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METABOLISMZ > DOC UY: CARBS REVIEW > Flashcards

DOC UY: CARBS REVIEW Flashcards

1
Q

Explain the biochemical derangement occurring in a patient who is suffering an acute myocardial infarction. What type of glycolysis prevails?

A
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2
Q

Why do you think that a genetic deficiency in muscle glycogen phosphorylase (McArdle disease) is a mere inconvenience, whereas a deficiency of liver glycogen phosphorylase (Hers disease) can be lethal?

A
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3
Q

In an oral glucose tolerance test, an individual in the basal metabolic state ingests a large amount of glucose. If the individual is normal, explain or illustrate biochemical changes that will occur?

A
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4
Q

Consider a type 1 DM patient who has neglected to take his insulin for the last 72 hours and has not been eating much as well. Please describe the activity level of the different hepatic enzymes involved in glycogen metabolism under these condition.

A
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5
Q

Essential fructosuria is a rare and benign genetic disorder caused by a deficiency of the enzyme fructokinase. Why is this disease benign, when a deficiency of aldolase B (hereditary fructose intolerance [HFI]) can be fatal? Why is there severe hypoglycemia in aldolase B deficiency? Explain.

A
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6
Q

Consider a type 1 DM patient who has neglected to take his insulin for the last 72 hours and has not been eating much as well. Please describe the activity level of the different hepatic enzymes involved in glycogen metabolism under these condition.

A
  • glycogenolysis
  • gluconeogenesis
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7
Q

A patient was started on antibiotic therapy with a combination of trimethoprim and sulfamethoxazole (TMP/sulfa) because he an allergy to penicillin.On the third day of therapy with TMP/sulfa for his infection, he was slightly jaundiced. His hemoglobin level had fallen by 3.5 g/dL from its value at admission, and his urine was red-brown.What is the biochemical derangement in this patient? Why is he jaundiced and why is his urine reddish-brown?

A

G6PD deficiency

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8
Q

Describe the glycolysis pathway

A

It is a catabolic pathway used by cell to generate ATP from glucose

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9
Q

What do anaerobic conditions limit?

A

ATP production per mole of glucose oxidized

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10
Q

Glycolysis is also known as

A

Embden meyerhoff pathway

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11
Q

In anaerobic condition how is glycolytic inhibition prevented?

A

NADH accumulates in cytoplasm; amount of NAD+ decreases

There’s insufficient NAD+ for G3P dehydrogenase step to proceed. Glycolysis is inhibited.

NAD+ is regenerated. Pyruvate to lactate via LDH.

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12
Q

ETC will not work in the absence of ______.

A

Oxygen

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13
Q

NAD+ used in glycolysis must be regenerated in order for glycolysis to continue

A

to generate reducing equivalents (NADH) for pyruvate dehydrogenase

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14
Q

Lactic Acidemia

A

Blood accumulates up to pH level of 7.2.
NADH/NAD+ ratio increases, leading to lactate formation.

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15
Q

T or F: ATP is formed by oxidative phosphorylation

A

False - Glycolysis synthesizes ATP via substrate-level
phosphorylation

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16
Q

Oxidative phosphorylation is found in _____.

A

areas with a lot of mitochondria such as in the heart

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17
Q

T or F: A molecule of pyruvate is formed from the oxidation of one glucose molecule .

A

False - Two molecules of pyruvate are formed from the oxidation of one glucose molecule .

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18
Q

If we start in G3P, how many pyruvate will be formed?

A

1 pyruvate

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19
Q

Pyruvate kinase is the rate-limiting enzyme of glycolysis

A

PFK

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20
Q

Two molecules of ATP are used in the beginning of the pathway

A

TRUE

  • Hexokinase
  • PFK-1
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21
Q

The net reaction for anaerobic glycolysis

A

Glucose + 2 ADP + 2 Pi → 2 lactate + 2 ATP + 2 H2O + 2 H

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22
Q

2 substrate level phosphorylation in glycolysis

A

Phosphoglycerate kinase step
Pyruvate kinase step

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23
Q

Iodoacetate blocks _____.

