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Physiology III > Metabolism 9 (Exam 4) > Flashcards

Metabolism 9 (Exam 4) Flashcards

1
Q

What are the 3 primary functions of the liver in regard to lipid metabolism?

A
  1. Degrade FA into compounds usable for energy
  2. Synthesize triglycerides (mainly from carbs, some from protein)
  3. Synthesize other lipids from FA (cholesterol/phospholipids)
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2
Q

What are two examples of situations where energy metabolism leans away from using carbs?

A

Starvation and Diabetes

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3
Q

In situations where energy metabolism leans away from utilizing carbs, what will happen in the liver?

A

Large amounts of triglycerides will rapidly appear (mobilization of FA from adipose tissue)

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4
Q

Why is it important to note that some cultures intake less fat?

A

Where you practice medicine could matter with regards to an animals diet. A pets diet tends to mimic the owners.

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5
Q

Adult dogs need ___ of daily calories from fat.

A

~5.5%

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6
Q

Adult cats need ___ of daily calories from fat.

A

~20%

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7
Q

What kind of diet have cats been shown to self select?

A 
High protein (52%)
High fat (36%)
Low carb (12%)
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8
Q

Most cells can use FA for energy, except for…?

A

Brain and RBCs

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9
Q

The glycolysis intermediate DHAP can be reduced (reversible reaction) to form what?

A

Glycerol-3-phosphate

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10
Q

What enzyme is the major link between carb and lipid metabolism?

A

Glycerol-3-phosphate dehydrogenase

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11
Q

Why can glycerol be immediately placed in the glycolytic pathway?
Why can FA not immediately enter?

A

Glycerol is immediately changed by intracellular enzymes to glycerol-3-phosphate and this allows it to enter the glycolytic pathway.
FA must be further processed in the mitochondria.

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12
Q

What helps FA enter the mitochondria?

A

Carnitine shuttle

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13
Q

Which FA have to use the carnitine shuttle to enter the mitochondria?

A

Long chain FA (> 14 C)

Small and medium chains can pass right through the membranes

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14
Q

Where do we get carnitine from?

A

It can be derived from the diet or can be biosynthesized from lysine and methionine

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15
Q

What is the second enzyme used in the carnitine shuttle? And what does it do?

A

CPT1

Allows the Fatty Acyl-carnitine to cross the outer mito membrane.

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16
Q

What is the third enzyme used in the carnitine pathway? What does it do?

A

CPT2
Breaks Fatty Acyl-Carnitine into Carnitine and Fatty acyl-CoA. By doing so, carnitine is recycled and Fatty acyl-CoA can continue to beta-oxidation

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17
Q

What helps Fatty Acyl-carnitine pass through the inner mito membrane?

A

Carnitine-Acylcarnitine Translocase (CACT)
This is an antiporter
It also takes carnitine back out of the mitochondria (recycling process)

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18
Q

What is the first enzyme used in the carnitine shuttle? What does it do?

A

Acyl-CoA Synthetase

This, using ATP, will combine CoA, FA, and carnitine to form = Fatty Acyl-Carnitine

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19
Q

What is beta-oxidation?

A

It is a catabolic (break down) process occurring in the mitochondria, where FA are used to generate Acetyl-CoA which is able to enter the CAC

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20
Q

During beta-oxidation what is the first step once we have Fatty Acyl-CoA?

A

The beta carbon of the fatty acyl-CoA binds with oxygen

So, the beta carbon is oxidized

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21
Q

After the beta-carbon of the Fatty Acyl-CoA is oxidized, what will happen?

A

The acetyl-CoA will split off (enter the CAC), and a new fatty acyl-CoA is formed (but it’s two carbons shorter)
This process will continue until everything is gone

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22
Q

How much ATP is produced from a single beta-oxidation cycle?

A

Max of 17

5 ATP from H liberated and 12 from a full CAC rotation

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23
Q

In terms of storage how do carbs and fats differ?

A

Carbs are stored as glycogen and storage is limited (few hundred grams)
But kilograms of fat can be stored in adipose tissue

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24
Q

What happens to excess ingested energy (fat, carbs, or proteins)?

