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Carbohydrates > Fructose and Galactose > Flashcards

Fructose and Galactose Flashcards

1
Q

Glucose (2)

A
  • at the center of carbohydrate metabolism

- major dietary sugar

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2
Q

Fructose (3)

A
  • ingested as monosaccharide or as part of sucrose
  • enter cells by facilitate diffusion on the GLUT% transporter
  • it is metabolized to intermediates of glycolysis
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3
Q 
Fructose metabolism (3)
-what happen, steps
A
  1. Fructokinase phosphorylates fructose, forming fructose-1-phosphate
  2. Fructose-1-phosphate is cleaved by aldolase B to dihydroxyacetone phosphate and glyceraldehyde
  3. Glyceraldehyde is then phosphorylated to glyceraldehyde-3-phosphate by triose kinase

ATP is necessary in step 1 and 3

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4
Q

Fructose metabolism

-characteristics (3)

A
  • Dihydroxyacetone-P and glyceraldehyde 3-phosphate are intermediates of the glycolytic pathway
  • Occurs in the liver and less in the small intestinal mucosa and proximal epithelium of the renal tubule
  • aldolase B is the rate-limiting enzyme
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5
Q

Defects in Fructose Metabolism (2)

A
  • Lack of hepatic fructokinase –> essential fructosuria (benign and asymptomatic)
  • Absence of aldolase B –> leads to hereditary fructose intolerance –> patients accumulate high amounts of fructose- 1- phosphate in their livers, which inhibits liver glycogen phosphorylate causing fructose induce hypoglycemia.
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6
Q

Consequences of High Fructose Intake (2)

A
  • in the liver, fructose increases fatty acid and triacylglycerol synthesis and VLDL secretion and LDL cholesterol
  • acute loading of the liver with fructose traps inorganic phosphate in fructose-1-phosphate and diminishes ATP synthesis
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7
Q

Galactose Metabolism

-characteristics (2)

A
  • ingested primary as lactose, which is converted to galactose and glucose in the intestine
  • converted to glucose in the liver
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8
Q 
Galactose Metabolism (3)
-steps, what happen
A
  1. Galactokinase catalyzes the phosphorylation of galactose using ATP
  2. Galactose-1-phosphate and UDP-glucose are converted to UDP-galactose and glucose-1-phosphate by galactose-1-P-uridyltransferase
  3. UDP-galactose is converted to UDP-glucose by UDP-glucose epimerase. It is reversible
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9
Q

Galactosemia (4)

A
  • Galactose-1-phosphate uridyl-transferase (GALT) deficiency
  • autosomal recessive disorder
  • prevents the person from processing galactose
  • accumulation of galactose-1-phosphate in nerve, lens, liver and kidney causes liver damage, severe mental retardation and cataracts
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10
Q

Regulation of carbohydrates metabolism

-mechanisms that are responsible for regulating the activity of enzymes (3)

A

1- changes in the rate of enzyme synthesis
2- covalent modification of reversible phosphorylation
3- allosteric effects

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11
Q

Major pathways of glucose utilization (4)

A
  • Storage –> glycogen, starch, sucrose
  • Oxidation via glycolysis –> pyruvate
  • Oxidation via pentose- phosphate pathway –> ribose-5-phosphate
  • Synthesis of structural polymers –> extracellular matrix and cell wall polysaccharides
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12
Q

Pentose phosphate pathway (4)

-characteristics

A
  • an alternative metabolic pathway for glucose oxidation in which NO ATP is generated
  • principal product: ribose-5-phosphate
  • occurs in the cytoplasm
  • two phases: oxidative and non-oxidative phase
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13
Q

3 intermediates of pentose phosphate pathway which are useful in other pathways

A
  • Ribose-5-phosphate
  • Fructose-6-phosphate
  • Glyceraldehyde-3-phosphate
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14
Q

Pentose phosphate pathway: oxidative phase

A

-3 reaction which forms: ribulose-5-phosphate, CO2, 2 NADPH for each molecule of glucose-6-phosphate oxidized

Glucose-6-phosphate + 2 NADP+ + H20 –> ribulose-5-phosphate + 2 NADPH + 2H+ + CO2

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15
Q

Pentose phosphate pathway: non-oxidative phase (3)

A
  • occurs in all cell types synthesizing nucleotides and nucleic acids
  • reversible
  • permits ribulose-5-phosphate to be converted to ribose-5-phosphate, fructose-6-phosphate and glyceraldehyde-3-phosphate
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16
Q

Regulation of pentose phosphate pathway (3)

A
  • Key regulatory enzyme: glucose-6-phosphate dehydrogenase
  • NADPH –> inhibitor
  • activity is stimulated by oxidized form of glutathione
17
Q

Complex carbohydrates

  • classification of complex carbohydrates
  • characteristics of each
A

-Glycoprotein or Proteoglycans

GP –> hetero-oligosaccharide which is covalently attached to a protein
PG –> proteins and glycosaminoglycan (hetero-polysaccharide) chains

18
Q

Glycoproteins (4)

A
  • short glycan chains –> 20 sugars
  • highly branched and do not have a repeating unit
  • usually contain –> amino sugars (N-acetlyglucosamine or N-acetyl-galactosamine), neural sugars (D-galactose and mannose, I- fucose), acidic sugar silic acid (N-acetylneuraminic acid)
  • usually found –> outer face of the plasma membrane, extracellular matrix and blood
19
Q