A

G3P dehydrogenase enzyme

In order to inhibit glycolysis.

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24
Q

Fluoride blocks ___________.

A

Enolase

This is to inhibit bacterial growth

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25
Q

Arsenic poisoning inhibits _____.

A

Glycolysis

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26
Q

What are the fates of lactate?

A
  • -
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27
Q

Glycolysis and Fate of Lactate in the heart

A
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28
Q

Other functions of Glycolysis

A
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29
Q

dissociation curves shiftts to _______-.

A

Right

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30
Q

The primary control of muscle glycolysis is the energy charge of the cell which is the ____.

A

the ratio of ATP to AMP

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31
Q

Glycolysis is stimulated as the energy charge of the cell ________.

A

falls—–a signal that the cell needs more ATP.

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32
Q

PFK and ATP levels relation

A
33
Q

PFK and ATP/AMP levels relation

A
34
Q

PFK and pH levels relation

A
35
Q

hexokinase vs fructokinase

A

Hexokinase is inhibited by its product

36
Q
A
37
Q

What inhibits PK?

A
  • ATP
  • Alanine
38
Q

Function of Glycolysis in the Liver

A

The liver maintains blood glucose: It stores glucose as glycogen when glucose is plentiful, and it releases glucose when the supply is low.

uses glucose to generate reducing power for biosynthesis and to synthesize building blocks for other molecules.

39
Q

Glucokinase phosphorylates glucose only when glucose is abundant because _________.

A

it has a HIGH Km for glucose

Its low affinity for glucose in the liver gives the brain and muscles first call for glucose when supply is limited and
* It ensures that glucose is not wasted when it is in abundant.

40
Q

Function of pacreatic glucokinase

A

detect changes in concentrations of glucose in the systemic circulation [note: this is same with hepatic glucokinase].

41
Q

When glucose is increased more glucose is phosphorylated by glucokinase, increasing glycolysis, and leading to increased formation of ATP.

A

…

42
Q

Explain MODY

A

mutated glucokinase.
km for glucose is above 200, thus moderate hyperglycemia not enough to induce insulin release.

[can be mistaken as Type I DM]

43
Q

Fructose 2,6-bisP

A
44
Q

PFK2

A
45
Q

High insulin/glucagon ratio causes ____________. to favor glycolysis

A

decreased cAMP and reduced levels of PFK2
……
[page 26]

46
Q

PDH is regulated by

A

rate of ATP utilization

47
Q

However, when tissues do not have an adequate supply of O2 to meet their ATP demands, the increased NADH/NAD ratio inhibits PDH, but AMP activates glycolysis. A proportion of the pyruvate is then reduced to lactate to allow glycolysis to continue.

A
48
Q

structure of glycogen

A
49
Q

8 to 10 residues – amylopectin (starch)

A
50
Q

glycogenin

A
51
Q

non-reducing ends

A
52
Q

Muscle glycogen is a fuel reserved for the production of ATP within that tissue whereas liver glycogen is a glucose reserve for the maintenance of blood concentration

A
53
Q

resting - fatty acids
high demands –> glucose

A
54
Q

the first and immediate source of glucose for the maintenance of blood glucose levels.

A

Liver glycogen

55
Q

In the liver, the G6P that is generated from glycogen degradation is hydrolyzed to glucose by glucose 6-phosphatase—an enzyme that is present only in the liver and kidneys.

A
56
Q

G6-Phosphatase is only present in kidney & liver. What does this imply?

A

Gluconeogenesis is only possible in kidney and liver

57
Q

Glycogen degradation thus provides a readily mobilized source of blood glucose as dietary glucose decreases, or as exercise increases, the use of blood glucose by muscles.

