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GI/Nutrition > 01d: FA Oxidation, Gluconeogenesis > Flashcards

01d: FA Oxidation, Gluconeogenesis Flashcards

1
Q

FA undergo oxidation in tissues, esp (X), for E. They can also be ocnverted to (Y) for storage in adipose tissue.

A 
X = muscle and liver
Y = triacylglycerols
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2
Q

List the four basic functions of FA.

A
  1. Major fuel source
  2. Building blocks (phospholipids, glycolipids)
  3. Protein modifies (hydrophobicity)
  4. Hormones/intracell messenger precursors
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3
Q

Palmitic acid has (X) number of C’s and the (sat/unsat) version is called (Y) with (Z) number of C’s.

A

X = 16
Unsat;
Y = palmitoleic acid
Z = 16

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4
Q

Oleic acid has (X) number of C’s and the (sat/unsat) version is called (Y) with (Z) number of C’s.

A

X = 18
Sat;
Y = stearic acid
Z = 18

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5
Q

T/F: Linoleic and linolenic acids are both unsaturdated with 18 carbons.

A

True (differ in number of double bonds)

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6
Q

Lipolysis, aka (X) breakdown, is a(n) (Y)-sensitive process.

A 
X = triglyceride/triacylglycerol 
Y = hormone
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7
Q

(X) acts on triglyceride to produce DAG, which is then acted on by (Y).

A 
X = adipose TG lipase
Y = hormone-sensitive lipase
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8
Q

TAG broken down to DAG then MAG. What acts on MAG to produce (X) product(s)?

A

MAG lipase;

X = glycerol and FA

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9
Q

List hormones that play important role in stimulating lipolysis.

A

Epi and glucagon

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10
Q

First step in FA oxidation is (X). This step involves ATP (production/breakdown) (to/from) (Y).

A

X = FA activation
Breakdown;
To
Y = AMP and PPi, which is then cleaved to 2Pi (two high-E bonds broken!!)

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11
Q

T/F: In FA activation, ATP is broken down into ADP and PPi.

A

False - into AMP and PPi, then PPi cleaved to 2 Pi

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12
Q

Activation of free FA is carried out by (X) enzyme. Essentially, FA and (Y) become (Z).

A 
X = Acyl-CoA Synthetase
Y = CoA
Z = Acyl-CoA
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13
Q

Second step in FA Oxidation is (X). What needs to be done for this step to occur?

A

X = Transfer to mitochondria

Carnitine replaces CoA on Acyl-CoA (to allow it to pass through translocase)

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14
Q

FA Ox: (X) enzyme responsible for addition of carnitine to FA Acyl group. (Y) enzyme responsible for putting the CoA back once FA is in (Z) compartment.

A 
X = CPT-I
Y = CPT-II
Z = mitochondrial matrix

CPT = carnitine palmitoyl transferase = carnitine acyltransferase

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15
Q

The translocase that’s important for shuttling FA to (X) compartment is in (Y) membrane and recognizes (Z).

A 
X = mitochondrial matrix
Y = inner mito
Z = carnitine
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16
Q

Third step in FA Oxidation is (X). In general, it starts with (Y) and ends with (Z) products.

A 
X = beta-oxidation
Y = Acyl-CoA
Z = Acetyl-CoA and Acyl-CoA (that's 2 C shorter)
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17
Q

How many NADH or FADH2

(required/produced) per cycle of FA beta-oxidation?

A

Produced;

1 of each

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18
Q

An important point of control in FA Oxidation is at that of (X) enzyme. Specifically, it’s inhibited by (Y), which is made by (Z).

A 
X = CPT-I
Y = malonyl-CoA
Z = acetyl-CoA carboxylase (ACC)
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19
Q

High levels of ACC enzyme is important for (stimulation/inhibition) of (X) enzyme/process. You’d expect ACC to be quite active as a result of (low/high) E states.

A

Inhibition;
X = FA oxidation (via CPT-I enzyme step)
High E

20
Q

In addition to controlling (X) process, ACC enzyme can be controlled. Specifically, (Y) inhibit(s) it in (low/high) E states.

A

X = FA oxidation (inhibits translocase step)
Y = PKA and AMPK (AMP-activated protein kinase)
Low E

21
Q

High PKA has (stimulatory/inhibitory) effect on FA oxidation by its direct (stimulatory/inhibitory) effect on (X).

A

Stimulatory;
Inhibitory (via phosphorylation);
X = ACC enzyme

22
Q

One of the most common inborn errors of metabolism is related to FA oxidation, a(n) (excess/deficiency) in (X) enzyme.

A

Deficiency;

X = Medium Chain Acyl-CoA Dehydrogenase (MCAD) deficiency

23
Q

Patient with Medium Chain Acyl-CoA Dehydrogenase (MCAD) deficiency would be (hyper/hypo)-glycemic. List the two reasons for this.

