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GI Part 2 > Fatty Acid Metabolism > Flashcards

Fatty Acid Metabolism Flashcards

1
Q

DO saturated fatty acids contain double bonds?

A

No

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2
Q

Are unsaturated FAs usually in the cis or trains formation?

A

Cis

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3
Q

What are the two essential. Amino acids? Are they saturated or unsaturated?

A

Linoleic acid
Linolenic acid
- they are unsaturated

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4
Q

How do you name the two essential fatty acids?

A

Rather than count from the head you count from the tail. The last carbon is called omega so if we have a double bond at the third to last carbon, we call it omega-3.

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5
Q

WHat are some sources of essential fatty acids?

A

SMASH

- salmon, mackerel, albacore, sardines, halibut

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6
Q

What is the first step in fatty acid synthesis?

A

Citrate shuttle - acetyl CoA can’t get from the mitochondrial matrix into the cytosol, so it comes together with oxaloacetate to form citrate through the work of citrate synthase. Citrate the can traverse the membrane. Once in the cytosol, citrate is cleaved back into Acetyl CoA and oxaloacetate.

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7
Q

What is the structure of a fatty acid?

A

Hydrocarbon chain with a terminal carboxyl group

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8
Q

What is the second step in fatty acid synthesis? Once Acetyl CoA is in in the cytosol.

A

An enzyme called Acetyl-CoA carboxylase converts Acetyl CoA into Malonyl-CoA through a carboxylation rxn.

  • This requires 1 ATP
  • This step is highly regulated
  • ABC - Requires ATP, requires Biotin as a cofactor, and it is a Carboxylase
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9
Q

What is Acetyl-CoA carboxylase? What are its allosteric regulators? What are its hormonal regulators? How do the hormonal regulators work?

A

Allosteric

Citrate –> +
Log chain fatty acyl-CoA –> -

Hormonal

Glucagon –> -, via AMPK, which phosphorylates and inactivates Acetyl-CoA Carboxylase
Insulin –> + activated via protein phosphatase dephosphorrylating Acetyl-CoA carboxylate and thus activating it.

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10
Q

What is the third step in fatty acid synthesis? Once we have malonyl CoA

A

We form palmitate through the enzyme Fatty Acid Synthase. FAS.

  • We consume 2 NADPH in this rxn.
  • palmitate is 16 carbons long
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11
Q

So what, now we have palmitate?? What happens now?

A

Palmitate can be lengthened or desaturated in order to make fatty acids necessary for the human body.

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12
Q

WHat would happen in a Diabetic patient It’s regards to FA synthesis?

A

Basically in diabetes we have too few insulin or the insulin receptors are not working properly. Therefore, we don’t have proper feedback from insulin. Normally insulin will cause there to be more FA synthesis as per earlier in the lecture. When this doesn’t happen, the Acetyl CoA gets shunted into ketone bodies instead.

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13
Q

Where. Does fatty acid synthesis. Occur?

A

Liver and adipose tissue

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14
Q

How do we store FAs?

A

In Triacylglycerol

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15
Q

What is the structure of Triacylglycerol?

A

3 fatty acids esterified to a glycerol molecule.

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16
Q

Where do we get the glycerol for Triacylglycerol? 2 ways

A

1) It can be recycled from VLDLs as they go from the liver to the adipose tissue. Once in the liver it is phosphorylated by glycerol kinase into Gllycerol-3-phosphate.
- Remember that in adipose tissue they don’t need the glycerol so it just goes back to the liver. Adipose tissue doesn’t have glycerol kinase.
2) Glucose is converted into DHAP and then into Glycerol-3-phosphate

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17
Q

Explain the process of Triacylglycerol synthesis?

A

We can get glycerol-3–phosphate in two ways as was mentioned earlier. Then from there, we convert glycerol-3-phosphate into TAG by the addition of FAs. In adipose tissue you are done because it can store TAGs. The liver can’t store TAGs so it ships them out to the adipose tissue by way of VLDL. Once in circulation, Lipoprotein Lipase (LPL) chops all of the TAGs into FAs. Then once in the adipose tissue it gets built back up into TAGs and the glycerol floats back to the liver.

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18
Q

How is synthesis of TAGs regulated?

A

By insulin. In a fed state, insulin stimulates both glycolysis and LPL. This will cause increased storage of FAs in the adipose tissue.

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19
Q

What are the triggers to release our stored TAGs from the adipose tissue? How do they work?

A

Stress hormones such as cortisol, epinephrine, and glycogen are responsible for this.

  • There are hormone-dependent lipase so found in the adipose tissue that cleave TAG into FAs and then they circulate around the body bound to albumin where they can be broken down for ATP.
  • In the liver, the stress hormones cause gluconeogenesis and fatty acid degradation to occur.
  • – as we mentioned earlier, if we have a buildup of Acetyl CoA then it will be converted to Ketone bodies, which can be used by the brain or muscle.
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20
Q

WHat is the role of perilipin???

