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biochemistry > Exam 2 flashcards > Flashcards

Exam 2 flashcards

1
Q

What are common dietary sources of fructose?

A

Fruits, honey, sucrose (table sugar), corn syrup, and sorbitol.

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2
Q

What enzyme phosphorylates fructose in the liver?

A

Fructokinase.

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3
Q

Why does fructose metabolism bypass PFK-1, the key regulatory enzyme in glycolysis?

A

Fructose enters glycolysis downstream of PFK-1, making it a rapid energy source.

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4
Q

What is essential fructosuria?

A

A benign autosomal recessive disorder caused by fructokinase deficiency, leading to fructose excretion in urine.

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5
Q

Why does essential fructosuria not cause severe symptoms?

A

Fructose is not trapped inside cells and is excreted in the urine.

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6
Q

What is hereditary fructose intolerance (HFI)?

A

A severe autosomal recessive disorder caused by aldolase B deficiency, leading to fructose-1-phosphate accumulation.

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7
Q

What are the symptoms of HFI?

A

Hypoglycemia, vomiting, hepatomegaly, jaundice, and failure to thrive.

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8
Q

How does HFI lead to hypoglycemia?

A

Fructose-1-phosphate accumulation inhibits glycogenolysis and gluconeogenesis.

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9
Q

How is HFI managed?

A

Avoiding fructose, sucrose, and sorbitol in the diet.

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10
Q

What metabolic disturbances are seen in HFI?

A

Hypoglycemia, lactic acidosis, hypophosphatemia, hyperuricemia, hypermagnesemia, and hyperalaninemia.

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11
Q

What tissues primarily metabolize fructose?

A

The liver and kidneys.

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12
Q

What happens to fructose in the absence of aldolase B?

A

It accumulates as fructose-1-phosphate, causing toxicity.

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13
Q

How does fructose contribute to triglyceride synthesis?

A

It bypasses glycolytic regulation and is rapidly converted to acetyl-CoA.

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14
Q

Why does fructose metabolism increase uric acid levels?

A

ATP depletion leads to increased purine degradation and uric acid production.

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15
Q

Why does fructose metabolism favor fat storage?

A

Excess acetyl-CoA from fructose metabolism is used in lipogenesis.

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16
Q

What role does sorbitol play in fructose metabolism?

A

Sorbitol can be converted to fructose via sorbitol dehydrogenase.

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17
Q

Why do diabetics have complications related to sorbitol accumulation?

A

High glucose levels increase sorbitol production, leading to cataracts and neuropathy.

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18
Q

What is the rate-limiting step of fructose metabolism?

A

Aldolase B activity.

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19
Q

Why does fructose have a lower impact on insulin secretion than glucose?

A

It bypasses glucokinase, which regulates insulin secretion in the pancreas.

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20
Q

How does high fructose consumption contribute to metabolic syndrome?

A

Increased lipogenesis, insulin resistance, and hyperuricemia.

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21
Q

What enzyme converts galactose to galactose-1-phosphate?

A

Galactokinase.

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22
Q

What is classic galactosemia?

A

An autosomal recessive disorder caused by galactose-1-phosphate uridyltransferase deficiency.

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23
Q

What are symptoms of classic galactosemia?

A

Vomiting, jaundice, hepatomegaly, mental retardation, cataracts, and failure to thrive.

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24
Q

How does galactosemia cause cataracts?

A

Accumulation of galactitol in the lens.

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25
Q

How is galactosemia diagnosed?

A

By detecting elevated plasma galactose and urine-reducing substances.

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26
Q

What is the treatment for galactosemia?

A

A galactose-free diet.

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27
Q

Why are individuals with galactosemia prone to E. coli infections?

A

The immune system is compromised due to metabolic disturbances.

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28
Q

How does galactose metabolism affect bilirubin conjugation?

A

Galactose-1-phosphate accumulation inhibits UDP-glucuronate synthesis.

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29
Q

What enzyme deficiency causes mild galactosemia with only cataracts?

A

Galactokinase deficiency.

