Acquiring and Utilizing Fuels Flashcards

1
Q

What are the names and functions of the five general glucose transporters?

A
GLUT1=constitutively active 
GLUT2=specialized function
GLUT3=constitutively active 
GLUT4=specialized function
Na/Glucose symporter
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2
Q

What is the name of the general fructose transporter?

A

GLUT5

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3
Q

Which transporter is responsible for transporting glucose into the blood stream through the intestines?

A

GLUT2

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4
Q

Which transporter is responsible for transporting glucose into the liver from the blood and why is that transporter used?

A

GLUT2–it has a generally lower Kt than other glucose transporters, so the liver will not absorb glucose and make glycogen unless other tissues are nourished first

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5
Q

What is Fanconi-Bickel disease?

A

Loss of GLUT2

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6
Q

Why might Fanconi-Bickel disease manifest as a case of hepatomegaly?

A

The liver can still absorb lactate from the body and conduct gluconeogenesis. The glucose made will be stored as glycogen that can never escape the liver

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7
Q

In what tissues is GLUT4 found? How is GLUT4 different than other glucose transporters?

A

Cardiac muscle, skeletal muscle, and adipose tissue; GLUT4 has a very high affinity for glucose compared to the other transporters

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8
Q

Where do cells store GLUT4 and what activates their activity?

A

GLUT4 is normally stored in intracellular vesicles; insulin and exercise prompt their secretion.

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9
Q

What is the metabolic value of ethanol?

A

Calories: ~7kcal/mol
Can only be stored as fat because the end product of metabolism is acetate
Contains no micronutrients, CHO, or proteins

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10
Q

What are the two major nutritional problems affiliated with excessive ethanol consumption?

A

1) Malnutrition from loss of other food sources

2) B vitamin deficiency

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11
Q

What is the first enzyme in alcohol metabolism, what reaction does it catalyze, where does the reaction happen, and what is the subsidiary byproduct of the reaction?

A

alcohol dehydrogenase
EtOH–>acetaldehyde
In mitochondria
NADH is produced

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12
Q

What is the second enzyme in alcohol metabolism, what reaction does it catalyze, where does the reaction happen, and what is the subsidiary byproduct of the reaction?

A

aldehyde dehydrogenase 2
acetaldehyde–>Acetate
In cytosol
NADH is produced

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13
Q

Where does Anabuse target and what is its effect?

A

Anabuse (disulfuram) knocks out ALDH2. As a result acetaldehyde increases, which, in the brain, triggers vomiting

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14
Q

What is the secondary reaction to degrade alcohol, and why is it a poor choice for metabolism?

A

CYP2E1, a cytochrome p450, can use NADPH to catalyze the reaction, but it has poor efficiency and will metabolize many drugs inappropriately (hence the reason the warning label may indicate not to take with EtOH)

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15
Q

What are four deleterious effects of excess ethanol on normal cellular metabolism?

A

1) Change in cellular redox state by absorbing too much NAD
2) Gluconeogenesis inhibited
3) loss of NAD shuts down Krebs cycle
4) increase in acetyl-CoA and NADH encourages liver cells to make more ketone bodies, and beta-hydroxybutyrate will be the preferential outcome

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16
Q

How does the body attempt to handle methanol ingestion? What are the overall consequences of its ingestion?

A

ADH converts methanol to formaldehyde which is converted to formic acid by ALDH. The body can clear some formic acid by shunting it to folic acid derivatives, but when those run out, they cause metabolic acidosis and can destroy the optic nerve

17
Q

How does the body attempt to handle ethylene glycol ingestion?

A

ADH and ALDH convert it to glycolic acid, which profoundly induces metabolic acidosis; the body may convert it to oxalic acid to clear the glycolic acid, but oxalic acid complexes with calcium and can crystalize in the kidney

18
Q

How is the anion gap calculated?

A

Cations (Na+K) - Anions (HCO3 and Cl)

19
Q

What compounds can increase the anion gap?

A

increase in lactate, ketones, or formates (they consume the available bicarbonate)

20
Q

What are four treatments for a patient who has ingested a toxic alcohol?

A

1) Hydration/dilution
2) Ethanol (competitive inhibitor)
3) Ventilation
4) 4-methylpyrazole—>blocks ADH
[bicarbonate not given as body can self-regulate]

21
Q

What is the ratio of ATP to creatine in muscle? Where is creatine made?

A

20:80

In the liver

22
Q

What enzyme is important in creating phosphocreatine? What reaction does it metabolize?

A

Creatine kinase

creatine+ATPphosphocreatine + ADP

23
Q

How does myokinase support continued cellular energy in exercise states? What’s a negative consequence of this reaction?

A

It can convert the reaction
2 ADP ATP+AMP

AMP is viewed as an excess purine and eliminated by the body as uric acid

24
Q

How is the imbalance in ATP, ADP, and AMP levels restored after exercise continues?

A

Start of glycolysis and fatty acid metabolism promotes restoration of ATP

25
Q

What two components promote the upswing in anaerobic metabolism during exercise?

A

AMP and phosphorylase kinase