A

We mentioned previously that when a Stress response occurs, TAGs are broken down into fatty acids. Well, in basal conditions it coats the TAGs so that the lipase can’t get to them and break them down So that they are stored. In times of energy deficit, perilipin phosphorylated, which allows lipase st of break down the TAGs into FAs.

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21
Q

With each addition of a malonyl CoA, which is a 3 carbon molecule, we only get a 2 carbon addition to the chain. What is the deal??

A

A CO2 is lost in each cycle.

22
Q

Where does desaturation/elongation occur??

A

Elongation - occurs in the ER and mitochondria

Desaturation - occurs in the ER

23
Q

WHere does The glycerol come from in Triacylglycerol synthesis?

A

Either in the breakdown of glucose, we form dihydroxyacetonephosphate (DHAP), which can be converted into glycerol phosphate.
Alternatively, in the liver only, we can use glycerol kinase to convert glycerol into glycerol phosphate

24
Q

How do we regulate Triacylglycerol synthesis?

A

Insulin will up regulate the conversion of glucose to DHAP as well as the lipoprotein lipase.
Ethanol impedes the ability for VLDL to be secreted into the blood stream from the liver which is why alcoholics often get fatty liver disease.

25
Q

What is the Energy output of beta oxidation?

A

1 FADH2

1 NADH

26
Q

Where does beta oxidation occur?

A

In the mitochondria of all cells

- the fatty acids come from the liver and mostly the adipose tissue where they get broken down in the mitochondria.

27
Q

Fatty acids can’t get into the mitochondria on their own. How do they get in?

A

Carnitine cycle.

28
Q

Carnitine Shuttle

A

Used to get the long chain fatty acids into the mitochondria (they can get into the cell via transporters).

  • 1) an enzyme called fatty acyl CoA synthase converts the fatty acid. Into an activated fatty acid - Fatty acyl CoA.
  • 2) CAT-I converts fatty acyl CoA into Fatty acyl carnitine so that it can now come into the mitochondria. It is on the outer membrane of the mitochondria.
  • – malonyl CoA inhibits this
  • 3) CAT-II basically brings us back. It converts fatty acyl carnitine into fatty acyl CoA.
  • 4) There is a transporter called CAT that allows for the transfer of carnitine in and out of the mitochondria.
29
Q

Fatty acyl CoA synthetase

A

Activates fatty acids into fatty acyl CoA

30
Q

CPT-I

A

converts fatty acyl CoA into fatty acyl carnitine so that it can enter the mitochondria

31
Q

CPT-II

A

Converts Fatty acyl carnitine into fatty acyl CoA

32
Q

CAT

A

allows carnitine to go in and out of the mitochondria. This allows carnitine to be recycled back into the cytosol for use to get fatty acyl CoA into the cell. Otherwise all of the carnitine will get stuck in the mitochondria.

33
Q

On a basic level, how does beta oxidation work?

A
  • Fatty acid chains are shorten by 2 carbons at a time until it is completely degraded into Acetyl CoAs
  • Each cycle has an output of 1 FADH2, 1 NADH, 1 Acetyl CoA.
  • notice that if you have an odd number chain length this will pose a problem.
34
Q

Why do unsaturated fatty acids yield less energy?

A

They are already partially oxidized, so there will be less FADH2. Remember, the whole point is to oxidize the fatty acids.
- when you metabolize fatty acids, you need to have additional enzymes to shift the position and change the geometry of double bonds.

35
Q

How do branched chain fatty acids get broken down?

A

Through alpha oxidation

  • it breaks down branched chain fatty acids into Acetyl CoA and propionyl CoA.
  • Phytatic acid is an example of one that if not broken down properly can lead to Refsum’s disease.
36
Q

Refsum’s Disease

A

A neurological disease caused by the inability to break down Phytatic acid due to a defect in alpha oxidation. You will have accumulation of Phytatic acid in nerve tissue.

37
Q

How do we break down odd numbered fatty acid chains?

A

1) The cabin chain is broken down until we have a 3 carbon molecule called proprionyl CoA.
2) An enzyme called Proprionyl CoA Carboxylase converts proprionyl CoA to methylmalonyl CoA.
- ABC so it requires ATP and biotin
3) methylmalonyl CoA is then interconverted into succinyl CoA through the use of methyl malonyl CoA mutase, using Vitamin B12 as a cofactor.
4) Succinyl CoA will then be converted to glucose.
- it is the only fatty acid that can be converted into glucose.

38
Q

How can we distinguish a Vitamin 12 deficiency vs A folate deficiency?

