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Biochemistry 2019 > Lecture 29 > Flashcards

Lecture 29 Flashcards

1
Q

Put the following substances in order of the amount of kCal they store (smallest to largest amount)

Glucose (blood)
TAGs (in fat and muscle)
Glycogen (liver and muscle)
Protein (muscle)

A

Glucose (blood)

Glycogen (liver and muscle)

Protein (muscle)

TAGs (in fat and muscle)

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2
Q

Pound for pound, TAGs contains about 6.75 times as much energy as _____.

A

Carbs (glycogen)

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3
Q

State the 3 sources of TAGs for humans

A

Dietary (processed in intestinal cells)

De Novo (in hepatocytes)

De Novo (in adipocytes)

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4
Q

State the 4 components that form a TAG

A

WATCH LECTURE

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5
Q

Compare glycerol, MAGs, DAGs, and TAGs in terms of their structures

A

Glycerol: Glycerol with 3 OH groups

MAG: Glycerol with 2 OH groups and a fatty acid chain

DAG: Glycerol with 1 OH group and 2 FA chains

TAG: Glycerol with 0 OH groups and 3 FA chains

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6
Q

Overexpression of Perilipin 1 does what? What effect does a knockout of Perilipin 1 cause?

A

overexpression of Perilipin 1 inhibits lipolysis

the knockout activates lipolysis

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7
Q

Describe the location, function and regulation of Perilipin

A

Perilipin coats lipid droplets in adipocytes and muscle cells

Functions to regulate lipolysis by controlling physical access to lipid breakdown enzymes

Perilipins are regulated by PKA, which promotes lipolysis by phosphorylating perilipin

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8
Q

What are the 2 hormone messengers that activate the mobilization of FAs out of adipocytes and what hormone inhibits this type of mobilization? Include the type of cell membrane receptor that each of these will use

A

Glucagon (released during hunger) and Epinephrine (released during exercise) activate the mobilization of FAs from adipocytes by interacting with an intramembranous GPCR

Insulin (released during fed state) inhibits this FA mobilization by interacting with intramembranous RTKs

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9
Q

Beginning with PKA (protein kinase A) state the mechanism that creates FAs + Glycerol from TAGs.

A

PKA activates Perilipin by phosphorylating it

Phosphorylated Perilipin activates ATGL (Adipose Triglyceride Lipase) by allowing it to bind to it’s CA (co activating factor)

Active ATGL (ATGL + CA) then makes DAGs from TAGs

PKA also activates HS lipase (hormone sensitive lipase) by phosphorylating it) and active HS lipase makes MAGs from DAGs

Lastly, MAG lipase carries out the final step by yielding FA + Glycerol from MAG

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10
Q

Explain the mechanism by which Insulin prevents the mobilization of FAs from adipocytes

A

Insulin interacts with it’s RTK Insulin receptor

The RTK activates PP1 (protein phosphatase), which inactivates HSL by dephosphorylating it

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11
Q

Where in the cell do FAs normally reside? what membrane(s) must it pass through in order to be broken down via beta-oxidation?(include where in the cell this beta-oxidation occurs)

A

FAs normally reside in the cytosol of the cell

In order to be broken down via beta-oxidation, FAs must pass through both the inner and outer mito membranes so they may be broken down in the mito matrix

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12
Q

briefly describe the 2 phases of FA breakdown and where they occur

A

Phase I: FA activation, which occurs in the cytosol

Phase II: Beta-oxidation (breaking FAs down, 2 carbons at a time) which occurs in the mito matrix

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13
Q

The outer mito membrane is not permeable to ______ and the inner mito membrane is not permeable to _____. Explain what occurs in order to get FAs across both of these membranes.

A

FA

FACoA

To cross the outer mito membrane: FA binds to CoA, forming Fatty Acyl CoA (which can pass through the membrane)

To cross the inner mito membrane: Carnitine removes the CoA from the FA and forms Fatty Acyl Carnitine (which can pass through the membrane)

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14
Q

What enzyme conducts the first reaction in any FA metabolism? Why is this enzyme activity important?

A

Acyl-CoA synthetase

It traps FA in cells (in the cytosol) and creates FA Acyl-CoA, which is a more metabolically active form of FA

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15
Q

Describe the 2 steps that occur to create FA Acyl-CoA from FA

A 
The carboxyl (CO2 end) of a FA reacts with ATP, forming Acyl Adenylate and PPi
(Acyl Adenylate has an AMP group, which makes sense bc the other 2 phosphates are in PPi)

Acyl Adenylate’s AMP group then reacts with the Sulfhydryl group of CoA to form Acyl-CoA + AMP

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16
Q

What is the significance of the PPi molecule that is formed by Acyl-CoA synthase activity?

A

PPi hydrolysis makes this reaction irreversible (makes it an effective method of trapping FA in the cell)

(PPi is broken into Pi + Pi, which provides energy for the cell)

17
Q

What is the rate limiting enzyme of the beta oxidation of FAs? what inhibits this enzyme?

