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KIN 217 - Human Biochemistry > Chapter 27 > Flashcards

Chapter 27 Flashcards

1
Q

Fatty Acids

A

Stored in adipose tissue as triacylglycerol’s (TAG)
- TAG = fatty acids linked to glycerol w/ ester linkages

Adipose tissue is located throughout the body, most prominent places are…
- Subcutaneous (below the skin)
- Visceral (around the internal organs)

TAG is stored in adipocytes as a lipid droplet

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2
Q

Fatty Acids are Processed in 3 Stages

A

Fatty acids into triacylglycerols in adipose tissues are made accessible in 3 stages:

  1. Degradation of TAG to release fatty acids and glycerol into blood for transport to energy-repairing tissue
  2. Activation of the fatty acids and transport into mitochondria for oxidation
  3. Degradation of the fatty acids to acetyl-CoA for processing by CAC
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3
Q

Seven-transmembrane-helix (7TM) receptors

A
  • transmit info initiated by signals as photons, hormones, neurotransmitters, odorants, etc.
  • change conformation in response to ligand binding and activate G-proteins
  • These receptors contain 7 helices that span the membrane bilayer
  • An example of a 7TM receptor that responds to chemical signals is called B-adrenergic receptor. This protein binds epinephrine (also called adrenaline), a hormone responsible for fight or flight response

Mutations in these receptors and their associated components cause a host of diseases. Examples of these mutations include…

  • Color blindness
  • Familial hypogonadism
  • Short stature due to mutated growth hormone receptor
  • Extreme obesity
  • Congenital hypothyroidism
  • Incomplete bowel innervation (Hirschsprung disease)
  • Precocious puberty
  • Night blindness
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4
Q

Ligand-receptor binding activates GTP-binding proteins (G-proteins) + Fatty Acid Release Steps

A
  1. Begins with fight or flight response or low blood glucose levels occurring, such as in the morning
  2. The ligand epinephrine is bound to its receptor, B2-adrenergic (a 7TM receptor)
  3. On the cytoplasmic portion, the Heterotrimeric G-protein consist of alpha, beta, and gamma subunits
  • GDP-bound G-alpha is inactive
  • GTP-bound G-alpha is active
  1. Upon ligand-receptor binding, a conformational change takes place within the receptor, which is relayed to the G-protein
  2. The G-protein releases the bound GDP in exchange for GTP. At the same time, the G-alpha-GTP now dissociates from the beta and gamma subunits
  3. Activated G-alpha-GTP then transitions towards membrane bound adenylate cyclase to activate this enzyme
  4. Activated adenylate cyclase then generates cAMP from ATP. cAMP now acts as a second messenger inside the cells to activate protein kinase A
  5. Activated PKA phosphorylates 2 key proteins: Perilipin and lipase
  6. Activation of Perilipin allows for the reorganization of the fat droplets, so that the TAG’s are accessible. Phosphorylation also releases coactivator ATGL
  7. ATGL initiates the mobilization of TAG by releasing a fatty acid from TAG to form DAG
  • ATGL removes first fatty acid from TAG to generate diacylglycerol (DAG)
  1. Phosphorylated lipase removes second fatty acid from DAG to generate monoacylglycerol (MAG) + a free fatty acid
  2. MAG-lipase completes fatty acid mobilization w/ production of a free fatty acid and a glycerol
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5
Q

STEP 1: Free Fatty Acids & Glycerol: Released into the Blood

A

Fatty acids (insoluble)
- Since fatty acids are not soluble in solution, the fatty acids will be bound to blood protein albumin

–> Albumin will transport fatty acids through blood to tissue cells that need fuel sources

Glycerol (soluble in plasma)
- The glycerol that’s released during lipolysis and absorbed by liver will be used in glycolysis or gluconeogenesis

