Exam 3 (Cole) Flashcards

1
Q

Names of the 3 ketone bodies produced in ketogenesis

A

Acetoacetate, acetone, B-hydroxybutyrate

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2
Q

Where does ketogenesis take place?

A

Mitochondria in the liver

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3
Q

What’s the starting substrate of ketogenesis?

A

Acetyl-CoA

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4
Q

Why do we make ketone bodies?

A

The brain can break them down since they are water-soluble form of lipid derived energy when glucose levels are low

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5
Q

Why are ketone bodies formed in uncontrolled type I diabetes?

A

Oxaloacetate gets used up for gluconeogenesis so acetyl-CoA can no longer be used in the citric acid cycle. Instead it goes to the mitochondria in the liver to create ketone bodies

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6
Q

What is the role of carnitine acyltransferases?

A

Transports fatty acids into the mitochondrial matrix

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7
Q

Why are ketone bodies formed in uncontrollable type I diabetes?

A

Too much glucose in the blood + low insulin causes fatty acids to be dumped into the liver. This causes low-yieldbeta oxidation where acetyl-CoA can no longer be used in the citric acid cycle (too little oxaloacetate) so undergoes ketogenesis. Too many ketone bodies are produced which can cause ketoacidosis

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8
Q

What are eicosinoids synthesized from?

A

Arachadonic acid

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9
Q

Which drug inhibits COX1 and COX2 (cyclooxygenase)?

A

NSAID’s (ibuprofen + asprin)

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10
Q

What’s the order of formation for eicosinoids?

A

Arachidonic acid –> cox1 / cox2 –> prostoglandins / thromboxanes

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11
Q

What do COX’s form before they become prostaglandin/thromboxane?

A

They form ring structures: 5-membered for prostaglandin, 6-membered thromboxane

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12
Q

What catalyzes the first step in the synthesis of leukotrienes?

A

Lipoxygenase

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13
Q

What is the role of malonyl-CoA

A

Inhibits carnitine acyltransferase I

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14
Q

Why is the entry of fatty acids into the mitochondria regulated?

A

If there’s an increase in malonyl CoA, that means that we’re synthesizing fatty acids. If we’re synthesizing, we do not need to break them down for energy so beta-oxidation is shut off

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15
Q

What is the product of acetyl-carboxylase in fatty acid synthesis?

A

Malolnyl-CoA

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16
Q

How do acetyl-CoA and NADPH get to the cytoplasm?

A

Citrate shuttle

17
Q

What is the regulated enzyme in fatty acid synthesis?

A

Acetyl-CoA carboxylase

18
Q

What does acetyl-CoA carboxylase require in fatty acid synthesis?

A

Biotin, because it’s a carboxylation reaction which requires 3 things and 1 of them is ATP

19
Q

Does acetyl-CoA carboxylase require ATP?

A

Yes

20
Q

What is the purpose of fatty acid synthesis?

A

During a fed state, we store energy by converting acetyl Co-A into fatty acids which can be stored as triglycerides in adipose tissue

21
Q

What is the purpose of hormone-sensitive lipase?

A

During a fasting state, we break down triglyerides into free fatty acids and glycerol to use as fuel

22
Q

What inhibits hormone sensitive lipase?

A

Insulin

23
Q

What is the purpose of making malonyl-CoA?

A

To drive fatty acid synthesis via energy release during condensation and loss of CO2

24
Q

How does citrate relate to fatty acid synthesis?

A

Citrate is a sign of being well-fed (TCA cycle very active), so it activates acetyl-CoA carboxylase

25
Q

What is the source of acetyl-CoA and NADPH used for fatty acid synthesis?

A

Citrate

26
Q

What happens to the regulation of acetyl-CoA carboxylase when cAMP levels go up?

A

Acetyl-CoA carboxylase gets inhibited because high levels of cAMP are a sign of fasted state and we don’t need to be making fatty acids if we’re starving

27
Q

When hormone sensitive lipase is active is acetyl-CoA carboxylase active or inactive?

A

Inactive

28
Q

Where does beta oxidation occur? What about fatty acid synthesis?

A

Beta Oxidation occurs in the mitochondria. Fatty acid synthesis occurs in the cytoplasm

29
Q

Is NADH or NADPH used in fatty acid synthesis?

A

NADPH

30
Q

Is NADH or NADPH a product of beta oxidation?

A

NADH

31
Q
A