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30
Q

What tissues lack sorbitol dehydrogenase, leading to galactitol accumulation?

A

The lens, kidneys, and Schwann cells.

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31
Q

How does galactose affect glycogen synthesis in well-fed states?

A

It is converted to glucose-1-phosphate and stored as glycogen.

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32
Q

What happens when aldose reductase converts excess galactose?

A

It forms galactitol, causing osmotic damage.

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33
Q

Why does galactosemia cause hyperbilirubinemia?

A

Inhibited UDP-glucuronate synthesis prevents bilirubin conjugation.

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34
Q

How does hypoglycemia occur in galactosemia?

A

Inhibited gluconeogenesis due to accumulated galactose-1-phosphate.

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35
Q

What dietary changes prevent symptoms of galactosemia?

A

Avoiding dairy and other galactose-containing foods.

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36
Q

What enzyme deficiency causes the most severe form of galactosemia?

A

Galactose-1-phosphate uridyltransferase deficiency.

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37
Q

How does galactose metabolism support brain function?

A

UDP-galactose is used for glycoprotein and glycolipid synthesis.

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38
Q

Why does UDP-galactose deficiency impact connective tissues?

A

It is required for glycosaminoglycan synthesis.

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39
Q

What is the first step in galactose metabolism?

A

Phosphorylation by galactokinase.

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40
Q

Why do symptoms of galactosemia appear early in infancy?

A

Milk consumption introduces galactose immediately after birth.

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41
Q

How does alcohol metabolism contribute to hypoglycemia?

A

Alcohol increases NADH levels, inhibiting gluconeogenesis by favoring lactate and malate formation.

42
Q

What enzyme metabolizes ethanol in the liver?

A

Alcohol dehydrogenase.

43
Q

What is the toxic intermediate produced during alcohol metabolism?

A

Acetaldehyde.

44
Q

What enzyme converts acetaldehyde to acetate?

A

Aldehyde dehydrogenase.

45
Q

Why does alcohol metabolism lead to lactic acidosis?

A

High NADH levels favor conversion of pyruvate to lactate.

46
Q

How does alcohol inhibit fatty acid oxidation?

A

High NADH levels delay oxidation and promote triglyceride accumulation in the liver.

47
Q

What condition results from excessive triglyceride storage in the liver?

A

Alcoholic steatosis (fatty liver).

48
Q

How does alcohol-induced hypoglycemia affect fasting individuals?

A

Inhibits gluconeogenesis, leading to dangerous blood sugar drops.

49
Q

Why is NAD+ depletion a major issue in alcohol metabolism?

A

NAD+ is needed for glycolysis, fatty acid oxidation, and the TCA cycle.

50
Q

How does alcohol consumption affect glycogen stores?

A

Depletes glycogen stores, increasing hypoglycemia risk.

51
Q

What metabolic shift occurs in chronic alcoholics?

A

Increased reliance on ketone bodies due to impaired glucose metabolism.

52
Q

What is the primary reason alcohol can worsen diabetic ketoacidosis (DKA)?

A

Increased NADH shifts metabolism toward ketogenesis.

53
Q

How does alcohol contribute to gout?

A

Increased NADH levels promote uric acid formation.

54
Q

What vitamin deficiency is common in chronic alcoholism?

A

Thiamine (Vitamin B1) deficiency.

55
Q

Why does alcohol delay the metabolism of lactate?

A

NAD+ is required to convert lactate back to pyruvate.

56
Q

How does alcohol affect the electron transport chain (ETC)?

A

Excess NADH inhibits the TCA cycle and reduces ATP production.

57
Q

What is Wernicke-Korsakoff syndrome?

A

A neurological disorder due to thiamine deficiency, common in alcoholics.

58
Q

Why does alcohol consumption cause mitochondrial dysfunction?

A

High NADH disrupts oxidative phosphorylation.

59
Q

How does binge drinking increase hypoglycemia risk in diabetics?

A

Alcohol metabolism inhibits gluconeogenesis and depletes glycogen.

60
Q

How does acetaldehyde contribute to alcohol toxicity?

