Glucose metabolism Flashcards

(48 cards)

1
Q

What is the regulatory enzyme of glycolysis ?

A

PFK-1

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2
Q

What is the regulatory enzyme of gluconeogenesis?

A

FBPase-1

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3
Q

Is glycolysis catabolic or anabolic in brain? Aerobic or anaerobic?

A

aerobic catabolic

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4
Q

Is glycolysis catabolic or anabolic in liver? Aerobic or anaerobic?

A

aerobic anabolic

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5
Q

Is glycolysis catabolic or anabolic in muscle? Aerobic or anaerobic?

A

can be anaerobic or aerobic catabolic

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6
Q

Is glycolysis catabolic or anabolic in RBC? Aerobic or anaerobic?

A

anaerobic catabolic

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7
Q

What is ultimate end product of anabolic glycolysis?

A

pryuvate to acetyl-CoA to fatty acid synthesis

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8
Q

overall formula for aerobic glycolysis

A

1 glucose => 2 pyruvate + 2 ATP + 2 NADH

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9
Q

overall formula for anaerobic glycolysis

A

1 glucose => 2 lactate + 2 ATP

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10
Q

How is PFK-1 modulated in liver?

A

F-2,6-bisphosphate phosphorylates to activate

F-2,6-bP is upregulated by insulin

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11
Q

How is PFK-1 modulated in muscle?

A

ratio of ATP/AMP regulates PFK-1

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12
Q

hepatic reciprocal regulation

A

insulin activates F-2,6-bP to phosphorylate PFK-1 and increase glycolysis

when F-2,6-bP is absent, FBP-1 is turned on and gluconeogenesis is turned on

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13
Q

muscle control of glycolysis

A

high AMP = activate PFK-1 (ratio of ATP to AMP is decreasing)

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14
Q

What does high ATP activate?

A

FBP-1

*do not need to run more glycolysis

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15
Q

citric acid cycle (TCA)

A

oxidizes acetyl-CoA to FADH2 and NADH

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16
Q

Does TCA require O2?

A

not directly

however, the ETC does require O2. If ETC can’t run due to low O2 conditions, then NAD+ and FAD+ will not be reformed and TCA will be inhibited

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17
Q

fatty acid oxidation and gluconeogenesis

A

gluconeogenesis uses glycerol from FA oxidation

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18
Q

What produces lactate?

A

the reduction of pyruvate

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19
Q

Where is F-2,6-bP found?

A

exclusively in the liver

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20
Q

4 components of metabolic syndrome

A

1) dyslipidemia
2) obesity
3) insulin resistance
4) HTN

21
Q

What should triglycerides be under?

22
Q

What is leading cause of mortality for individuals with metabolic syndrome?

23
Q

What 2 pathways does the Cori cycle connect? How?

A

anaerobic glycolysis and gluconeogenesis

lactate from anaerobic glycolysis makes glucose in gluconeogenesis (pyruvate intermediate)

glucose from gluconeogenesis makes lactate in anaerobic glycolysis (pyruvate intermediate)

24
Q

3 sources of carbon for gluconeogenesis

A

lactate, glycerol, and amino acids

25
What are 2 main amino acids for gluconeogenesis?
alanine and glutamine
26
Where is GLUT-1 found?
most mammalian cells
27
Where is GLUT-2 found?
liver, pancreatic B-cells, renal tubules, intestines
28
Where is GLUT-3 found?
brain and placenta
29
Where is GLUT-4 found?
muscle and adipose, regulated by insulin
30
Why does GLUT-2 have a lower affinity for glucose? (liver + intestine)
in liver, want to uptake glucose for storage, so want to uptake glucose when there are higher amounts in intestine, glucose amounts will be high after a meal, so low affinity works there too
31
what is most excess glucose stored as?
mostly triglycerides *more energy than glycogen
32
Why does low affinity for GLUT-2 work for pancreatic B-cells?
when glucose levels are high the transporter will work this signals insulin release only when there are high levels of blood glucose
33
Why is C-peptide useful?
can see how much insulin is produced insulin has a shorter half-life, so C-peptide is easier to measure
34
General steps of insulin release (6 steps)
1) glucose enters B-cell through GLUT-2 2) go through glycolysis + ATP levels rise 3) K+ channels close 4) membrane depolarization 5) Ca2+ channels open 6) insulin released
35
What enzymes triggers the GLUT-4 receptor expression?
PI3 kinase
36
where does ketongenesis occur?
in the liver
37
what regulates ketonegenesis?
insulin decreases in T1DM, no insulin to downregulate ketonegenesis which can lead to ketoacidosis
38
Where does gluconeogensis occur?
liver and kidneys
39
Effects of ESRD on metabolism
can cause severe hyperglycemia if insulin is not being produced at all by the kidneys
40
3 times when insulin resistance is normal
1) pregnancy (want high blood sugar for baby) 2) puberty 3) steriod / glucocortiod use
41
Is insulin resistance always T2DM?
No! most of the time not
42
What causes T2DM?
insulin resistance combined with beta cells inability to make more insulin to overcome resistance
43
Diabetic fasting glucose level
> 126 mg/dL
44
Normal fasting glucose level
< 100 mg/dL
45
Diabetic HA1c
> 6.5 %
46
Normal HA1c
< 5.6 %
47
diabetic 2-hour oral glucose tolerance
> 200 mg/dL
48
normal 2-hour oral glucose tolerance
< 140 mg/dL