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Biochem BLOCK 2 > Metabolism of other Mono-and Disaccharides > Flashcards

Metabolism of other Mono-and Disaccharides Flashcards

1
Q

fructose and galactose

A
  • occur in significant amounts in the diet (primarily in disaccharides)
  • make important contributions to energy metabolism
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2
Q

What is an important component of structural carbohydrates?

A

galactose

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3
Q

fructose

A
  • significant source of calories (10%) in typical western diet
  • comes from sucrose, high fructose corn syrup, honey, fruits
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4
Q

fructose entry into cells

A

NOT insulin dependent

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5
Q

fructose mediated by what transporter?

A

GLUT 5

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6
Q

fructose and insulin secretion

A

does not promote insulin secretion

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7
Q

fructose metabolization

A

Bypasses the PFK-1 step, which means that it is metabolized more rapidly than glucose

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8
Q

step 1 of fructose metabolism

A
  • phosphorylation of fructose
  • enzymes-fructokinase and hexokinase
  • IRREVERSIBLE
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9
Q

fructokinase

A
  • phosphorylation of fructose
  • in liver (mostly), kidney, and small intestinal mucosal cells
  • uses ATP
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10
Q

hexokinase

A
  • phosphorylation of fructose
  • high Km (low affinity) for fructose, therefore it does not usually contribute significantly
  • acts in all other tissues
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11
Q

step 2 of fructose metabolism

A
  • cleavage of fructose 1-phosphate
  • enzyme: aldolase B
  • DHAP and glyceraldehyde formed
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12
Q

DHAP

A

formed from the cleavage of fructose 1-P with enzyme Aldolase B
can directly enter glycolysis (or gluconeogensis)

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13
Q

glyceraldehyde

A

product of the cleavage of fructose 1-P with enzyme aldolase B

  • can be phosphorylated to glyceraldehyde 3-P (via triose kinase) and enter glycolysis
  • can also be converted to glycerol to enter other pathways
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14
Q

Conversion of glucose to fructose via sorbitol

A

-enzyme: aldose reductase and sorbitol dehydrogeanse

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15
Q

aldose reductase

A
  • conversion of glucose to fructose via sorbitol
  • found in many tissues including lens, retina, schwann cells of peripheral nerves, liver, kidney, cells of ovaries and seminal vesicles
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16
Q

sorbitol dehydrogenase

A
  • conversion of glucose to fructose via sorbitol

- ONLY found in the liver, ovaries, and seminal vesicles

17
Q

Tissues that express only aldose reductase

A

will be damaged by long term elevation of blood glucose because it can make sorbitol but not further metabolize it.

18
Q

excess glucose

A

converted to sorbitol

19
Q

sorbitol accumulation

A

results in osmotic uptake of water, which can account for some of the symptoms seen in DM patients

  • cataracts
  • retinopathy
  • nephropathy
  • peripheral neuropathy
20
Q

conversion of mannose to fructose 6-P

A
  • mannose is C-2 epimers of glucose
  • very little in the diet, most is synthesized intracellularly by fructose or recycled
  • important component of glycoproteins
  • substrate for hexokinase
  • mannose is substrate for phosphomannoseisomerase
21
Q

substrate for hexokinase

A

mannose. phosphorylated to mannose 6-P

22
Q

substrate for phosphomannoseisomerase

A

mannose 6-P (hexokinase phosphorylated mannose to form this)

-converts mannose to fructose 6-P

23
Q

essential fructosuria

A
  • lack of fructokinase
  • autosomal recessive (1:130,000)
  • benign
  • fructose accumulates in urine
24
Q

Hereditary fructose intolerance (fructose poisoning

)

A
  • autosomal recessive (1:20,000)
  • absence of adores B, intracellular trapping fructose
  • severe hypoglycemia, vomiting, jaundice, hemorrhage, hepatomegaly, renal dysfunction, hyperuricemia, and lacticacidemia
  • fructose, sucrose, and sorbitol can cause hepatic failure and death
  • therapy: rapid detection and removal and fructose and sucrose from diet
25
Q

Why does fructose get trapped in cell in fructose poisoning?

A

absence of aldolase B, fructose is phosphorylated as in normal pathway, however builds up because can’t be further metabolized

26
Q

production of fructose 1-P in someone with fructose poisoning

A
  • ties up much of the available cellular phosphate, which means the liver and kidney cells are comprised
  • leads to hepatomegaly, jaundice, hypoglycemia, and renal dysfunction
  • large amount go AMP building up due to lack of ATP production results in AMP being degraded and resulting hyperuricemia
27
Q

galactose metabolism

A
  • isomer of glucose (C-4 epimer)
  • dietary source-lactose from milk and milk products
  • some from lysosomal degradation of complex carbs
  • transport into cells is NOT insulin dependent
  • metabolism is 2 steps to UDP galactose
28
Q

step 1 of galactose metabolism

A

-phosphorylation of galactose with enzyme galactokinase

29
Q

step 2 of galactose metabolism

A

formation of UDP galactose

  • enzyme: galactose 1-phosphate uridyltransferase (GALT)
  • transfer reaction
  • UDP galactose can be converted to UDP-glucose and enter glucose metabolic pathways
30
Q

galactokinase deficiency

A
  • rare autosomal recessive
  • elevation og galactose in blood and urine
  • causes galactitol accumulation if galactose is present in the diet
  • elevated galactitol can cause cataracts
  • dietary restriction
31
Q

aldose reductase in galactose metabolism

A
  • physiologically unimportant in galactose metabolism unless galactose levels are too high
  • elevated galatitol can cause cataracts
32
Q

classic galactosemia

A
  • GALT deficiency
  • autosomal recessive
  • galactosemia and galactosuria, vomitting, diarrhea, jaundice
  • accumulation of galactose 1-P and galactitol in nerve, liver, lens, and kidney tissue causes liver damage, severe mental retardation, and cataracts
  • prenatal Dx is possible by chorionic villus sampling
  • rapid dx and removal of galactose from diet
33
Q

synthesis of lactose

A
  • milk sugar produced by lactating mammary glands
  • synthesized in golgi
  • enzyme: lactose synthase
34
Q

lactose synthase

A

complex of 2 proteins

  • A: B-D-galactosyltransferase found in a number of body tissues
  • B: a-lactalbumin: its synthesis is stimulated by the peptide hormone prolactin

Biochem BLOCK 2 (14 decks)

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