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6
Q

STEP 2: Describe how the Fatty Acids get linked to CoA

A

–> Fatty acids separate from albumin in bloodstream and diffuse across cell membrane w/ assistance of transport proteins
- In cells, fatty acids are shuttled about in association w/ fatty-acid binding proteins
- Activation and attachment to CoA is required before oxidation

–> Fatty acids must be activated by reaction w/ CoA to form acyl-CoA

  • Activation takes place on outer mitochondrial membrane, where it’s catalyzed by acyl-CoA synthetase
  • Activation takes place in two steps: (partial reactions are freely reversible)
    1. Fatty acid reacts w/ ATP to form acyl adenylate, and the other 2 phosphoryl groups of the ATP substrate are released as pyrophosphate
  1. Sulfhydryl group of CoA attacks acyl adenylate to form acyl-CoA and AMP

–> Reaction is driven forward by hydrolysis of pyrophosphate by pyrophosphatase, rendering reaction irreversible (b/c of pyrophosphatases)

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7
Q

STEP 2: Describe how fatty acid entry into the mitochondrial matrix works

A
  1. After being activated by linkage to CoA, fatty acid is transferred to carnitine; rection catalyzed by carnitine acyltransferase I (CAT I), generating acyl carnitine
  • required for transport of acyl carnitine across inner mitochondrial membrane into mitochondrial matrix
  1. Translocase transports acyl carnitine into matrix of mitochondria
  2. In mitochondria, carnitine acyltransferase II (CAT II) transfers fatty acid to CoA
  3. Fatty acyl CoA is now ready to be degraded
  4. Carnitine returns to cytoplasmic side in exchange for acyl carnitine (repeats)

acyl-CoA + carnitine <=> acyl carnitine + CoA

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8
Q

STEP 3: explain the 4-steps to fatty acid oxidation in the mitochondria

A
  • Fatty acid oxidation = degrading the fatty acids two carbon atoms one at a time
    –> also called B-oxidation b/c oxidation it takes place at beta carbon atom
  • B-oxidation takes place in 4-reactions that are repeated:Oxidation of B-carbon atom
    Hydration of trans-∆2-enoyl CoA
    Oxidation of L-3hydroxyacyl CoA
    Cleavage of the 3-ketoacyl CoA
  1. Oxidation of B-carbon atom occurs, catalyzed by acyl-CoA dehydrogenase ~ this generates enol-CoA w/ trans double bond between C2 and C3
  • Electrons are transferred to FAD to generate FADH2, which then enter ETC
  1. Hydration of the double bond between C2 and C3 occurs by enzyme enoyl-CoA hydratase ~ this results in L-isomer of 3-hydroacyl CoA
  2. Oxidation of L-isomer of 3-hydroacyl CoA occurs by L-isomer of 3-hydroacyl CoA dehydrogenase ~ this generates 3-ketoacyl CoA and NADH
  3. Cleavage of 3-ketoacyl CoA by B-ketothiolase occurs ~ this forms acetyl-CoA and a fatty acid chain that is 2-carbons shorter than when the reaction started
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9
Q

Fatty acid oxidation takes place with 4-repeating steps: oxidation, hydration, oxidation and cleavage. In each round ______________________________ is formed

a) an acetyl-CoA (shortened by 2-C), 1-FADH2, 1-NADH
b) an acetyl-CoA (shortened by 2-C), 2-FADH2, 2-NADH
c) an acetyl-CoA (shortened by 1-C), 1-FADH2, 3-NADH

A

a) an acetyl-CoA (shortened by 2-C), 1-FADH2, 1-NADH

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10
Q

In the degradation of palmitate, a 16-carbon fatty acid, complete oxidation of palmitoyl-CoA will yield…

a) 7-acetyl-CoA, 7-FADH2, 7-NADH, and 7-protons
b) 8-acetyl-CoA, 7-FADH2, 7-NADH, and 7-protons
c) 6-acetyl-CoA, 3-FADH2, 3-NADH, and 3-protons

