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Nutritional physiology > 21. Metabolic and physiological 'regulation' > Flashcards

21. Metabolic and physiological 'regulation' Flashcards

1
Q

Insulin: stimulates X. What happens?

A

Insulin stimulates lipoprotein lipase: if you had a high glucose meal, fatty acids are released from chylomicrons to make triglycerides in the adipocytes.

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2
Q

Metabolism changes with fasting. What happens with overnight fast?

A

Glycogen stores in liver used: gluconeogenesis important

Adipocytes do not take up glucose

Some muscle glucose uptake, much less.
Protein and fat breakdown in muscles more important

Fatty acids used for ATP (beta ox). Glycerol can be used for gluconeogenesis

Gut also produces glucose, and alanine

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3
Q

What happens upon starvation?

A

Muscle cells don’t take up glucose
More dependent on protein and fatty acid ox

Ketone bodies: Acetoacetate +beta hydroxybutyrate used by the brain

Kidney more important for gluconeogenesis. Produces glucose from aa’s.

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4
Q

What organs take up 60% of REE?

A

brain, liver, heart, kidneys

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5
Q

When fasting, brain still uses 4-5 g glucose/hr = 96-120 gr/day
Blood level: ~ 5 mM = 0.9 g/L
Hepatic glucose prod. = 180 g/day. Brain consumes what fraction of this?

A

About 2/3

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6
Q

Both glycogenolysis (glycogen-> glucose) and gluconeogenesis contribute both about 50% glucose production when fasting. These processes are induced by..? inhibited by ..? (hormones)

A

induced by glucagon
Inhibited by insulin

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7
Q

In post-absorptive state, most important organs in descending order for standard meal glucose production are.. (choose: kidney, intestine,liver)

And for fasting (24-48 hr)?

And in post-absorptive state of protein-rich diet?

A
  1. liver (70-75%)
  2. kidney (15-20%)
  3. intestine (5-7)
  4. kidney (50-55)
  5. Liver (20-25)
  6. Intestine (20)
  7. Kidney (40-45)
  8. Liver (40)
  9. Intestine (17-20)
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8
Q

What enzymes are very much regulated in glycolysis? What do they have in common?

A
  1. Hexokinase
  2. Phosphofructokinase
  3. Pyruvate kinase

They do not have a reverse pathway

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9
Q

Regulation of three glycolysis enzymes

Low conc of energy: ….. (same for pyruvate drhydr complex)
Hormonal regulation: by 1 and 2

A

enzyme flux will increase
insulin & glucagon

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10
Q

Insulin: expressed with..

Causes
1
2
Stimulates 3

A

high levels glucose in circ.
1 Glucose uptake
2. “” usage in cell
3. hexokinase, phosphofructokinase, pyruvate kinase

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11
Q

Glucagon: expressed when..
Inhibits 1, 2

A

fasting
> inhibits pyruvate kinase (to slow down the use of glucose)
> inhibits glycogen synthase

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12
Q

PFK1: Phosphofructokinase. Inhibited by? Stimulated by?

A

 Inhibited by high levels of ATP, acetyl-CoA, citrate. (Citrate needs to be present in the cytosol. Is only present in the cytosol with high flux of TCA cycle)
 Stimulation by AMP, low levels of O2

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13
Q

What reaction does pyruvate dehydrogenase complex start?

A

Pyruvate -> acetyl-CoA. Highly regulated.

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14
Q

High levels of 1 and 2 stimulate PDH (pyruvate dehydrogenase) kinases, which 3 the complex by phosphorylation

A

1 Acetyl-CoA
2. NADH
(its products)
3. inactivate

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15
Q

High levels of 1 or 2 or 3 inhibit PDH kinases: dephosphorylation results in 4 complex again.

A

1 pyruvate
2 CoA
3 NAD
4 active

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16
Q

What does insulin stimulate/block?

A

Stimulates glycolysis, blocks gluconeogenesis

17
Q

What do glucagon & cortisol stimulate?
What hormones stimulate opposing enzymes?

A

stimulate gluconeogenesis, higher production of glucose.
Glucagon: makes sure there is enough glucose available

Insulin & glucagon stimulate opposing enzymes

18
Q

What is the rate-limiting enzyme of TCA? By what is this enzyme regulated?

A

Citrate synthase

  • energy (inhibited by high ratio’s of ATP over ADP, acetyl-CoA over CoA and NADH of NAD)
  • product of the enzyme (citrate) or succinyl-CoA (another intermediate): also inhibiting
19
Q

Fatty acids in cytoplasm: can be transported into mito’s, used through beta ox to produce CO2, oxygen, energy. Transporter enzyme = ?

