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Block 1 - Week 1 > Lipid Mobilization and Oxidation > Flashcards

Lipid Mobilization and Oxidation Flashcards

1
Q

Where does dietary lipid digestion occur?

A

It begins in the stomach and continues in the small intestine

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2
Q

Where and how are Cholesteryl Esters, Phospholipds, and Triacylglycerols with long-chain fatty acids degraded?

A

In the small instestine by pancreatic enzymes

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3
Q

What are the important pancreatic enzymes?

A
  • Cholesterol Esterase
  • Phospholipase A2
  • Pancreatic Lipase
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4
Q

How does Cystic Fibrosis affect the pancreatic enzymes?

A

Thickened mucus prevents these enzymes from reaching the intestine

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5
Q

How is TAG from milk fat degraded?

A

TAG in milk contains short- to medium-chain-length FAs and are degraded in the stomach by Acid Lipases (Lingual Lipase and Gastric Lipase)

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6
Q

Why, where, and how does emulsification occur?

A
  • Why: hydrophobic nature of lipids requires them to be emulsified for efficient degradation
  • Where: Small intestine
  • How: Peristaltic action (mechanical mixing) and Bile Salts (Detergents)
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7
Q

What are the 3 primary products of dietary lipid degradation?

A
  1. ) 2-monoacylglycerol
  2. ) Cholesterol (nonesterified/free)
  3. ) Free FA
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8
Q

What forms Mixed Micelles?

Why are they important?

A
  • The 3 primary products of dietary lipid degradation + fat-soluble vitamins
  • Facilitate dietary lipid absorption by Intestinal Mucosal Cells (Enterocytes)
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9
Q

Chylomicrons

A

Lipoprotein (lipid and protein) comprised of TAG, Cholesteryl Esters, and Apolipoprotein (apo) B-48 assembled with fat-soluble vitamins inside the Intestinal Mucosal Cells (Enterocytes)

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10
Q

What type of FAs enter the blood directly?

A

Short- and medium-chain FAs

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11
Q

How do Chylomicrons enter the blood?

A

They first enter into the Lymph and then enter the blood

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12
Q

Where and how are Chylomicrons degraded?

A

In the Capillaries of Muscle and Adipose tissue by Lipoprotein Lipase (with Apo C-II coenzyme)

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13
Q

What is Fat Maldigestion and what does it cause?

A

Malabsorption which causes Steatorrhea (lipids in the feces)

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14
Q

Carnitine

A
  • Specialized carrier that transports long-chain Acyl groups from Cytosol into the Mitochondrial Matrix
  • Obtained from the diet (primarily meat products)
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15
Q

Phytanic Acid

A
  • Branched chain fatty acid, product of chlorophyll metabolism
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16
Q

How many carbons do Short Chain Fatty Acids (SCFAs) have?

A

2-5 carbons

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17
Q

How many carbons do Medium Chain Fatty Acids (MCFAs) have?

A

6-12 carbons

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18
Q

How many carbons do Long Chain Fatty Acids (LCFAs) have?

A

13+ carbons

19
Q

What are the fat soluble vitamins?

A

A, D, E, K

20
Q

How do Polyunsaturated Fats impact health?

A
  • Precursor to Hormones (Ex. Prostaglandins)

- Reduce Total and LDL Cholesterol (Lower Heart Disease)

21
Q

Prostaglandins

A
  • Hormone
  • Polyunsaturated Fats are a precursor to
  • Stimulate Endothelial Cells that line blood vessels to release Nitric Oxide (Vasodilator, lowers BP)
22
Q

Nitric Oxide

A
  • Vasodilator, released by Endothelial Cells when stimulated by Prostaglandins
  • Lowers BP
23
Q

Preferred energy source in the body

A

Carbohydrates > Fats > Proteins > Ketone Bodies

24
Q

Where, when, and how are Ketone Bodies produced?

A
  • In the Liver Mitochondria
  • Made during prolonged Fasting or Exercise
  • Made with Type 1 DM or Alcoholism
  • Made by using Acetyle-CoA
25
Q

How are Ketone Bodies used as energy?

A
  • Ketone Bodies are released from the Liver into the blood
  • Can be picked up by the majority of cells
  • Reconverted to Acetyl-CoA in the cell
  • Acetyle-CoA enters the mitochondria to produce ATP
26
Q

What are the 3 main Ketone Bodies?

