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Winter-Prufungen > deck_Biochem-p2-7211 > Flashcards

deck_Biochem-p2-7211 Flashcards

1
Q

This type of molecule has:

  1. Limited or no solubility in water so must be transported in blood w/a protein
  2. Extractable with organic solvents
A

lipid

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2
Q

This molecule is characterized by a carboxyl end group and a long hydrophobic tail of CH2 units

A

Fatty acid

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3
Q

If a molecule has no double bonds, it is called:

A

saturated

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4
Q

If a molecule has 1-2 double bonds, what is it called?

A

mono-unsaturated

poly-unsaturated

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5
Q

The position of the first double bond in the chain is the: ____, noted with a w

A

end carbon

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6
Q

What are the 2 essential fatty acids that can’t be synthesized?

A 
linoleic acid (w-6)
linolenic acid (w-3).

The w-6 tells us that the terminal double bond is 6C’s from the w end.

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7
Q

Linoleic acid (w-6) is used to make another key unsaturated fatty acid in the body: _____ (AA)

A

arachadonic acid

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8
Q

Linolenate is used to make:

A

docasahexanoic acid

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9
Q

Trans vs. Cis: what does it mean, what are the implications (2)?

A
  1. A trans fatty acid creates an unsaturated fatty acid that has the thermal/biological properties of saturated fatty acids…it is not natural.
  2. Has a low melting pt (solid at RT)
  3. Increases atherosclerosis.
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10
Q

Fatty acids are stored in adipose tissue as _______ consisting of a glycerol backbone with three fatty acid chains in ester linkage.

A

triglyceride

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11
Q

Stores of this _____ molecule contribute > 100,000 calories to our fuel depots!!

A

triglyceride. It is the major fuel at the beginning of starvation. Di and mono-glycerides are the absorptive form.

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12
Q

In what organs does fatty acid take place?

A

liver and lactating mammary gland.

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13
Q

Where in the cell does fatty acid synthesis take place?

A

CYTOPLASM

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14
Q

How does ATP-citrate lyase contribute to the synthetic pathway?

A

Citrate (cytoplasm) + ATP + CoA + H2O –> Acetyl-CoA + ADP + Pi + OAA

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15
Q

How is ATP-citrate lyase regulated?

A

Presence of ATP/citrate. High ATP/high citrate –> rxn proceeds. Because if there is high ATP, isocitrate DH is blocked, so citrate builds up.

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16
Q

How does ACC (acetyl-CoA-carboxylase) contribute to FA synthesis?

A

Acetyl CoA –> Malonyl CoA

*required vitamin: BIOTIN

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17
Q

How is ACC regulated?

A
  • Biotin (req’d vitamin)
  • Rate-limiting step + highly regulated
  • Regulated by: citrate (causes the dimers to polymerize), phosphorylation (inactivates it via AMPK. )
  • Example: high epinephrine/glucagon -> PKA –> kinase –> phosphorylates ACC –> inactivated.

High insulin –> ACC not phosphorylated –> active.

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18
Q

What are the 2 isoenzymes of ACC, and where do they work/what do they do?

A

1) ACC-alpha: makes FAs. It is the CYTOSOLIC form. Occurs in liver, mammary gland.
2) ACC-beta: controls OXIDATION of fatty acids. Mitochondrial enzyme. Where? Muscle, liver.

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19
Q

How does FA Synthase contribute to the FA synthesis pathway?

A

-It is a dimer w/8 catalytic centers.
-Required vitamin: pantothenic acid.
Steps:
-1) Acetyl group (from Acetyl CoA) is transferred to the SH group of ACP (acyl carrier protein domain).
-2) Acetyl group transferred to the Cys residue’s holding site, on the enzyme still.
3) Now there’s an empty spot in ACP. Malonate fills it.
4) Acetyl group on Cys condenses w/ malate group in ACP, losing a CO2 (ok b/c it means energy is lost - drives rxn fwd).
5) Double bonds created - so must be reduced by NADPH. Repeat 6 more times to create butyrl.

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20
Q

Where is fatty acid synthase expressed?

A 
lipogenic tissues (liver).  vs.
ACC (muscle, hearts)
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21
Q

What is malic acid enzyme?

A

Malate –> pyruvate via conversion of NADP+ to NADPH. impt for generating enough energy.

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22
Q

Where does NADPH come from?

A
  1. 6 moles from pentose phosphate pathway

2. Malate –>Pyruvate

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23
Q

Complete oxidation of FAs or partial oxidation to ketones contributes…

A

substantially to the necessary energy in most tissues.

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24
Q

newly made FAs in the liver are exported as triglyceride via ______ these proteins.

A

VLDL

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25
Q

Newly ABSORBED FAs in the intestine are exported as triglyceride in what _____?

A

Chylomicrons

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26
Q

How are the FAs of the triglyceride released prior to their uptake into adipocyte (and so they can be re-eseterified within the adipcyte)

A

Lipoprotein lipase

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27
Q

Do mammals have enzymes to introduce double bonds at carbon atoms beyond C9 in the hydrocarbon chain.

A

No.

28
Q

Where does FA oxidation occur (organs)?

A

Liver (metabolism from FAs provides energy for gluconeogenesis)

Muscle (skeltal and cardiac- their oxidation - major source of fuel.)

29
Q

Why is FA oxidation called B-oxidation?

A

b/c oxidation begins at the B carbon.

30
Q

Where does ketone genesis occur?

A

Take me to the liver. Used by the brain and mitochondria.

31
Q

What is the essential requirement for the FAS pathway?

A

Pantothenic Acid.

32
Q

FAs expressed only in____ .

A

lipogenic tissues.

33
Q

This is the process by which fatty acids (stored in the form of TAGs) are mobilized for oxidation.

