Glucose metabolism Flashcards

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?

A

150

22
Q

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

A

heart attack

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
Q

What are 2 main amino acids for gluconeogenesis?

A

alanine and glutamine

26
Q

Where is GLUT-1 found?

A

most mammalian cells

27
Q

Where is GLUT-2 found?

A

liver, pancreatic B-cells, renal tubules, intestines

28
Q

Where is GLUT-3 found?

A

brain and placenta

29
Q

Where is GLUT-4 found?

A

muscle and adipose, regulated by insulin

30
Q

Why does GLUT-2 have a lower affinity for glucose? (liver + intestine)

A

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
Q

what is most excess glucose stored as?

A

mostly triglycerides

*more energy than glycogen

32
Q

Why does low affinity for GLUT-2 work for pancreatic B-cells?

A

when glucose levels are high the transporter will work

this signals insulin release only when there are high levels of blood glucose

33
Q

Why is C-peptide useful?

A

can see how much insulin is produced

insulin has a shorter half-life, so C-peptide is easier to measure

34
Q

General steps of insulin release (6 steps)

A

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
Q

What enzymes triggers the GLUT-4 receptor expression?

A

PI3 kinase

36
Q

where does ketongenesis occur?

A

in the liver

37
Q

what regulates ketonegenesis?

A

insulin decreases

in T1DM, no insulin to downregulate ketonegenesis which can lead to ketoacidosis

38
Q

Where does gluconeogensis occur?

A

liver and kidneys

39
Q

Effects of ESRD on metabolism

A

can cause severe hyperglycemia if insulin is not being produced at all by the kidneys

40
Q

3 times when insulin resistance is normal

A

1) pregnancy (want high blood sugar for baby)
2) puberty
3) steriod / glucocortiod use

41
Q

Is insulin resistance always T2DM?

A

No! most of the time not

42
Q

What causes T2DM?

A

insulin resistance combined with beta cells inability to make more insulin to overcome resistance

43
Q

Diabetic fasting glucose level

A

> 126 mg/dL

44
Q

Normal fasting glucose level

A

< 100 mg/dL

45
Q

Diabetic HA1c

A

> 6.5 %

46
Q

Normal HA1c

A

< 5.6 %

47
Q

diabetic 2-hour oral glucose tolerance

A

> 200 mg/dL

48
Q

normal 2-hour oral glucose tolerance

A

< 140 mg/dL