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EOM 1 - Test 4 > Hardman - Oxidation of Fatty Acids > Flashcards

Hardman - Oxidation of Fatty Acids Flashcards

1
Q

Cystic Fibrosis

A

Pancreatic dysfunction

Growth failure, ADEK deficiency, bone disease

Not digesting fats

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2
Q

Need for Lipids

A
  • Building blocsk for phospholipids and glycolipids
  • Modification of proteins
  • Fuel
  • Hormones and intracellular messaging
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3
Q

3 Sources of Fatty Acids

A
  1. Diet
  2. Storage lipid droplets
  3. Fats synthesized in liver
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4
Q

Dietary Fats

A

90% TAGs

Multiple enzymes needed to digest each type

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5
Q

Stomach Fat Digestion Enzymes

A

Acid resistance lingual lipases

Gastric lipases

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6
Q

Enzyme which removes first two FA’s from TAGs?

Which does it remove?

A

Pancreatic Lipase removes FA at carbons 1 and 3

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7
Q

Colipase

How is it activated?

A

Anchors lipase at the lipase-aqueous interface

Cleavage by trypsin

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8
Q

Enzyme for digestion of cholesterol esters

A

Cholesterol esterase from pancreas

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9
Q

Enzymes for phospholipid (ex. phosphatidylcholine) digestion

Which carbons do these remove?

A
  1. Phospholipase A2 (#2 Carbon)
  2. Lysophospholipase (#1 Carbon)
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10
Q

How is lipid digestion hormonally controlled?

A

Cholecystokinin (CCK) - from jejunum and duodenum

(+) Gall Bladder - bile release

(+) Pancrease - enzyme release from exocrine cells

Secretin - produced in response to low pH of chyme (rich in bicarb)

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11
Q

What happens to fatty acids following intestinal lipase processing?

A

The TAGs which have been degraded to FAs / Glycerol are taken up by intestinal mucosa, and converted back into TAGs, and packaged on chylomicrons

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12
Q

What apolipoproteins label chylomicrons?

A

B-48

C-III

C-II

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13
Q

Chylomicron components

How do these components reach tissues?

A

TAGs incorporated with cholesterol, apolipoproteins (ApoC-II)

Move through lymphatic system and bloodstream to tissues

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14
Q

What enzyme converts chylomicrons to their components?

How is it activated?

A

Lipoprotein Lipase

Activated by apoC-II in capillary

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15
Q

What are fatty acids associated with when transported to other cells?

A

Albumin

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16
Q

Glycerol use during fat synthesis

A

Used by liver to produce glycerol-3-phosphate for:

glycolysis

gluconeogenesis

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17
Q

How are fatty acids transported into the cellular cytoplasm?

A
  1. Travel blood as TAGs (chylomicrons)
  2. Membrane bound lipases break down for transit
  3. Reform as TAGs in cytoplasm
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18
Q

MCAD

Medium Chain Acyl-CoA Dehydrogenase Deficiency

A

Symptoms: Lethargy, vomiting, appetite supression

Tests: Hypoketotic, hypoglycemia

19
Q

3 Stages for Mobilization of fatty acids as fuel

A
  1. Mobilization
  2. Activation and Transport to mitochondria
  3. Breaking down FA to acetyl-CoA
20
Q

What regulates mobilization of storage fatty acids?

Think: Under what conditions would you start to tap into your stored fatty acids?

A

Hormonally controlled lipase–activated by glucagon / epinephrine

Your glucose stores are low, and you need to produce energy if you’re burning your fat stores

21
Q

What is the fate of glycerol when all the FAs are cleaved off?

A

Enters glucose pathway, need to add phosphate first

Converted to Glycerol 3-Phosphate

22
Q

What is required for transport of FAs into mitochondria?

A

Activation w/ Acetyl-CoA (ATP dependent)

23
Q

What two major organ systems do not use Fatty Acids for fuel?

A

RBCs (no mitochondria)

Brain (blood brain barrier)

24
Q

What carriers activated fatty acids into mitochondria?

Hint: Hardman reaaaally emphasized this

25
Do all fatty acids require carnitine?
No, short/medium (\< 12 Carbons) can cross without carnitine
26
What are sources for **carnitine**?
1. Meat 2. Synthesized from **lysine and methionine** by liver or kidney--**not skeletal or heart muscle**
27
What is the membrane enzyme that is responsible for transfering acyl group from long chain fatty acid to carnitine? What inhibits this? Why?
**Carnitine Acyltransferase I** aka **Carnitine Palmitoyltransferase** aka **CPT - I** **(all same thing)** **_INHIBITED BY MALONYL CoA_** **_Malonyl CoA is the first commited step of Fatty Acid Synthesis--can't have breakdown/synthesis going on at the same time!_**
28
Carnitine Deficiency (or CPT-1) Source? Results?
Source: Liver Disease **Vegetarian Diet** **Burns, Pregnancy** Hemodialysis (kidney disease) Gentics Results: 1. **Inability to synthesize glucose during a fast--low blood sugar, coma, death** **2. Sustain exercise**
29
Steps for Fatty Acid B-Oxidation
Oxidation Hydration Oxidation Thiolysis - Shortened by 2-carbons each cycle
30
What are the electron acceptors in B-Oxidation?
FADH2, NADH
31
What type of enzyme drive an oxidation rxn?
Dehydrogenase
32
What are net products each OHOT round of B-Oxidation?
1 FADH2 1 NADH 1 Acetyl CoA
33
How many cycles would a n-(even)-carbon require for complete oxidation?
(n/2) - 1 -1 because the last step cuts four carbons into two Acetyl CoA, so in reality the true "net" would be 2 Acetyl CoA for the last step
34
Total ATP from complete B-Oxidation of Palmitate?
106 ATP
35
If B-Oxidation handles even carbon fatty acids, what about **Odd**?
Final step (5-carbon) yields: 3-carbon **Propionyl CoA** and 2-carbon **Acetyl CoA** - Propionyl CoA converted to **Succinyl CoA** (5-carbon) to enter Citric Acid Cycle
36
What coenzymes or vitamins are required for conversion of propionyl coa to succinyl coa?
Biotin (B7, Vitamin H) B12
37
What additional steps are required for unsaturated fatty acid processing in B-Oxidation?
Odd # Double Bonds: Isomerase Even # Double Bonds: Reductase is**_o**_ - _**o_**dd r**_e**_d - _**e_**ven
38
Refsum Disease
Genetic defect in **peroxisomal enzyme** responsible for initial step in oxidation of phytanic acid Symptoms: Retinitis pigmetosa, progressive peripheral neuropathy, skeletal malformations, severe motor weakness
39
a-Oxidation | (alpha-ox)
Takes place in peroxisomes **branched** chain fatty acids **very long** chain fatty acids **hydrogen peroxide** byproduct
40
Ketosis 3 major ketone bodies
Ketone bodies formed from acetyl CoA when fat degradation predominates Ketone Bodies: 1. Acetoacetate 2. 3-hydroxybutyrate 3. Acetone
41
Conversion of 3-Hydroxybutyrate or Acetone from Acetoacetate depends on what?
NADH/NAD+ ratio, High NADH = 3-hydroxy butyrate High NAD+ = Acetone
42
What will excess acetyl CoA eventually lead to?
High ketone production
43
Diabetic Ketosis
Absence of insulin: 1. Liver cannot provide ocaloacetate 2. Insulin normally decreases fatty acid metabolism -- Liver will produce large amount of ketone bodies, lowering pH
44

EOM 1 - Test 4 (19 decks)

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