Glycosaminoglycans (GAG) (2)

A
  • unbranched acidic polysaccharides that consist of repeating disaccharide units
  • composed of an amino sugar and uronic acid
20
Q

Pentose phosphate pathway: oxidative phase

-particularly important in: (3)

A
  • liver, lactating mammary glands and adipose, which are active in NADPH dependent biosynthesis of fatty acids
  • testes, ovaries and placenta which are active in the NADPH dependent biosynthesis of steroid hormones
  • erythrocytes, which require NADPH to keep glutathione reduced
21
Q

Examples of common Glycosaminoglycans (5)

A
  • Hyaluronic acid
  • Chondroitin sulfate
  • Keratan sulfate
  • Dermatan sulfate
  • Heparin
22
Q

Hyaluronic acid (6)

A
  • largest (n=5,000 - 30,000)
  • negative charges bind lots of water and cations
  • Glucuronic acid + N-acetylglucosamine
  • β(1–>3): inside / β(1–>4): between disaccharides
  • abundant in vitreous humor of eye and synovial fluid of joints
  • viscous solutions (low concentrations) and hydrated gel (high concentrations)
23
Q

Sulfated glycosaminoglycans (4)

A
  • GAG’s that carry sulfate group in the form of sulfate esters
  • sulfate groups contribute additional negative charges
  • much shorter
  • covalently bound to amino acid side chains in a core protein
24
Q

Chondroitin Sulfate (3)

A
  • component of cartilage, tendons, ligament and aorta
  • Glucuronic acid + N-acetlygalactosamine
  • β(1–>3): inside / β(1–>4): between disaccharides
25
Q

Keratan Sulfate (3)

A
  • found in cornea, cartilage and intervertebral disks
  • Galactose + N-Acetylglucosamine
  • β(1–>4): inside / β(1–>3): between disaccharides
26
Q

Dermatan sulfate (3)

A
  • contributes to the flexibility of the skin, present in blood vessels and heart valves
  • Iduronic Acid + N-Acetylgalactosamine
  • β(1–>3): inside / β(1–>4): between disaccharides
27
Q

Heparin (4)

A
  • formed by mast cells and basophils
  • anticoagulant and lipid- cleating properties
  • Glucuronic acid + Glucosamine
  • α(1–>4): inside / α(1–>4): between disaccharides
28
Q

Proteoglycan (4)

A
  • core protein with its covalently attached GAGs
  • major components of the amorphous ground substance of CT
  • are responsible for the slimy consistency of mucus secretions
  • contain: heparan sulfate and chondroitin sulfate (less common)
29
Q

Large proteoglycan aggregates

A

Composed mostly of collagen (type I and II) and aggrecan

30
Q

Aggrecan (5)

A
  • Core protein of 2316 amino acids
  • Two globular domains at the amino end
  • Keratan sulfate and chondroitin sulface (more of them) domain
  • Globular domain at the carboxyl end
  • Hyaluronic acid molecules binds up a few hundred aggrecan molecules
31
Q

Aggrecan molecule

  • function
  • how does it work (4)
A

-act as a lubricant, absorbs and dissipates impact forces

  • GAG’s have negatively charged group, which means they will be attracted to H20 molecules.
  • when aggrecan molecules are in their initial position –> a lot of H20 molecules will be absorbed and attached to them
  • when an impact is applied, H20 molecules leave , slightly deforming the molecule
  • as soon as force is released, H20 molecules will rush back
32
Q

Synthesis of proteoglycans (3)

A
  • they are processed through the secretory pathway
  • core protein is made by ribosomes on the rough ER
  • polysaccharides are constructed in the ET and golgi apparatus
33
Q

Degradation of proteoglycans (2)

A
  • extracellular proteoglycans are endocytosed and sent to the lysosomes
  • polysaccharide chains of the GAGs are degraded by the stepwise removal of monosaccharides from the nonreducing end
34
Q

Mucopolysaccharides (4)

A
  • deficiency of only one of the required lysosomal enzymes can interrupt the ordered sequence of GAg degradation
  • undegraded GAGs accumulate in the lysosomes
  • partially degraded polysaccharide appears in blood and urine
  • Lysosomal storage disease –> mucopolysaccharidosis
35
Q

Mucopolysaccharidosis (3)

A
  • enzyme deficiency is generalized, affecting all organ systems
  • inheritance is autosomal recessive or X-linked recessive
  • symptoms develop gradually
36
Q

Problems caused by the buildup of GAGs in the tissues (3)

A
  • Defects in the degradation of keratan sulfate and dermatan sulfate –> CT abnormalities
  • hearing loss, short stature
  • valvular heart disease
37
Q

Accumulation of Heparan sulfate

-consequences

A

-mental retardation and neurological degradation

IT IS THE ONLY IMP GAG IN THE CNS

38
Q

GAG’s that do not accumulate

A

-chondroitin sulfate and hyaluronic acid

they can be degraded by lysosomal hyaluronidase and endoglycosidase

39
Q

Treatment of mucopolysaccharidoses (3)

A
  • Replacement of the missing enzyme
  • after injected into the bloodstream, the enzyme is endocytosed and targeted to the lysosomes
  • limitations: high cost, formation of antibodies to the enzyme, inability of the enzymes to enter the brain

Carbohydrates (4 decks)

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