A

Hypoglycemic;

  1. Tissues forced to consume glucose since FA not available
  2. Gluconeogen not possible without FA Ox
24
Q

(X) is an important alternate E product/fuel for brain in severe starvation. These are produced primarily in (Y) from (Z) compound.

A 
X = ketone bodies
Y = liver mitochondria (ketogenesis)
Z = acetyl-coa
25
Q

Ketone body synthesis: interconversion can occur when (X) compound undergoing either decarboxylation, to yield (Y), or reduction, to yield (Z).

A 
X = acetoacetate
Y = acetone
Z = D3-Hydroxybutyrate
26
Q

Which, if any, ketone bodies can be efficiently reconverted via (ketogenesis/ketolysis) to (X). What’s the fate of (X)?

A

Ketolysis;
Acetoacetone and D3-hydroxybutyrate
X = acetyl-coa (2 molecules)

TCA Cycle

27
Q

In (X) disease, there’s a very high blood level of ketone bodies. This is because (presence/absence) of (Y) results in unrestrained (Z).

A

X = diabetic ketoacidosis
Absence
Y = insulin
Z = lipolysis (even in presence of high glucose)

28
Q

T/F: Gluconeogenesis has same energy requirements as glycolysis (2 ATP per glucose).

A

False - 6 ATP (or GTP) per glucose

29
Q

The (first/second/third) enzyme of gluconeogenesis, (X), has a required activator: (Y).

A

First;
X = pyruvate carboylase
Y = acetyl-coa

30
Q

Insulin (stimulates/inhibits) gluconeogenesis. This is (direct/indirect) via (stimulating/inhibiting) (X).

A

Inhibits;
Indirect;
Inhibiting
X = FA lipolysis (and thus acetyl-coa formation, which is required for gluconeogen)

31
Q

The first two steps of gluconeogen, involving (X) enzymes, are highly coordinated by liver with corresponding (Y) enzyme.

A 
X = pyruvate carboxylase and PEP carboxykinase
Y = pyruvate kinase
32
Q

The liver exercises high control/regulation over (X) and (Y) early glycolytic enzymes. It also regulates the two corresponding gluconeogenesis enzymes, which are:

A 
X = glucokinase 
Y = PFK

Glucose-6-phosphatase and fructose-1,6-BPase

33
Q

Fructose-2,6-BP, which (stimulates/inhibits) PFK, (stimulates/inhibits) the corresponding gluconeogenesis enzyme (X).

A

Stimulates;
Inhibits;
X = Fructose-1,6-BPase

34
Q

Key enzyme involved in Cori cycle is (X). And in alanine cycle is (Y).

A 
X = lactate dehydrogenase
Y = alanine aminotransferase (ALT)
35
Q

(Alanine/Cori) cycle is active in high muscle activity.

A

Cori

36
Q

Unlike (X), ketone bodies don’t need to be carried on albumin to travel in bloodstream. Why?

A

X = FAs

They’re water-soluble

37
Q

Reciprocal control: Fructose-1,6-BPase is inhibited by high levels of (X), which are the factors that stimulate (Y) glycolytic enzyme.

A 
X = Fructose-2,6-BP and AMP
Y = PFK
38
Q

Control of gluconeogenesis and glycolysis is possible by adaptive responses. In other words, starvation/low carb diet will have which general effect on gluconeogen/glycolytic enzymes?

A

Gluconeogen enzymes upregulated

39
Q

(X) glycolytic enzyme must be inhibited for gluconeogenesis to proceed. This justifies the heavy regulation put on (X), such as its required activator: (Y).

A 
X = pyruvate kinase
Y = fructose-1,6-BP
40
Q

The main points of Cori/alanine cycles is that liver receives lactate/alanine, converts them to (X) via (Y), and sends the much-needed product back to (Z).

A 
X = pyruvate, then glucose
Y = gluconeogenesis
Z = muscle (via blood)
41
Q

EtOH ingestion inhibits gluconeogenesis due to (depletion/accumulation) of (X).

A

Accumulation;

X = NADH

42
Q

Fuel stores in muscle include (X); these stores are for (muscle/other tissues).

A

X = glycogen and TAGs;

Muscle alone

43
Q

Fuel stores in liver include (X); these stores are for (liver/other tissues).

A 
X = glycogen;
Other tissues (brain, muscle)
44
Q

Fuel stores in adipose include (X); these stores are for (muscle/other tissues).

A 
X = TAGs;
Other tissues (liver, muscle)
45
Q

T/F: An overflow of excess lipids results in fat accumulation outside adipose tissue (muscle, liver).

A

True

GI/Nutrition (17 decks)

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