) to pick up the acetyl group.
-releases CO2

41
Q

E2:

A

uses lipoamide to transfer the acetyl group from TPP to CoA (from B5)
-reduces the lipoamide and creates acetyl CoA

42
Q

What’s left for E3? Resetting the coenzymes to reuse

A

-FAD resets lipoamide, becoming FADH2

-NAD+ resets FADH2 back to FAD, becoming NADH

43
Q

What resets the NADH back to NAD+?

A

NADH can then be reoxidized to NAD+ through the electron transport chain (ETC), which is a series of redox reactions that generate a proton gradient across the inner mitochondrial membrane. This proton gradient is then used to drive ATP synthesis by ATP synthase.

44
Q

Glycolysis prep step:

A

Pyruvate dehydrogenase complex

45
Q

Step one: Creation of citrate enzyme:

A

citrate synthase

46
Q

Step two enzyme:

A

aconitase hydratase
-reaction involves an aconitate intermediate

47
Q

Step three, enzyme:

A

Citrate
Exergonic reaction: helps pull previous reaction forward

-produces NADH and CO2

48
Q

Step four enzyme:

A

Alpha keto glutarate dehydrogenase (complex)

-exergonic reaction

-Produces NADH & CO2

49
Q

Step 5 enzyme:

A

succinyl CoA synthetase

-Thioester bond broken; energy released

Involves substrate level phosphorylation.

50
Q

Step 6 enzyme:

A

Succinate
-FADH2 produced

(this one is attached to the inner mitochondrial membrane)

Also serves as part of the ETC and is the entry point for FADH2 from CAC into ETC.

51
Q

Step 7 enzyme:

A

Fumarase
-water is added across the db

52
Q

Step 8 enzyme:

A

malate
-NADH generated
-endergonic rxn

53
Q

First hald following glycolysis:

A

Start with 3 C pyruvate
Energy yield: 2NADH and 1 GTP (ATP)

54
Q

Second half:

A

Conversion of succinate to oxaloacetate
-Energy yield: 1 NADH and 1 FADH2
-Cycle goes back to the beginning: oxaloacetate + acetyl CoA to make citrate

55
Q

1=PDH complex
Inhibited by:

A

Acetyl CoA, NADH
-Product inhibition
ATP
-indicates high energy

56
Q

1=PDH complex
activated by:

A

CoA, NAD+
-substrate activation

AMP
-indicates low energy

Ca+2
-released during muscle contraction, signifies need for more energy

57
Q

2= citrate synthase:

A

Inhibited by:
Citrate
-product inhibition

NADH, ATP
-Products of CAC, indicate high energy

Succinyl CoA
-Product of CAC, used to make energy (GTP)

58
Q

If we have access to acetyl CoA, what can the liver do with it?

A

Store it as ketone bodies for other tissues to use (ketogenesis)

-Brain, heart, skeletal muscle can break down ketone bodies (ketolysis) when needed for energy

59
Q

Ketolysis (extra-hepatic)

A

Liver lacks enzyme that converts acetoacetate to acetoacetyl CoA:
-Liver does not use the ketone bodies that or makes.

60
Q

When would you liver use acetyl CoA for ketogenesis as opposed to CAC?

A

In times of low blood sugar
For example, during starvation or when following the Atkins (high protein, low carb) diet, the liver makes ketones to send out to other tissues.

61
Q

Which two of the following would apply in the liver when blood sugar is low?

A. Beta oxidation is decreased
B. Beat oxidation is Increased
C. Gluconeogenesis is decreased
D. Gluconeogenesis is increased

A

B. Beat oxidation is Increased.
D. Gluconeogenesis is increased

62
Q

Uncontrolled type 1 diabetes mellitus (DM) can cause buildup of ketone bodies:

A

Autoimmune condition where insulin-secreting beta cells of pancreas are damages/destroyed.

-Results in low insulin and high blood sugar levels

63
Q

If ketogenesis normally results from low blood sugar, why does it happen with high blood sugar in uncontrolled DM?!

A

decreased insulin levels, increased fatty acid breakdown, inefficient ketone body utilization, and receptor resistance. These factors contribute to an accumulation of ketone bodies in the bloodstream, leading to the potential for ketoacidosis.

64
Q

When insulin is high;

A

glucagon is low

65
Q

When insulin is low:

A

glucagon is high

66
Q

IN DM, insulin is low despite hyperglycemia:

A

beta cells are damaged

67
Q

In DM we have:

A

Hyperglycemia with high glucagon

68
Q

Ketosis:

A

High level of ketones

Not usually a problem

-ketone bodies are used, expired, or excreted in the urine
(excretion of ketones is used as a measure of Atkin’s diet)

69
Q

Diabetic ketoacidosis:

A

high levels of ketones combined with low blood pH and hyperglycemia.

-seen in uncontrolled diabetes mellitus

Low blood pH= acidosis: from buildup of ketone bodies

Hyperglycemia: from low insulin, high glucagon

Leads to diuresis: increased urination from osmotic pull of glucose.
-leads to electrolyte imbalances, as ions are excreted due to excessive urination

(untreated can cause coma, and death)

70
Q

If a patient comes to you in the initial stages of diabetic ketoacidosis:

What warning sign might you be able to detect while they are in your office with you?

What complaint might they have that is related to the hyperglycemia?

A

There are several warning signs that a patient might exhibit in the initial stages of diabetic ketoacidosis (DKA) while in your office:

Increased thirst and urination (polydipsia and polyuria): As blood sugar levels rise, the body attempts to excrete excess glucose through increased urination, leading to dehydration and excessive thirst.

Rapid, deep breathing (Kussmaul respiration): As the body tries to compensate for the acidity caused by ketone accumulation, it increases its respiratory rate to expel carbon dioxide and buffers the acidic environment. This can manifest as rapid, deep breathing, known as Kussmaul respiration.

Fruity odor on breath (acetone breath): Ketones, particularly acetone, have a characteristic fruity odor that can be detected on the breath of individuals with DKA.

Excessive fatigue and weakness: As blood sugar levels rise and ketones accumulate, the body’s cells struggle to utilize glucose for energy, leading to fatigue and weakness.

Vomiting and nausea: The accumulation of ketones can irritate the stomach lining, causing nausea and vomiting.

Headache: Elevated blood sugar levels and dehydration can contribute to headaches.

Dry, flushed skin: Dehydration can lead to dry, flushed skin.

Extreme hunger despite high blood sugar: Despite high blood sugar levels, individuals with DKA may experience extreme hunger due to the body’s inability to utilize glucose effectively.

In addition to these physical signs, patients with DKA may also present with complaints related to their hyperglycemia:

Frequent urination (polyuria): Increased urination is a common complaint associated with hyperglycemia. This is because the body tries to excrete excess glucose in the urine to maintain normal blood sugar levels.

Frequent thirst (polydipsia): Excessive thirst is a natural counterpart to polyuria. As the body loses fluids through frequent urination, it triggers a compensatory thirst mechanism to replenish lost fluids.

Fatigue and weakness: The inability to effectively utilize glucose for energy can lead to fatigue and weakness. This can make daily activities challenging and can impact the patient’s quality of life.

Headaches: Elevated blood sugar levels can disrupt the normal balance of fluids and electrolytes in the body, leading to headaches.

Blurred vision: Changes in blood sugar levels can affect the clarity of vision. Individuals with hyperglycemia may experience blurred vision or difficulty focusing.

BMS 100 Final (6 decks)

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