A

CPT1 = CAT 1 = CARNITINE

20
Q

CPT1 is a …. step for lipid metabolism

A

limiting

21
Q

CPT1 is inhibited by..

A

Malonyl-CoA (intermediate in fatty acid synthesis)

When there is a lot of fatty acid synthesis happening in the cytosol, CPT1 = inhibited. “don’t start oxidizing we are synthesizing’

22
Q

What happens with leptin (produced by adipose tissue) regulation? How does this cause an increased fatty acid oxidation?

A
  1. Signals to brain + muscle.
  2. In muscle: phosphorylates AMPK (low energy ATP), becomes active.
  3. Then, phosphorylates ACC, which becomes inactive.
  4. ACC regulates conversion of acetyl-CoA to malonyl-CoA.
  5. Less malonyl-CoA: ‘no fatty acid synthesis!’, no inhibition of CPT1: therefore leptin results in increase of fatty acid oxidation.
23
Q

Mice that lack ACC , lack ..? They are ..?

A

(lack fatty acid synthesis), are very lean.

24
Q

Problem with leptin: high levels of leptin -> you become …?

A

Problem with leptin: high levels of leptin -> you become a bit insensitive for it. Does not phosphorylate AMPK as much. AMPK stays inactive, ACC does not become inactivated. Still fatty acid synthesis.

25
Q

No leptin: super hungry: obese, easily everything stored as leptin

A

Sad life

26
Q

What do lipases do?

A

Lipases hydrolyze ester bonds in triacylglycerol.

27
Q

What does insulin do in terms of triglycerides?

A

Insulin inhibits the use of triglycerides as energy source and stimulates the storage of glucose as fatty acids.

  • Simulates glycolysis
  • production of fatty acids
  • production of gl-3-p
  • pentose phosphate pathway for NADH for making triglycerides.
28
Q

Insulin: both regulation for lipolysis and glycolysis

A

ok

29
Q

 At least 4 of the 16.5 ATP formed by complete oxidation of glycerol (via dihydroxyacetone phosphate: DHAP) are obtained by substrate level phosphorylation. True/false

A

False.

= ATP or GTP production in one step. Look at DHAP in glycolysis: because we are talking about complete oxidation.

DHAP -> pyruvate = 2x ATP. Then you get 1x acetyl-CoA: in TCA cycle there is one step of direct phosphorylation (GDP -> GTP).
So 3x

29
Q

 At least 4 of the 16.5 ATP formed by complete oxidation of glycerol (via dihydroxyacetone phosphate: DHAP) are obtained by substrate level phosphorylation. True/false

A

False.

= ATP or GTP production in one step. Look at DHAP in glycolysis: because we are talking about complete oxidation.

DHAP -> pyruvate = 2x ATP. Then you get 1x acetyl-CoA: in TCA cycle there is one step of direct phosphorylation (GDP -> GTP).
So 3x

30
Q

Alanine, tryptophan, iso-leucine are glucogenic amino acids (meaning: they can be converted into glucose. True/False

A

True

They can all make OAA and go outside of the TCA cycle. Precursors for only acetyl-CoA are not glucogenic because they are completely oxidized. Tryptophan can make acetyl-CoA but ALSO pyruvate).

31
Q

 Glucogenic amino acids can follow two metabolic pathways: gluconeogenesis or direct oxidation. Which component is, in most cases, a common intermediate for both pathways? (A) 3-phosphoglyceraldehyde (B) phosphoenolpyruvate (C) pyruvate (D) acetyl-CoA

A

B) phosphoenolpyruvate

32
Q

 Rank these fatty acids for their ATP yield upon complete oxidation (A) (C18:0) < (C16:0) < (C18:2) < (C18:3) (B) (18:0) < (C16:0) < (C18:3) < (C18:2) (C) (C:16:0) < (C18:0) < (18:2) < (C18:3) (D) (16:0) < (C18:3) < (C18:2) < (C18:0).

A

In every spiral, you remove 2C and produce 1FADH and 1 NADH. (=4 ATP) + acetyl-CoA. FADH production happens when going from 1- bound C to double bond C. 1.5 ATP yield less (FADH). C16:0 = 74 = 28 ATP + 70 = 98 ATP.
C18:0 = 84 = 32 ATP + 80 = 112 ATP. C18:2 = 112-1.52 = 109 ATP. C18:3 = 112-1.53 = 107.5 ATP

33
Q

 The pathway from pyruvate to acetyl-CoA is (A) lactic acid producing (B) part of gluconeogenesis (C) metabolically irreversible (D) requires more energy than it produces

A

(C) metabolically irreversible

Nutritional physiology (26 decks)

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