A

They will be converted to fat due to the amazing storage capabilities of fat

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25
Q

How do carbs and fat differ in terms of energy density?

A

A gram of fat has 2.5 times the calories of energy for a gram of glycogen

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26
Q

Overall, why is it more beneficial to the body, to store energy in the form of fat?

A

We can store more fat, and it’s more energy dense

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27
Q

Define Lipodystrophy

A

Abnormal distribution of fat in the body, the body is unable to maintain/produce healthy fat tissue

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28
Q

If there is an inability to store fat, where is it usually deposited?

A

In ectopic, or abnormal, sites like the liver, muscle, pancreas and kidney

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29
Q

Absence of fat is associated with what?

A

Insulin resistance
Hypertriglyceridemia (high blood fat)
NAFLD (Non-alcoholic fatty liver disease)
MetSyn (metabolic syndrome)

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30
Q

What is a common fat related disorder in Galloway calves?

A

Hepatic lipodystrophy (absence of adipose tissue, leading to lipid accumulation in the liver)

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31
Q

What common fat related disorder is common in pigs?

A

Adipogenesis (adipocyte hyperplasia)

32
Q

What common fat related disease is associated with cats?

A

Hepatic Lipidosis (Feline Fatty Liver)

33
Q

Define Ketosis. Where does it occur?

A

Degradation of FA for energy (occurs in the liver)

34
Q

Define ketone bodies

A

Ketone bodies are water-soluble molecules that contain the ketone groups produced from fatty acids by the liver. They are readily transported into tissues outside the liver, where they are converted into acetyl-CoA —which then enters the citric acid cycle and is oxidized for energy.

35
Q

What are the three ketone bodies?

A

Acetoacetic acid
Beta-hydroxybutyric acid
Acetone

36
Q

What is crazy about acetoacetic acid and Beta-hydroxybutyric acid?

A

Their transport is so rapid that their concentration rarely rises above 3 mg/dl, but very large quantities are actually moved due to their high solubility into tissues

37
Q

What combines with a lack of carb metabolism to create a very high mobilization of FA from tissues?

A

Low insulin
High glucagon
Increased glucocorticoid production

38
Q

Why can a limitation of oxaloacetate cause extreme acidosis?

A

Oxaloacetate is required to bind to acetyl-CoA, so without it, there will be a build up (20x) of acetoacetic acid and Beta-hydroxybutyric acid

39
Q

What is a cool way that you can diagnose acidosis?

A

The acetone can be smelled on the breath, as it is “blown off” with exhalation

40
Q

Why does the keto diet work and not cause major damage to the body?

A

With a slow change, the body can adapt to use far more acetoacetic acid than usual after a few weeks, even the brain can derive 50-75% of their energy from fats

41
Q

Who can benefit from keto?

A

Those with seizures, type 2 diabetes, and of course those wanting to lose weight

42
Q

What are the components of a phospholipid?

A

One or more FA, one phosphoric acid radical, and usually a nitrogenous base

43
Q

What cells form phospholipids?

A

All cells can form them, but the liver makes 90% of them

The intestinal epithelium also forms quite a few during absorption

44
Q

What Lecithins or glycerophospholipids did we discuss?

A

Phosphatidylcholine, phosphatidylethanolamine, phosphatidylinositol, and phosphatidylserine

45
Q

What are lecithins?

A

Phospholipids that are structural components in the cell membrane that can also have emulsification properties

46
Q

What are Cephalins?

A

These are phospholipids that contain the amino acids serine or ethanolamine (like thromboplastin)

47
Q

What is thromboplastin (a cephalin) used for?

A

Clotting

48
Q

What is sphingomyelin?

A

A phospholipid that usually has a phosphocholine or ceramide and is present in the myelin sheath as an electrical insulator

49
Q

What is the basic structure of cholesterol?

A

A sterol nucleus that is synthesized from multiple acetyl-CoAs

50
Q

How is a basic sterol modified?