A

b) 8-acetyl-CoA, 7-FADH2, 7-NADH, and 7-protons

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11
Q

The complete oxidation of palmitate yields ____ molecules of ATP

a) 104
b) 106
c) 128
d) 132

A

b) 106

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12
Q

Describe fatty acid degradation concerning unsaturated & odd-chain fatty acids

A

Beta oxidation is straight-forward for complete degradation of saturated fatty acids that have even # of carbon atoms, but degradation of unsaturated fatty acids and/or those w/ odd chain carbons require additional steps

Degradation of unsaturated and odd-chain fatty acids:
- Requires additional steps
- Requires additional enzymes: isomerases and/or reductases

–> isomerase enzyme facilitates the conversion of a cis-double bond into a trans double bond, required to complete beta oxidation of the fatty acid

–> reductase enzymes are required for polyunsaturated fatty acids

  • Unsaturated fatty acids are not fully reduced due to at-least 1-double bond, thus slightly less energy will be captured

Polyunsaturated fatty acid (PFAs) require:
- cis-Δ3-enoyl CoA isomerase
- 2,4-dienoyl-CoA reductase
- Ex. Linoeoyl-CoA

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13
Q

Unsaturated fatty acids w/ odd numbers of double bonds require _____

a) isomerase
b) reductase
c) isomerase and reductase

A

a) isomerase

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14
Q

Unsaturated fatty acids w/ even numbers of double bonds require _____

a) isomerase
b) reductase
c) isomerase and reductase

A

c) isomerase and reductase

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15
Q

Example: Degradation of Palmitoleoyl-CoA (Monosaturated Fatty Acid)

A

 Beta oxidation of degradation of plamitoleoyl-CoA results in formation of cis-Δ3-enoyl CoA

 cis-Δ3-enoyl CoA cannot be processed by acyl-CoA dehydrogenase

 An isomerase enzyme (cis-Δ3-enoyl CoA isomerase) will shift the cis-Δ3-enoyl CoA into trans-Δ2-enoyl CoA

 trans-Δ2-enoyl CoA is a normal substrate for β oxidation

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16
Q

Polyunsaturated fatty acid (PFAs) require…

a) cis-Δ3-enoyl CoA isomerase AND 2,4-dienoyl-CoA reductase

b) cis-Δ2-enoyl CoA isomerase AND 1,3-dienoyl-CoA reductase

c) cis-Δ3-enoyl CoA isomerase AND 1,4-dienoyl-CoA reductase

A

a) cis-Δ3-enoyl CoA isomerase AND 2,4-dienoyl-CoA reductase

17
Q

Explain how the fatty acid chain length is considered for fatty acid degradation

A
  • Chain length also needs to be considered for fatty acid degradation
  • For B-oxidation of an odd #ed fatty acid chain, routine B-oxidation will occur until a 3-C propionyl-CoA is generated at the last thiolysis reaction (propionyl-CoA + acetyl-CoA instead of 2 acetyl-CoA entities)
  • Biotin enzyme propionyl-CoA carboxylase adds a carbon to propionyl-CoA to form methylmalonyl-CoA (4-C)
  • Succinyl-CoA, a CAC component, is formed from methylmalonyl-CoA by methylmalonyl-CoA mutase (a vitamin b12-requiring enzyme)
18
Q

Ketone bodies…

a) are a fuel source derived from fats
b) are synthesized in the liver
c) all of the above

A

c) all of the above

19
Q

Ketone bodies: Acetoacetate, D-3-hydroxybutyrate, Acetone

A
  • Are synthesized from acetyl-CoA in liver mitochondria
  • Are secreted into blood for use as fuel source by some tissues (ex. heart muscle)

D-3-hydroxybutyrate
- Formed upon reduction of acetoacetate

Acetone
- Generated by spontaneous decarboxylation of acetoacetate

In tissues using ketone bodies, D-3-hydroxybutyrate is oxidized to acetoacetate, which is metabolized to 2 molecules of acetyl-CoA