A
58
Q

Glycogen synthesis requires the formation of α-1,4-glycosidic bonds to link glucosyl residues in long chains and the formation of an α-1,6-branch every 8 to 10 residues.

A
59
Q
  • Most of glycogen synthesis occurs through the lengthening of the polysaccharide chains of a preexisting glycogen molecule (a glycogen primer) in which the reducing end of the glycogen is attached to the protein glycogenin. To lengthen the glycogen chains, glucosyl residues are added from UDP-G to the nonreducing ends of the chain by glycogen synthase.
A

GLYCOGEN SYNTAHSE

60
Q
A

amylo-4,6-transferase (branching enzyme)

61
Q

glycogen synthase absence

A

Persistent fasting hypoglycemia

62
Q

T or F: Glycogen synthase cannot form the a -1,6- glycosidic linkages

A

TRUE

63
Q

T or F: Glycogen has more alpha-1,6 linkages than alpha-1,4 linkages

A

FALSE

64
Q

T or F: Glycogen synthase form amylose chain then a branching enzyme removes a block of about 7 glucosyl residues from a growing chain and transfer it to another chain to produce an a-1,6 linkage.

A

TRUE

65
Q

Branching Enzyme Nomenclature

A

Amylo-4,6-transferase

1,4-a glucan branching enzyme

Amylo-(1,4→1,6)-transglycosylase

Alpha-1,4-glucan-6-glycosyltransferase

Alpha-glucan-branching glycosyltransferase

66
Q

Glycogenolysis doesn’t involve hydrolysis reaction but a _____-.

A

phosphorolysis reaction (breaking of a bond using a phosphate ion
as a nucleophile).

67
Q

Why g1P?

Glycogen phosphorylase starts at the nonreducing end of a chain and successively cleaves glucosyl residues by adding phosphate to the anomeric carbon of the terminal glycosidic bond, thereby releasing glucose 1-phosphate and producing a free 4α-hydroxyl group on the glucose residue now at the end of the glycogen chain.

A
68
Q

Two catalytic activities of Glycogenolysis

A

The debrancher enzyme, which catalyzes the removal of the four residues closest to the branch point, has two catalytic activities: it acts as a transferase and as an α-1,6-glucosidase.

69
Q

One glucose and approximately seven to nine glucose 1-phosphate residues are released for every branch point. [this occurs only in the liver]

A
70
Q

NOMENCLATURE CONCERNS WITH ENZYMES THAT METABOLIZE GLYCOGEN

A

Both glycogen phosphorylase and glycogen synthase will be covalently modified to regulate their activity.
* When it is activated by covalent modification, glycogen phosphorylase is referred to as glycogen phosphorylase a; when the covalent modification is removed and the enzyme is inactive, it is referred to as glycogen phosphorylase b.
* Glycogen synthase, when it is not covalently modified, is active and can be designatedas glycogensynthaseaorglycogensynthaseI.
* Whenglycogensynthaseiscovalentlymodified,itisinactiveintheformof glycogen synthase b or glycogen synthase D

71
Q

Skeletal muscle glycogen produces glucose 1- phosphate and a small amount of free glucose.

A
72
Q

glucagon has no effect in the muscle

A
73
Q

malignant hyperdermia

A
74
Q

the effects of Ca in muscle result principally from the release of Ca from the sarcoplasmic reticulum after neural stimulation, and not from epinephrine- stimulated uptake;

A
75
Q

An increase of glucagon and decrease of insulin during the fasting state initiates a cyclic adenosine monophosphate (cAMP)-directed phosphorylation cascade, which results in the phosphorylation of glycogen phosphorylase to an active enzyme and the phosphorylation of glycogen synthase to an inactive enzyme

As a consequence, glycogen degradation is stimulated, and glycogen synthesis is inhibited

A
76
Q

carb loading

A
77
Q

orange as a source of glucose

A
78
Q
A

METABOLISMZ (7 decks)

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