A

Carnitine Acyltransferase (Carnitine + Acyl CoA = Acyl Carnitine + CoA)

Malonyl CoA inhibits Carnitine Acyltransferase
(this makes sense bc Malonyl CoA is the product of ACC, which is the rate limiting enzyme of FA synthesis)(can’t breakdown and synthesize FAs at the same time)

18
Q

Describe the mechanism of the Translocase that escorts Acyl carnitine and Carnitine across the inner mito membrane (include the directions it moves these molecules)

A

This translocase is an anti porter that brings Acyl carnitine into the mito matrix while simultaneously moving Carnitine out of the mito matrix (into the intermembrane space of the mito)

This allows Acyl CoA to cross the membrane and recycles Carnitine back to the intramembranous space after it has helped Acyl CoA cross the membrane.

19
Q

Compare Carnitine acyltransferase I and Carnitine Acyltransferase II

A

Carnitine Acyltransferase I: removes CoA and adds Carnitine in the intermembrane space of the mito
(Carnitine + Acyl CoA = Acyl Carnitine + CoA)

Carnitine Acyltransferase II: adds CoA and removes Carnitine in the mito matrix
(Acyl Carnitine + CoA = Acyl CoA + Carnitine)

20
Q

State the 4 steps of beta oxidation of FAs in the mito matrix. Include the enzyme that begins beta oxidation and where FADH2, NADH is synthesized in this process.

A
  1. Oxidation: Acyl CoA Dehydrogenase (ACAD) begins beta oxidation and creates FADH2
  2. Hydration: Water is added
  3. Oxidation: NADH is created
  4. Thiolysis: 2 Carbons are cleaved off and Acetyl CoA is created (will go to TCA cycle to generate 12 ATP)
21
Q

how many ATP will FADH2 yield? What about NADH? How many ATP will 1 molecule of Acetyl CoA yield if it enters the Citric Acid cycle?

A

FADH2 = 2 ATP

NADH = 3 ATP

Acetyl CoA = 12 ATP

22
Q

True or False:

The beta oxidation of FAs directly forms ATP, hence why FA breakdown occurs in times of ATP need. explain.

A

False

Beta oxidation of FA’s yield FADH2, NADH, and Acetyl CoA which then serve as substrates for other reactions to yield ATP. Therefore beta oxidation does not DIRECTLY yield ATP.

FADH2 delivers electrons to the CoQ/ubiquinone of the ETC
NADH delivers electrons to Complex I of the ETC
Acetyl CoA generates ATP via the TCA cycle

23
Q

State the following contribution to ATP yeild for the following products after the beta oxidation of 1 molecule of palmitate (16 C FA).

FADH2:
NADH:
Acetyl CoA:
Total ATP produced:
Net ATP produced:
A 
FADH2: 7 x 2 = 14 
NADH: 7 x 3 = 21
Acetyl CoA: 8 x 12 = 96
Total ATP produced: 131
Net ATP produced: 129 (bc 2 ATP are used to activate the palmitate molecule)

(7 FADH2/NADH bc those come from the BONDS between the 2 carbon “units” of FAs)
(8 Acetyl CoA bc those come from the 2 carbon UNITS of FAs)

24
Q

Briefly describe the relationship between lipid and carbohydrate oxidation.

A

Acetyl CoA is formed by the oxidation of FAs and OOA is formed by digesting carbohydrates from food.

Without sufficient carb intake, there will not be enough OAA to combine with Acetyl CoA and begin glycolysis (citric acid cycle begins with Citrate)

“Fats burn in the flame of carbohydrates”
If you eat too few carbs, Acetyl CoA accumulates and the body will enter ketosis, which creates ketone bodies from the excess Acetyl CoA.

25
Q

State the names of the 3 ketone bodies that can be formed from Acetyl CoA by the body to provide energy during fasting/starvation. Where in the body are all of these ketones bodies produces?

A
  1. Acetoacetate
  2. Beta-Hydroxybutyrate
  3. Acetone

All 3 of these are produced in the liver only

26
Q

Describe the precursor molecules for the following 2 ketone bodies.

Acetoacetate:

Hydroxybutyrate:

Acetone:

A

Acetoacetate: High levels of Acetyl CoA (and no carb intake to “burn” them via the citric acid cycle)

Hydroxybutyrate: Acetoacetate (NADH is needed also)

Acetone: Acetoacetate

27
Q

Describe the pathway that occurs beginning with Hydroxybutyrate when there are low levels of 2 acetyl CoA.

A

Hydroxybutyrate (loses a proton) oxidizes into Acetoacetate

Acetoacetate becomes Acetoacetyl CoA via CoA transferase

Acetoacetyl CoA becomes 2 Acetyl CoA via Thiolase

(This is basically making Acetyl CoA from a ketone)

28
Q

Describe the steps that occur and lead to death in diabetic ketoacidosis

A
  1. OAA levels drop
  2. CAC slows (bc of the lack of OAA)
  3. Free FAs are released from Adipose tissue stores
  4. Ketone bodies are formed from the FAs to provide energy
  5. accumulation of ketones decreases blood pH
  6. Coma and death result from low blood pH

Biochemistry 2019 (32 decks)

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