Blood glucose level, diabetes, fructose/galactose (PPP not incl.) Flashcards

1
Q

What are blood glucose ranges

  • in postabsorptive state
  • after carbohydrate meal
  • during starvation
A
  • postabsorptive phase: 4.5 - 5.5 mmol/L
  • after carbs: 6.5 - 7.2 mmol/L
  • starvation: 3.3 - 3.9 mmol/L

​lower glucose level possible if hypoglycemia develops slowly

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2
Q

Describe the Cori cycle.

A
  1. glycolysis in mm. produces pyruvate
  2. pyruvate converted to lactate
  3. lactate exported into blood stream
  4. lactate taken up by liver
  5. incorporated into gluconeogenesis
  6. glucose exported into blood stream
  7. glucose taken up by mm.
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3
Q

What are the effects of hyperglycemia in the liver?

A
  1. incr. glucose uptake by GLUT 2
  2. glucokinase activated due to high [glucose]
  3. incr. glycogenesis due to activation of PP1 → enhanced glycogen synthase activity
  4. decr. glycogenolysis due to glucose sensory function of glycogen phosphorylase
  5. active PDC incr. FA synthesis
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4
Q

What are the effects of hyperglycemia in the pancreas?

A
  1. incr. glucose uptake by GLUT 2
  2. glucokinase triggers insulin secretion from pancreatic β-cells
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5
Q

What are the effects of hyperglycemia in peripheral tissue (muscle, adipocytes)?

A
  1. incr. amount of GLUT 4 in membranes due to insulin
  2. incr. glycogenesis
  3. decr. glycogenolysis
  4. incr. glycolysis due to upregulation of PFK1
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6
Q

What are the long term effects of hyperglycemia?

A

insulin represses all enzymes involved in gluconeogenesis, esp. PEPCK → decr. gluconeogenesis

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7
Q

What are the effects of hypoglycemia in the liver?

A

incr. gluconeogenesis

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8
Q

What causes the incr. risk of hypoglycemia during pregnancy?

A
  • limited ketogenesis in the fetus
  • incr. glucose demand of the fetus, due to brain/body rate
  • no gluconeogenesis bc PEPCK is repressed, no G6Pase
  • glycogen storage is limited
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9
Q

Distinguish btw the types of diabetes mellitus.

A
  • type I: insulin deficiency due to destruction of pancreatic β-cells
  • type II: insulin resistance
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10
Q

What might be a long term effect of diabetes?

A

decr. amount of PEPCK due to long-term repression by insulin

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11
Q

What is glucoseuria?

A

more glucose secreted into renal tubules than can be reabsorbed (limited rate of 2 mmol/min)

→ exceeding renal threshold, hence excreted w/ urine

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12
Q

Which transporters are involved in galactose/fructose uptake in the intestine?

A
  • galactose: actively pumped into cell by SGLT, then leaves entercoyte basolaterally via GLUT 2
  • fructose: passive diffusion via GLUT 5 into cell, then leaves enterocyte basolaterally via GLUT 2, 5
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13
Q

Briefly describe the main steps of fructose metabolism in the liver and sperms.

A
  1. fructokinase: fructose + ATP → F1P + ADP
  2. aldolase B: F1P → DHAP + glyceraldehyde
  3. triosekinase: glyceraldehyde + ATP→ glyceraldehyde-3P + ADP

⇒ DHAP + glyceraldehyde-3P can be introduced for glycolysis or gluceneogenesis

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14
Q

How differs the fructose metabolism in per. tissue from the fructose metabolism in the liver?

A

no fructokinase, but hexokinase (can process glucose and fructose):

fructose + ATP → F6P + ADP

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15
Q

What is the difference btw glucose and fructose metabolism in the liver?

Why is it clinically important?

A

metabolism of fructose happens much faster b/c it bypasses the main regulatory step of glycolysis (PFK1) and also causes incr. activity of glucokinase

⇒ uncontrolled NADH + acetyl-CoA production leads to incr. TAG and cholesterol synthesis in the liver (fatty liver)

= risk factor of obesity + metabolic syndrome

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16
Q

What are 2 inborn defects of fructose metabolism?

A
  • essential fructosuria
  • fructose intolerance
17
Q

Which defect causes essential fructosuria?

Consequence?

A

defects of fructokinase
fructose accumulates in blood after meals and is excreted into urine

18
Q

Which defect causes fructose intolerance?

Consequence?

A

defects of aldose B
→ accumulation of F1P

effects on glycogen metabolism:

  • glycogenesis ↑​
  • phosphorylase activity ↓↓

effects on glycolysis:

  • glucokinase​ activity ↑​↑
  • pyruvate kinase activity ↑​↑

⇒ severe abdominal distress, nausea, vomiting, hypoglycemia, hyperuricemia after fructose consumption, liver damage, gout, renal failure

19
Q

Describe the polyol pathway.

Why is it important?

It is regulated by?

Which enzymes are involved?

A

important in sperms to provide E source, regulated by testosterone level

NOTE: NADPH/H+ used, NADH/H+ produced

20
Q

Briefly describe the main steps of galactose metabolism.

What happens with its products?

A

unlike fructose, galactose can only be metabolized in the liver

  1. galactokinase: galactose + ATP → galactose-1P + ADP
  2. galactose-1P uridyltransferase:
    galactose-1P + UPD-glucose → G1P + UDP-galactose
  3. phosphoglucomutase: G1P → G6P
21
Q

How is UDP-galactose recycled?

A

converted to UDP-glucose by 4-epimerase, NAD+ used as coenzyme

BUT: reversible

22
Q

Differentiate btw the 3 types of galactosemia.

Consequences?

A
  • type 1: malfunctioning galactose-1P uridyltransferase (= classic galactosemia)
  • type 2: malfunctioning galactokinase
  • type 3: malfunctioning 4-epimerase

→ accumulation of intermediates of galactose metabolism (e.g. galactose-1P, galacticol)

⇒ can lead to brain damage, cataracts, jaundice, hepatomegaly, kidney damage

23
Q

How are glycoproteins produced from galactose?

A
24
Q

Explain the steps of lactose synthesis in the lactating mammary gland.

A
  1. glucose transported into gland by GLUT 1/3
  2. hexokinase → G1P
  3. first 2 steps of glycogenesis: G1P → UDP-glucose
  4. 4-epimerase → UDP-galactose
  5. lactose synthase
    UPD-galactose + glucose → UDP + lactose