Glycogen metabolism Flashcards

(40 cards)

1
Q

• A homopolymer of __
• Linkage: __
• Branching: __ (at about every 8-10 residues)

A

a-D-glucose

a-1,4

a-1,6

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2
Q

Glycogen as a

A

Fuel Reserve

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3
Q

mobilized to maintain blood glucose levels in between meals

A

Glycogen

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4
Q

from glycogen CAN PROVIDE ENERGY whenever the requirement is sudden (as in during strenuous activity)

A

Glucose

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5
Q

__ glycogen is degraded for
• DISTRIBUTION TO OTHER ORGANS through the blood
• maintaining PROPER BLOOD GLUCOSE LEVELS

A

Liver

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6
Q

Muscle glycogen is degraded for its use in

A

energy production

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7
Q

Release of Glc as Glc-1-P

Glucose released is __ without consuming ATP.

A

already phosphorylated

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8
Q

Release of Glc as Glc-1-P

Glc-1-P cannot __ the cell and go to the bloodstream.

A

leave

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9
Q

Release of Glc as Glc-1-P

It readily enters the glycolytic pathway once it’s converted to glucose-6-P by

A

phosphoglucomutase

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10
Q

Release of Glc as Glc-1-P

Action of glycogen phosphorylase continues until
there are about _ residues left from the branch
point

A

4

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11
Q

Re-modeling of Glycogen

Re-modeling prior to further degradation occurs near the

A

branch point

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12
Q

De-branching

a-1,6 glycosidic bond is cleaved by an

A

a-1,6-glucosidase

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13
Q

De-branching

Released glucose from de-branching is converted
to glucose-6-P and can enter

A

glycolysis

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14
Q

Fate of Glc-1-P in the Liver
• Glucose-1-P is

A

dephosphorylated

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15
Q

Fate of Glc-1-P in the Liver

Free glucose exits the hepatic cells and goes
into the blood stream for:
• maintaining __ blood glucose levels in between meals
• __ to other organs (brain and muscles)

A

proper, transport

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16
Q

Glc-6-phosphatase is present in the

A

liver only.

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17
Q

Fate of Glc-1-P in the Muscle

Muscle cells _ glycogen for its own need

19
Q

Fate of Glc-1-P in the Muscle

Glucose-1-P → Glucose 6-P →

20
Q

Muscle cells __ glucose-6-phosphatase.

21
Q

the activated form of glucose that serves as GLUCOSE
DONOR for glycogen synthesis
• UTP – __ __

A

UDP-Glucose

uridine triphosphate

22
Q

BRANCHING ENZYME
• Breaks the a-1,4 link and forms the a-1,6 branch.

23
Q

Branching occurs at about every __ residue

24
Q

Branching __ solubility of glycogen

25
Glycogenolysis and glycogenesis are
reciprocally regulated
26
Conditions that promote synthesis inhibit degradation and __
vice versa
27
employed in response to the blood glucose level
Regulation
28
Normal blood glucose level:
70-100 mg/100 mL
29
Stimulates UPTAKE OF GLUCOSE from the bloodstream
INSULIN
30
Promotes glycogenesis and inhibits glycogenolysis
INSULIN
31
EPINEPHRINE (in __) and GLUCAGON (in __) • Stimulates glycogen BREAKDOWN to glucose
E- muscle G- liver
32
After a carbohydrate rich meal • Blood glucose level __ • Pancreas will secrete __ • __ is promoted
elevates insulin Glycogenesis
33
After not eating for a long period of time • Blood glucose level __ • Pancreas secretes __ • __ is promoted in the liver
decreases glucagon Glycogenolysis
34
DURING STRESS (strenuous exercise, excitement, beating deadlines, cramming for exams etc.) • Adrenal glands secrete
epinephrine
35
__ is stimulated in the muscle • The so-called “__” • Epinephrine is also called __
Glycogenolysis “Adrenaline Rush” adrenaline
36
Why do we FEEL LETHARGIC after a carbohydraterich meal? • After such meal, blood glucose level
increases
37
Lethargic after meals? __ is secreted by the pancreas and glycogen synthesis is __
Insulin, activated
38
Lethargic after meals? No __ is available for energy production so the person feels lethargic
glucose
39
Insulin-dependent diabetis • Deficiency in insulin may be caused by: • AUTOIMMUNE DESTRUCTION of pancreatic cells secreting insulin • MUTATION of insulin structure
Diabetes Mellitus Type 1
40
Insulin-resistant diabetis • Patient is NON-RESPONSIVE to insulin • Due to DEFECT IN THE STRUCTURE of the insulin receptor • Insulin CANNOT PROMOTE UPTAKE OF GLUCOSE from the blood
Diabetes Mellitus Type 2