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Physiology Metabolism > Metabolism 7: TAG Degradation, Fatty Acid Oxidation, Ketone Bodies > Flashcards

Metabolism 7: TAG Degradation, Fatty Acid Oxidation, Ketone Bodies Flashcards

1
Q

What is HSTL?

A

Hormone-Sensitive Triacylglycerol Lipase: Cleaves TAGs into glycerol and 3 fatty acids in the adipose tissue

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2
Q

What effect does epinephrine/glucagon have on HSTL?

A

Stimulates and activates it.

Epinephrine works via cAMP and PKA to phosphorylate HSTL -> Activates it

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3
Q

What effect does insulin have on HSTL?

A

Antilipolytic-Inhibits activity by dephosphorylation

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4
Q

What effect does prostaglandin have on HSTL?

A

Antilipolytic- inhibits activity

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5
Q

What role do thyroid and adrenal cortical hormones have on HSTL?

A

They are permissive. Do not activate but are required for normal activity

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6
Q

Which part of TAG breakdown can be used to create glucose?

A

Glycerol

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7
Q

How much of total dietary caloric intake should TAG consumption comprise?

A

<30%

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8
Q

What kind of condition stimulates mobilization of TAGs?

A

When there is a need for substrates for energy production

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9
Q

What is perilipin?

A

Coats the surface of fat droplets. It must be phosphorylated by PKA iin order for HSTL to translocate to surface of the fat droplet and hydrolyze TAGs

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10
Q

What are the possible fates of released FA from TAG breakdown?

A

Enter circulation->bind Albumin-> carried to muscle, liver, etc -> undergo beta oxidation and energy production

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11
Q

What are the possible fates of glycerol from TAG breakdown

A

transported to kidney and liver

Phosphorylated by glycerol kinase to generate glycerol-3-phosphate for use in gluconeogenesis

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12
Q

What does the increased circulating levels of FAs from TAG breakdown increase?

A

Beta-oxidation of fatty acids
Ketone body formation
Gluconeogenesis

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13
Q

What does the increased circulating levels of FAs from TAG breakdwon inhibit?

A

Fatty acid biosynthesis

Glycolysis

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14
Q

How does circulating levels of FAs inhibit fatty acid biosynthesis?

A

Fatty-AcylCoA allosterically inhibits Acetyl-CoA Carboxylase (rxn: Acetyl-CoA ->Fatty Acyll CoA

Inhibit produciton of Malonyl CoA

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15
Q

What is the only physiological inhibitor of carnitine palmitoyl transferase-1?

A

MAlonyl CoA: product of fatty acid biosynthesis

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16
Q

What also increases as beta oxidation of fatty acid increases?

A

Ketone Body formation

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17
Q

How does an increase in ATP by tissues metabolizing fatty acid impact glycolysis?

A

It inhibits it by inhibiting PFK-1 (Signaling that we have enough ATP)

18
Q

What can the increased ATP production from fatty acid metabolism be used for?

A

Gluconeogenesis

19
Q

Which organs are good users of fatty acids?

A

Liver, Kidney Cortex, Heart, Skeletal Muscle

20
Q

Which organs do not/cannot use fatty acids for energy?

A

RBCs, Brain, Nervous System, Adrenal Medulla, Lens

21
Q

What is hte major energy producing pathway in the body?

A

Mitochondrial Beta Oxidation of Fatty Acids

22
Q

What does the complete beta-oxidation of palmitic Acid produce? How much ATP?

A

8 Acetyl-CoA
7 NADH
7 FADH2

Total 106 ATP

23
Q

What does a single cycle of beta oxidation generate?

A

1 Acetyl CoA, NADH, FADH2

24
Q

How are fatty acids degraded?

A

Sequential removal of 2 carbon units

25
Q

What does carnitine do?

A

Transports long chain fatty acids into the mitochondrial matrix for beta oxidation (Carnitine –> Acyl Carnitine)

26
Q

What does an inhibition of carnitine transport result in?

A

Inhibited fatty acid oxidation

Decreased ATP production

27
Q

What is CPT-1?

A

Carnitine Palmitoyl Transferase I: Transports fatty acid chains by placing them on carnitine to form acylcarnitine

28
Q

What is the rate limiting enzyme for fatty acid beta oxidation?

A

CPT-1

29
Q

How does Malonyl CoA affect CPT-1?

A

It is the only known inhibitor of carnitine palmitoyl trasnferase and blocks the formation of acylcarnitine

Thus it inhibits fatty acid oxidation

30
Q

What is malonyl CoA a product of?

A

The rate limiting eznzyme Acety-CoA Carboxylase in fatty acid biosynthesis

31
Q

What is Primary Carnitine Deficiency Disorder?

A

Defect in carnitine transporter

32
Q

What is SEcondary Carnitine Deficiency Disorder?

A

Defect in CPT-II or CPT-I

33
Q

What deficiency accounts for 10% of Sudden Infant Death Syndrome(SIDS)

A

Deficiency of medium chain FA-CoA Dehydrogenase

34
Q

How are long, medium, and short chain fatty acids beta-oxidized differently?

A

They use separate AcylCoA Dehydrogenases (LCAD, MCAD, SCAD)

35
Q

Where are ketone bodies formed?

A

ONLY in the Liver Mitochondria

36
Q

What usually accompanies ketone body formation?

A

High rate of beta oxidation of fatty acids in liver

37
Q

What are the ketone bodies?

A

Acetoacetate, Beta hydroxybutyrate, Acetone

38
Q

Which ketone body is formed spontaneously without enzyme?

A

Acetone from acetoacetate via decarboxylation rxn

39
Q

What is HMMG-CoA Synthase?

A

Mitochondrial enzyme only found in liver that acts in ketone body formation

40
Q

Does the liver also use ketone bodies for energy?

A

No. They do not have the acetoacetate:succinyl-CoA Transferase enzyme (thiophorase) for ketone utilization

41
Q

What happens to the ketone bodies once they are formed?

A

generated in liver -> released into circulation -> transported to other tissues (mitochondria of muscle, brain, etc) for energy production

Physiology Metabolism (11 decks)

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