A

Lipolysis

34
Q

These enzymes _____ catalyze hydrolytic reactions to produce free fatty acids + glycerol.

A

Lipases

35
Q

Which lipases are within the adipocyte?

A

1) ATGL: adipose triglyceride lipase
2) HSL: hormone-sensitive lipase
3) MGL: monoglyceride lipase

36
Q

Which lipases within the adipocyte are highly regulated during: feeding/fasting, by gene expression, and by phosphorylation?

A

ATGL

HSL

37
Q

This is a lipase that is made in the adipocyte, but is secreted onto the capillary endothelium. It acts on VLDL and chylomicrons. Lipoprotein TG –> FA

A

Lipoprotein lipase

38
Q

This is a lipase that is responsible for the hydrolysis of ingested TG in the Small Intestine.

A 
Pancreatic lipase 
Ingested TG (and DG & MG) --> FA
39
Q

Fatty acids circulating in the plasma and bound to albumin are called…

A

free fatty acids (non-esterified fatty acids). They are available to several tissues as fuel and can be converted into ketone bodies in the liver.

40
Q

All tissues except for ___ and ___ can oxidize fatty acids for generation of energy.

A

except for brain and RBCs

41
Q

In muscle (skeletal and cardiac), _____ = the preferred fuel for oxidative metabolism creating ATP.

A

fatty acids

42
Q

Where does fatty acid oxidation take place?

A

mitochondria

43
Q

This protein allows fatty acids to be taken up into cells prior to oxidation.

A

CD36

44
Q

After uptake, this type of enzyme catalyzes the formation of a fatty acyl thioester conjugate w/ Coenzyme A. This rxn takes place on the OUTER mitochondria membrane and requires ATP. This reaction produces Fatty Acyl CoA.

A

fatty acyl-coA synthase

45
Q

The long-chain fatty acyl CoA (>12 C) cannot get across the inner mitochondrial membrane, so it is carried across by a carrier _____. This takes off the CoA and transports the long-chain acyl group into the mitochondrial matrix.

A

carnitine

46
Q

In B-oxidation, The acyl group is transferred from CoA to carnitine via this enzyme: _____.

A

Carnitine Palmitoyl Transferase I (CPT-1), also called CAT-1 (Carnitine Acyl Transferase I)

47
Q

How is CAT-1 (CPT-1) regulated?

A
  • It is allosterically inhibited by Malonyl CoA, a product of the ACC-B reaction. So if there is lots of glucose/high glycolytic rate –> lots of Malonyl CoA –> fatty acyl CoA can’t make it into the mitochondria for oxidation. That is good because we already have an oxidative fuel (lots of glucose) at that time.
48
Q

Once fatty-acyl carnitine is formed, it is translocated across the inner membrane, and is reformed. The acyl group is transferred from the carninitine to the CoA in the mitochondrial matrix. What enzyme catalyzes this re-formation?

A

CPT-2/CAT-2 (Carnitine Palmitoyl Transferase)

49
Q

In B-oxidation (occurs inside mitochondrial matrix), the fatty acyl CoA’s are oxidized initially at what Carbon? There is then a series of steps that releases a ___ (#)C fragment in the form of Acetyl CoA.

A

Oxidized initially at B-carbon

2-C fragment released in each cycle

50
Q

Starting with palmitoyl CoA (16C), how many B-oxidation cycles does it undergo for the goal of ___ acetyl CoA’s?

A

7 B-oxidation cycles

8 Acetyl Co-A’s

51
Q

What does the initial dehydrogenase reaction in B-oxidation yield?
(Acyl CoA –> trans-enoyl CoA)

A

FADH2

52
Q

What does the second dehydrogenation reaction in B-oxidation yield?

A

NADH

53
Q

8 acetyl CoA’s are formed and are available for complete combustion in TCA if _____ is present. This requires continued oxidation of glucose.

A

OAA

54
Q

What is the net ATP produced from B-oxidation of fatty acids?

A

106 mol per mol palmitate

55
Q

About ___x as much ATP is generated from 1 mol fatty acid as from 1 mol glucose.

A

3x

56
Q

These molecules are water-soluble oxidative fuel. Can be utilized by muscle (especially heart and skeletal muscle) and by brain.

A

ketone bodies

57
Q

Where does ketogenesis occur?

A

liver

58
Q

What happens if levels of OAA are low –> conversion of acetyl CoA to citrate is low –> how is acetyl CoA disposed of? What does this pathway generate?

A

ketogenesis, expressed only in the liver.

Generates: acetoacetate and B-hydroxybutyrate. Acetone is also formed via spontaneous, non-enzymatic decarboxylation.

59
Q

Ketones are taken up into cells via ________.

A

Monocarboxylate transporter (MCT-1)

60
Q

What are the four items needed for complete combustion in TCA cycle?

A

1) Mitochondria
2) Oxygen
3) Succinyl CoA
4) OAA

61
Q

The energy yield for ketones is ____ than that of glucose.

A

Energy yield for ketones is greater than that of glucose and it requires less oxygen.

62
Q

During starvation, what is the preferred fuel for the brain?

A

Ketones

63
Q

What could cause excessive accumulation of ketones (acidosis/ketoacidosis)?

A
  1. Low levels/deficiency of insulin
  2. Mutations in MCT-1
  3. Mutations in ketone utilization genes
64
Q

The ____ the brain/body ratio, the faster ketosis develops under nutrient limitaiton.

A

larger

65
Q

What are the 2 reasons why Acetyl CoA can’t be used for glucose synthesis?

A
  1. PDH rxn is irreversible (so can’t form pyruvate)
  2. PEP can’t be formed via PEP-CK b/c we have no synthesis of new OAA. OAA must be formed de novo for net glucose synthesis to occur.

Winter-Prufungen (11 decks)

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