A

Side chains to form cholesterol, cholic acid (basis for bile acids), or many steroid hormones

51
Q

About 70% of cholesterol in lipoproteins are in the form of ____?

A

Cholesterol esters

52
Q

Do we see more endogenous or exogenous cholesterol?

A

Endogenous cholesterol is formed in cells to a much greater extent than exogenous. Most of the circulating cholesterol was produced by the liver.

53
Q

Why does ingested cholesterol not change the plasma cholesterol level very much?

A

Inhibition of essential enzyme for endogenous cholesterol

54
Q

Why can high saturated fat increase blood cholesterol by 15-25%?

A

Increased fat deposition in the liver provides increases in acetyl-CoA for production of cholesterol

55
Q

Why can unsaturated fat depress blood cholesterol?

A

We are not sure, the mechanism is unknown

56
Q

Why will a lack of insulin or thyroid hormone increase cholesterol?

A

Mainly due to changes in the activation of enzymes for metabolism

57
Q

Why are genetic disorders like an LDL (low-density lipoprotein) receptor mutation so bad?

A

It prevents the liver from adequately removing cholesterol-rich LDLs from the blood, thus liver has no negative feedback and goes on a rampage of producing cholesterol

58
Q

What are some diseases associated with dogs that have high cholesterol?

A

Nephrotic syndrome (bunch of extra stuff in the interstitial space)
Hypothyroidism
Cholestasis (flow of bile slows or stops altogether)

59
Q

What is a disease associated with cats with high cholesterol?

A

Cholestasis

60
Q

What is a major use of cholesterol?

A

80% is converted to cholic acid for use in bile

61
Q

What hormones can cholesterol be used to form?

A

Adrenocortical hormones
Progesterone/estrogen in ovaries
Testosterone in the testes

62
Q

What use does cholesterol have in the skin?

A

It’s resistant to water-soluble substances and chemical agents, prevents water evaporation

63
Q

What is the most important use of cholesterol?

A

Structural components of cell membranes

64
Q

What is atherosclerosis?

A

It is a disease of middle to large size arteries, where plaques form on the inside surfaces of arterial walls

65
Q

What is arteriosclerosis?

A

Thickened or stiffened blood vessels of all size

66
Q

What is the general pathway for Atherosclerosis?

A
  1. Damage occurs to vascular endothelium
  2. Adhesion molecules attach
  3. Monocytes and lipids will accumulate (mostly LDLs)
  4. Monocytes will enter the intima, differentiate to macrophages, and oxidize lipoproteins (now a foam cell)
  5. Macrophage foam cells aggregate and cause a fat streak
  6. Continued fatty growth bulges into the artery and reduces blood flow
67
Q

Why can atherosclerosis become deadly?

A

The fatty growths can rupture or cause blood clots to form

68
Q

50% of all U.S. and Europe deaths are from ____.

A

Vascular disease

69
Q

What type of animals can get atherosclerosis?

A

Herbivores:

  • Dogs, cats, tigers, lions eat a lot of saturated fat and don’t get plaque buildup (unless the thyroid is removed)
  • Rabbits, mice, guinea pigs, opossums and nonhuman primates all are models of athero
70
Q

When FA are mobilized out of the adipose tissue, where are they deposited? Why?

A

Liver, this is where they are broken down

71
Q

What are the components or products of triglyceride break down?

A

FA and glycerol

72
Q

What transports long-chain FA into the mitochondria for beta-oxidation?

A

Carnitine Shuttle

73
Q

Is beta-oxidation an effective means of generating ATP? What type is best?

A

Yes. Longer chain FA are best because they produce more ATP

74
Q

In the event of low carbs, the liver generates excess acetyl-CoA. What happens?

A

Production of acetoacetic acid, beta-hydroxybutyric acid and acetone (ketosis)

75
Q

Outside of the cell membrane composition, what is cholesterol converted to?

A

Cholic acid for use in bile

76
Q

Which type of animal is predisposed to developing atherosclerosis?

A

Herbivores

Physiology III (4 decks)

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