A

In a vitamin B12 deficiency, You Will have increased levels of methylmalonic acid because you can’t convert it into Succinyl CoA

39
Q

What is the yield of breakdown of an odd number chain fatty acid?

A

1 FADH2, 1 NADH, 1 Acetyl CoA, 1 Succinyl CoA

40
Q

CPT-1 deficiency

- also carnitine deficiency

A

Symptoms: Muscle pain during exercise, increased fatty acid in the blood, hypoketotic, hypoglycemic

  • this makes sense because when you exercise you initially use up all of your glycogen stores and then you start to break down fatty acids. If you can’t break down the fatty acids then you will get muscle pain. You will of course have increased FAs in the blood because you can’t bring them into the mitochondria. You will be hypoketotic because you are not making Acetyl CoA from fats and you will be hypoglycemic because you can’t break down fats to make glucose.
  • will also have increased carnitine in the blood and hepatomegaly

Treatment: Eat short chain and medium chain fatty acids.

41
Q

CPT-II deficiency

A

Adult - affects causes muscle pain and fatigue following exercise
Infantile - manifests in first 24 months of life. Will cause hypoketotic hypoglycemia. Will progress to hepatomegaly and cardiomyopathy.
Neonatal - symptoms begin within hours to first few days of life. Respiratory failure, hepatomegaly, seizures, hypoglycemia, cardiomegaly. The cardiomegaly will lead to fatal arrhythmias.

42
Q

What enzyme is needed to break down medium chain fatty acids?

A

MCAD - medium chain acyl CoA dehydrogenase

43
Q

Signs of MCAD deficiecy

A

Hypoketotic hypoglycemia
Increased acyl carnitines in the blood and urine
Hyperammonemia - result of liver damage
Dicarboxylic acids in the blood and urine
High concentration of medium chain fatty acids in the blood and urine

Treatment: don’t fast and constant feeding

44
Q

Deficiency in methylmalonyl CoA mutase

A

If you remember, this is the enzyme that converts methylmalonyl CoA into Succinyl CoA to be used in TCA or gluconeogenesis. It needs vitamin B12 as a cofactor.

  • A deficiency in the enzyme vitamin B12, of intrinsic factor will have the same symptoms
  • will lead to peripheral neuropathy
  • will have methylmalonic acid in the urine
45
Q

Why do ketone bodies get formed?

A

In states of starvation, a lot of fatty acids are broken down. We know that one of the products is Acetyl CoA which can enter the TCA cycle. Eventually, the amount of Acetyl CoA exceeds the amount that can enter the TCA cycle, so Acetyl CoA starts to get converted into ketone bodies to be used by the heart and skeletal muscles, while leaving whatever glucose is around to go to the brain
- also in a fasting state, we are deficient in oxaloacetate because it is being used in gluconeogenesis. Therefore, TCA cycle has difficulty proceeding.

46
Q

How are ketone bodies formed?

A

They start off with the same two reactions as in the creation of cholesterol. Once we get up to HMG CoA, in ketone body synthesis we use HMG CoA lyase (as opposed to in cholesterol when we used HMG CoA reductase). From there, we make our ketone bodies.
- also, ketone body synthesis occurs in the mitochondria whereas cholesterol synthesis occurs in the cytosol and ER (both of the liver)

47
Q

What are the three ketone bodies?

A

Acetoacetate
Acetate
Beta hydroxybuterate

48
Q

How are ketone bodies actually used?

A

They get to the peripheral tissues and essentially the opposite reaction occurs where we build back up Acetyl CoA.
- acetoacetate –> acetoacetyl acid –> 2 Acetyl CoA

49
Q

Why doesn’t the liver use up all of the ketone bodies if it is made there?

A

Because it lacks the enzyme CoA transferase, which means that it is unable to break down the ketone bodies into Acetyl CoA. This way it saves the ketone bodies for the tissues that need them.

50
Q

How does ketogenesis get regulated?

A

Increased Acetyl CoA = increased ketogenesis

Decreased blood glucose = increased ketogenesis

51
Q

What happens to Levels of ketone bodies and fatty acids in the blood as time goes by?

A

They go up.

  • fatty acids start to go up 3-4 hours after a meal
  • ketone bodies follow the trend of FAs
  • after 2-3 days of starvation, ketone bodies can begin to enter the brain cells and power the brain.
52
Q

Why does diabetes induce Ketosis

A

Absence of insulin leads to increase plasma glucose levels and thus lowered cellular glucose levels –> inability to replenish TCA cycle intermediates (oxaloacetate) –> Acetyl CoA from fatty acid degradation can’t be used in the TCA cycle –> Acetyl CoA is shunted into ketogenesis –> lowered pH –> disturbs function of CNS

GI Part 2 (16 decks)

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