20
Q

In tissues using ketone bodies, D-3-hydroxybutyrate is oxidized to ________, which is metabolized to ___ molecules of acetyl-CoA

a) acetoacetate; 3
b) acetate; 2
c) acetoacetate; 2

A

c) acetoacetate; 2

21
Q

Enzymes catalyzing the formation of ketone bodies from acetyl-CoA (Acetoacetate, D-3-hydroxybutyrate, Acetone)

A
  1. 3-ketothiolase
  2. hydroxymethylglutaryl CoA synthase
  3. hydroxymethylglutaryl CoA cleavage enzyme
  4. D-3-hydroxybutyrate dehydrogenase
22
Q

True or False: Animals can convert fatty acids into glucose

A

False

  • Fats are converted into acetyl-CoA, which is then process by CAC
  • Oxaloacetate (CAC intermediate) is a precursor to glucose
  • Acetyl-CoA derived from fats can’t lead to net synthesis of oxaloacetate or glucose b/c, although 2 carbons enter cycle when acetyl-CoA condenses w/ oxaloacetate, 2 carbons are lost as CO2 before oxaloacetate is regenerated
23
Q

Metabolism in Context

A
  • Fatty acids metabolism can be altered by physiological conditions
  • In diabetes, excess amount of ketone bodies can lead to life threatening conditions
  • Ketone bodies = moderately strong acids ~ access production = acidosis ~ in diabetic patients is called diabetic ketosis
24
Q

Diabetic ketosis

A
  • results when insulin is absent
  • In absence of insulin, or when insulin is not functioning, glucose cannot enter cells ~ energy must be derived from fats leading to production of acetyl-CoA
  • Access amounts of acetyl-CoA cannot be processed b/c of lack of glucose derived oxaloacetate
  • Access ketones bodies generated in liver are released into blood ~ this will contribute to diabetic acidosis
  • Fatty acids release from adipose tissue is enhanced in absence of insulin function
25
Q

Discuss ketone bodies with regards to starvation

A

Ketone bodies are crucial for starvation

  1. During starvation, protein degradation is initially the source of carbons for gluconeogenesis in liver
  2. Glucose is than released into blood for brain to use (glucose = predominant fuel for brain)
  3. After days of fasting, brain begins to use ketone bodies as fuel. Ketone body usage curtails protein degradation and prevents tissue failure
26
Q

With regards to ketone bodies and the depletion of TAG, a person’s survival time is mainly determined by the ______ of TAG deposits

a) size
b) shape
c) texture
d) pigment

A

a) size

27
Q

True or False: Ketones bodies are synthesized from fats, which are the largest energy store in the body

A

True

28
Q

After depletion of TAG, protein degradation ________, and _____ inevitable results from a _____ of heart, liver, or kidney function

a) decreases; death; loss
b) accelerates; death; loss
c) remains the same; degradation; gain in

A

b) accelerates; death; loss

29
Q

With regards to fuel reserves of the different organs for a typical male, which of the following provide the greatest fuel reserve?

a) liver
b) adipose tissue (or fat tissue)
c) blood
d) brain
e) muscle

A

b) adipose tissue (or fat tissue)

30
Q

Metabolism: Adapting to Starvation

A
  • As starvation continues, there is an adaptation w/ a shift to fatty acid oxidation and the accumulation of ketone bodies
  • Liver exports ketones, brain begins to use them
  • Gluconeogenesis and protein degradation will also slow-down
31
Q

During the degradation of unsaturated fatty acids, the double bonds must be reduced. The reductant used to reduce the double bonds is

a) cytochrome
b) FADH2 formed during other steps of fatty acid degradation
c) NADH formed during other steps of fatty acid degradation
d) NADPH

A

d) NADPH

32
Q

Degradation of an 18- carbon unsaturated fatty acid would be expected to yield hoe many NADH and FADH2 per fatty acid molecule?

a) 6
b) 8
c) 7
d) 9

A

b) 8

KIN 217 - Human Biochemistry (34 decks)

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