A
  • Acetoacetate
  • B-Hydroxybutyrate
  • Acetone
27
Q

Fasting timeline

A
  1. ) 12 hours: Glycogenolysis (Pancreas releases Glucagon –> Liver breaksdown Glycogen to Glucose)
  2. ) 24 hours: Gluconeogenesis (Liver makes new glucose)
  3. ) 1-3 days: Breakdown of fatty acids for energy: Fatty Acids –> (B-Oxidation) –> Acetyl-CoA (Except for Brain Cells, FAs can’t cross Blood Brain Barrier, Brain Cells can only use Glucose or Ketone Bodies for energy)
28
Q

Why use Acetyl-CoA for Ketone Body production?

A
  • In a starvation state, low levels of Oxaloacetate (normally Acetyl-CoA + Oxaloacetate –> Citrate in TCA cycle)
  • When low levels of Oxaloacetate, Acetyle-CoA builds up
  • Liver uses this build up to make Ketone Bodies
29
Q

1st step of Ketone Body production

A

2x Acetyle-CoAs –> (Acetyl-CoA Acyl-Transferase) –> Acetoacetyl-CoA + Free CoA

30
Q

2nd step of Ketone Body production

A

Acetoacetyl-CoA + Ac-CoA –> (HMG-CoA Synthase) –> 3-Hydroxy-3-Methylglutaryl-CoA + Free CoA

Note: This is the rate limiting step

31
Q

What is the rate limiting step of Ketone Body production?

A

The second step:

Acetoacetyl-CoA + Ac-CoA –> (HMG-CoA Synthase) –> (AKA HMG-CoA) + Free CoA

32
Q

3rd step of Ketone Body production

A

HMG-CoA –> (HMG-CoA Lyase) –> Acetoacetate (Ketone Body + Ac-CoA

33
Q

Possible 4th step of Ketone Body

A

Acetoacetate (Ketone Body) –> (B-Hydroxybuteryate Dehydrogenase) –> B-Hydroxybuterate (Another Ketone Body)

34
Q

How is Acetone made?

A

Some Acetoacetate (Ketone Bodies) in the blood spontaneously lose a carbon and become Acetone (Metabolically useless Ketone Body, exhaled from lungs)

35
Q

What Ketone Body is useless? What implication does this have?

A

Acetone –> Gets exhaled from the lungs –> Explains Fruity Smelling Breath in Diabetic Ketoacidosis

36
Q

What happens to the blood pH as a result of Ketone Bodies being in the blood?

A
  • Ketone Bodies are Acids –> Lowers Blood pH

- Metabolic Acidosis

37
Q

What cells can’t use Ketone Bodies (Acetoacetate and B-Hydroxybutyrate) for energy and why?

A
  • Red Blood Cells because they don’t have Mitochondria

- Liver cells because they don’t have the Enzyme Thiophorase which converts Acetoacetate to Acetoacetyl-CoA

38
Q

How is B-Hydroxybutyrate converted back to Acetoacetate one in the peripheral tissues?

A
  • Enzyme B-Hydroxybutyrate Dehydrogenase

- Makes an NADH in the process

39
Q

How is Acetoacetate used as energy in the cells?

A

Acetoacetate + [Succinyl-CoA] –> (Thiophorase) –> Acetoacetyl-CoA + [Succinate]

Acetoacetyl-CoA –> (B-Ketothiolase) –> 2x Acetyl-CoAs + [CoA]

Acetyl-CoA can now enter TCA Cycle to make ATP

40
Q

What hormone induces Triglyceride breakdown in Adipocytes?

A

Hormone Sensitive Lipase (HSL)

41
Q

What is the role of the protein Albumin?

A

Carries fatty acids to target cells, like Live Cells, which are capable of fatty acid oxidation

42
Q

Step 1 of fatty acid oxidation

A

Once inside the target cell:

FA –> (Fatty Acyl-CoA Synthetase uses 2 ATP) –>
Fatty Acyl-CoA

43
Q

Where are the enzymes required for B-oxidation of fatty acids?

A

In the Mitochondrial Matrix

44
Q

Step 2 of fatty acid oxidation

A

Fatty Acyl-Coa –> (CPT-1 aka CAT-1) –> Fatty Acyl-Carnitine

Block 1 - Week 1 (6 decks)

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