Homework 14 Flashcards

(14 cards)

1
Q

You have two populations of people, one without diabetes and one with untreated type I diabetes. For each population, you set out to measure the activity of liver cell phosphofructokinase-1 (PFK-1) one hour after eating a meal. Remember PFK-1 catalyzes reaction #3 in glycolysis.
What do you predict about PFK-1 activity in people without diabetes as compared to people with type I diabetes?

I. PFK-1 activity will be lower in nondiabetics than diabetics.
II. PFK-1 activity will be higher in nondiabetics than diabetics.
III. PFK-1 activity will be about the same in nondiabetics than diabetics.

A

II.

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2
Q

Which of the following statements correctly explains why PFK-1 activity will be higher in nondiabetics than type I diabetics?

I. Insulin normally stimulates glycolysis in liver cells, but the lack of insulin signal in type I diabetics reduces activation of glycolysis.
II. Insulin normally stimulates glycolysis in liver cells, but the decrease in responsive insulin receptors in type I diabetics reduces activation of glycolysis.
III. Glucagon normally stimulates glycolysis in liver cells, but the decrease in responsive glucagon receptors in type I diabetics reduces activation of glycolysis.
IV. Glucagon normally stimulates glycolysis in liver cells, but the lack of glucagon signal in type I diabetics reduces activation of glycolysis.

A

I.

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3
Q

Increased glucose levels in the ___ stimulate glycolysis, which provides ___ for oxidation in the ___.

A

Cytosol, pyruvate, mitochondrion

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4
Q

The resultant acetyl-CoA can return to the ___ (as ) ___ and generate precursors for increased fatty acid synthesis. The increased intracellular glucose also stimulates glycogen synthesis.

A

Cytosol, citrate

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5
Q

Which of the following is the most important factor regulating flux through the citric acid cycle?

I. Concentration of intermediates
II. The ratio of [NAD+]/[NADH]
III. Hormonal control of α-ketoglutarate dehydrogenase levels
IV. Allosteric inhibition of fructose-1,6-bisphosphatase by F-2,6-BP

A

II.

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6
Q

During fatty acid synthesis, a build-up of fatty acids ___ the activity of ___ .

A

Inhibit, acetyl CoA carboxylase

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7
Q

Which regulatory mechanism ensures that fatty acids formed in the cytoplasm are not immediately oxidized?

A

Inhibition of carnitine acyltransferase by malonyl CoA

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8
Q

Hexokinase is the first enzyme in glycolysis, and there are different versions of this enzyme in animal cells. Hexokinase IV in liver cells has a KM value that is substantially higher than the KM for hexokinases expressed in other cell types. What is the significance of this fact?

A

The higher KM reflects lower affinity for its substrate, and therefore this kinase is only operational when glucose levels are high.

High KM represents lower affinity, and this enzyme would only be active when glucose concentrations are high. Thus, this high KM ensures that the liver cells export the glucose they are creating, and do not use this glucose for its own energy needs unless the concentrations are high.

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9
Q

In the cell, ATP, ADP, NADH, and NAD+ are internal signals that allosterically effect the activity of citric acid cycle enzymes. High levels of ATP and NADH decrease the activity of citric acid cycle enzymes, while ADP and NAD+ increase the activity. One of these citric acid cycle enzymes is isocitrate dehydrogenase and its substrate is isocitrate. Given this information, answer the following question.

Which of the following predictions is a plausible explanation for how ADP activates isocitrate dehydrogenase?

I. When binding to isocitrate dehydrogenase, ADP decreases the K50 for isocitrate.
II. When binding to isocitrate dehydrogenase, ADP increases the K50 for isocitrate.
III. When binding to isocitrate dehydrogenase, ADP dephosphorylates the enzyme.
IV. When binding to isocitrate dehydrogenase, ADP phosphorylates the enzyme.

A

I.

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10
Q

Select ALL of the following that are directly used to control fatty acid oxidation in cells.

I. negative feedback regulation if free fatty acids accumulate
II. changing the activity of the acylcarnitine shuttle
III. targeting the acetyl-CoA transport shuttle in the mitochondrial membrane
IV. altering the activity of the oxidoreductase enzymes in β-oxidation

A

I and II

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11
Q

Ketone bodies are produced in  ___ cells when there is excess ___.

A

Liver, acetyl CoA

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12
Q

In diabetic liver cells, an increased rate of ___ can lead to excessive production of ketone bodies.

A

Fatty acid oxidation

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13
Q

Why do diabetics have low stores of glycogen in their cells?

A

Difficulty transporting glycose from the blood into their cells

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14
Q

When blood glucose levels are high, untreated diabetics have difficulty transporting glucose ___________ the cell, therefore, the concentration of glucose in the cytoplasm is _____.

A

Inside, low

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