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Biochem Final > Glycogen and Carb metaolism > Flashcards

Glycogen and Carb metaolism Flashcards

1
Q

Glycogenin, Glycogen Synthase, Branching Enzyme

A

polymerization of glucose (glycogen synthesis)

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2
Q

First step of glycogen synthesis

A

activate glucose

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3
Q

Primer protein for glycogen synthesis

A

Glycogenin

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4
Q

Transfers glucose from UDP-glucose to non-reducing ends forming alpha(1,4) glycosidic bonds

A

Glycogen Synthase (glycogen synthesis)

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5
Q

Cleaves off short fragments from alpha (1,4) chains and connects to make alpha (1,6) linkages

A

Branching Enzyme (glycogen synthesis)

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6
Q

Location of glycogen synthesis

A

cytosol

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7
Q

Releases glucose-1-phosphate from glycogen

A

glycogen phosphorylase (glycogen degradation)

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8
Q

Transfers branches and releases glucose

A

debranching enzyme (glycogen degradation)

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9
Q

Beta cells of pancreas

A

insulin

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10
Q

Alpha cells of pancreas

A

glucagon

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11
Q

Hormone released from adrenal medulla

A

epinephrine

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12
Q

Phosphorylation of glycogen phosphorylase

A

becomes active (glycogen degradation)

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13
Q

Phosphorylation of glycogen synthesis

A

becomes inactive

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14
Q

What organ synthesizes glycogen but do not respond to glucagon? They lack what enzyme that releases glucose to bloodstream?

A

muscles, lack glucose-6-phosphatase (G6P»Glucose)

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15
Q

Main source of blood glucose before breakfast.

A

glucoNEOgenesis

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16
Q

Main source of blood glucose during well-fed state.

A

glycogen degradation

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17
Q

muscle weakness/ exercise intolerance

enlarged liver

A

general symptoms of glycogen storage disease

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18
Q

defect in glucose-6-phosphatase

A

Type I GSD- van Gierke disease

inability to convert G6P to glucose for release to bloodstream

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19
Q

acid maltase deficiency

A

Type II GSK - Pompe disease

glycogen accumulation due to deficiency in the enzyme that catalyzes glycogen breakdown in lysosomes

20
Q

defective glycogen debranching enzyme

A

Type III GSD - Cori disease

21
Q

defective glycogen phosphorylase in muscles

A

Type IV GSD - McArdle disease

unable to use stored glycogen

22
Q

buildup of NADH, CAC is inhibited, gluconeogenesis is inhibited (no pyruvate and OAA from CAC). NADH gets used up by lactate dehydrogenase and malate dehydrogenase

A

alcohol metabolism makes NADH

- causes lactic acidosis and hypoglycemia (inhibition of gluconeogenesis)

23
Q

gel-like component of ECM comes from what?

A

proteoglycans (acidic and basic)

24
Q

large molecules that consist mainly of acidic modified sugars

A

proteoglycans

25
Q

where does glycosylation of proteins occur?

A

ER and Golgi

26
Q

facilitate the excretion of poorly water-soluble metabolites

A

acidic carbohydrates are abundant in ECM

27
Q

N-acetylglucosamine added

A

Heparan Sulfate

Keratin Sulfate

28
Q

N-acetylgalactosamine added

A

Chondroitin Sulfate

29
Q

Both sugars added

A

Dermatan Sulfate

Heparin

30
Q

no sugar added

A

hyaluronic acid

31
Q

degradation of proteoglycans

A

in lysosomes

32
Q

proteins linked to long polymers of C-6 acids and aminosugars which are sulfated in the Golgi after synthsis

A

proteoglycans

33
Q

mannose, galactose, and fucose

A

required for glycosylation of proteins

34
Q

made by fructose-6-phosphate

A

mannose and fucose

- heavy regulation of PFK1 in glycolysis

35
Q

genetic disease

- defective proteoglycan-degrading hydrolases leading to skeletal deformation and intellectual disability

A

Mucopolysaccharidosis (MPS)

36
Q

Accumulation of dermatan sulfate and heparan sulfate caused by defective enzyme iduronate sulfatase
- X-linked recessive

A

Hunter

37
Q

accumulation of dermatan sulfate and heparan sulfate caused by defective enzyme alpha-iduronase
- auto-recessive

A

Hurler-Scheie

38
Q

accumulation of heparan sulfate caused by different defects of heparan sulfate degradation (A,B,C,D roots)

A

Sanfilippos’s (A, B, C, D)

39
Q

occurs in the liver and require production of UDP-glucuronic acid to serve as a substrate

A

glycosylation

40
Q

increases water solubility and is a common path for the body to excrete poorly water-soluble molecules such as hemoglobin

A

glycosylation

41
Q
  • glucuronate linked to a glucosamine and is the backbone of ECM
  • also allow newly synthesized proteoglycans to be integrated into the meshwork of ECM
A

hyaluronic acid

42
Q
  • lack mitochondria thus do not undergo CAC or oxidative phosphorylation
  • depends on glycolysis for energy
  • can perform anaerobic reactions to produce lactate
  • utilizes Cori cycle
  • utilizes PPP for NADPH and/or ribose synthesis
A

RBCs

43
Q
  • can perform glycogen synthesis and degradation
  • can fully metabolize glucose via glycolysis, CAC and ox. phos
  • perform PPP when needed
  • can perform anaerobic reactions to produce lactate
A

skeletal muscles

44
Q
  • can perform glycogen synthesis and degradation
  • can fully metabolize glucose via glycolysis, CAC and ox. phos
  • perform PPP when needed
  • cannot perform anaerobic reactions to produce lactate
A

cardiac muscles

45
Q
  • fully metabolize glucose
  • makes and degrades glycogen
  • performs Cori cycle
  • performs PPP if needed
  • does not perform anaerobic reactions
A

hepatocytes

Biochem Final (21 decks)

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