A

It forms adducts with proteins, leading to liver damage.

61
Q

What is the primary function of the electron transport chain (ETC)?

A

To generate ATP through oxidative phosphorylation.

62
Q

Where is the ETC located?

A

In the inner mitochondrial membrane.

63
Q

What is the final electron acceptor in the ETC?

A

Oxygen (O₂).

64
Q

What happens to oxygen at the end of the ETC?

A

It combines with electrons and protons to form water.

65
Q

What complex in the ETC is NOT a proton pump?

A

Complex II (Succinate dehydrogenase).

66
Q

How does NADH contribute to the ETC?

A

It donates electrons to Complex I.

67
Q

What is the role of FADH₂ in the ETC?

A

It donates electrons to Complex II.

68
Q

What molecule shuttles electrons between Complex I/II and Complex III?

A

Ubiquinone (CoQ).

69
Q

What molecule transfers electrons from Complex III to Complex IV?

A

Cytochrome c.

70
Q

What enzyme synthesizes ATP using the proton gradient?

A

ATP synthase (Complex V).

71
Q

How does proton movement drive ATP synthesis?

A

Protons flow back into the matrix through ATP synthase.

72
Q

What is the role of the proton gradient in oxidative phosphorylation?

A

It stores energy used to drive ATP production.

73
Q

What happens when ETC complexes are inhibited?

A

ATP production decreases, leading to cell death.

74
Q

What toxin inhibits Complex IV?

A

Cyanide.

75
Q

What toxin inhibits Complex I?

A

Rotenone.

76
Q

What is the effect of an uncoupling agent like thermogenin?

A

It dissipates the proton gradient, generating heat instead of ATP.

77
Q

How does the malate-aspartate shuttle function?

A

It transfers electrons from cytosolic NADH into the mitochondria.

78
Q

What disease is linked to ETC dysfunction?

A

Leigh syndrome.

79
Q

What happens when mitochondria are damaged?

A

ATP production decreases, leading to energy deficits.

80
Q

How is ATP transported out of the mitochondria?

A

Via the ATP/ADP translocase.

81
Q

What enzyme breaks down triglycerides in adipose tissue?

A

Hormone-sensitive lipase.

82
Q

What molecule transports free fatty acids in the blood?

A

Albumin.

83
Q

Where does beta-oxidation occur?

A

In the mitochondria.

84
Q

What is the primary product of beta-oxidation?

A

Acetyl-CoA.

85
Q

How are long-chain fatty acids transported into mitochondria?

A

Via the carnitine shuttle.

86
Q

What enzyme activates fatty acids for beta-oxidation?

A

Acyl-CoA synthetase.

87
Q

What deficiency impairs fatty acid transport into mitochondria?

A

Carnitine deficiency.

88
Q

What are ketone bodies?

A

Acetoacetate, β-hydroxybutyrate, and acetone.

89
Q

When are ketone bodies produced?

A

During fasting or low-carbohydrate diets.

90
Q

What organ cannot use ketone bodies for energy?

A

The liver.

91
Q

What is the rate-limiting enzyme in ketogenesis?

A

HMG-CoA synthase.

92
Q

How does insulin affect fat metabolism?

A

It inhibits lipolysis and promotes fat storage.

93
Q

What hormone stimulates lipolysis?

A

Glucagon.

94
Q

How does beta-oxidation provide energy?

A

By generating NADH and FADH₂ for the ETC.

95
Q

What is the fate of odd-chain fatty acids?

A

They produce propionyl-CoA, which enters the TCA cycle.

96
Q

What is the function of lipoprotein lipase?

A

It breaks down triglycerides in lipoproteins for tissue uptake.

97
Q

What is the main storage form of lipids in the body?

A

Triglycerides.

98
Q

What are the major sources of dietary fat?

A

Triglycerides, phospholipids, and cholesterol.

99
Q

What is the role of bile salts in fat digestion?

A

They emulsify fats to aid in digestion.

100
Q

What is the primary energy source during prolonged fasting?

A

Fatty acids and ketone bodies.

biochemistry (9 decks)

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