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PLE > Biochemistry: Carbohydrates > Flashcards

Biochemistry: Carbohydrates Flashcards

1
Q

ETC Complex I Inhibitors

A

BPAR

Barbiturates - CNS depressant
Piericidin A - NADH dehydrogenase inhibitor, antibiotic
Amytal - barbiturate derivative
Rotenone - pesticide

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2
Q

ETC Complex II Inhibitors

A

MCT

Malonate - competitive inhibitor of the enzyme succinate dehydrogenase
Carboxin - fungicide
TTFA - Thenoyltrifluoroacetone, a chemical compound used pharmacologically as a chelating agent

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3
Q

ETC Complex III Inhibitors

A

AD

Antimycin A - piscicide (fish poison)
Dimercaprol/BAL - also called British anti-Lewisite, is a medication used to treat acute poisoning by arsenic, mercury, gold, and lead

Complex III and/or IV inhibition: ETC will no longer work!

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4
Q

ETC Complex IV Inhibitors

A

CCSH

Cyanide
Carbon monoxide
Sodium azide - gas-forming component in many car airbag systems
Hydrogen sulfide

Complex III and/or IV inhibition: ETC will no longer work!

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5
Q

Examples of compounds that increase the permeability of the inner mitochondrial membrane to protons, ETC proceeds without establishing proton gradient

Name?
Effects?
Examples?

A

Name: Uncouplers
Effects: Increased oxygen consumption, decreased NADH/NAD and FADH/FAD ratio, decreased ATP synthesis
Examples: Synthetic - 2,4 dinitrophenol (pesticide), aspirin (hyperpyrexia in overdose leads to ETC uncoupling); Uncoupling protein - thermogenin (brown fat)

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6
Q

ATP Synthase Inhibitor

A

a. k.a. Complex V Inhibitors

ex. Oligomycin - a macrolide

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7
Q

GLUT 1 transporter found in

A 
Brain
Colon
Kidney
Placenta
RBCs

Glucose uptake

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8
Q

GLUT 2 transporter found in

A

Kidney
Liver
Pancreas
Small intestine (BM)

Rapid uptake or release of glucose

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9
Q

GLUT 3 transporter found in

A

Brain
Kidney
Placenta

Glucose uptake

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10
Q

GLUT 4 transporter found in

A

Adipose tissue
Heart muscle
Skeletal muscle

Insulin-stimulated glucose uptake

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11
Q

GLUT 5 transporter found in

A

Small intestine (lumen)

Absorption of glucose

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12
Q

SGLT 1 transporter found in

A

Kidney
Small intestine

Sodium-dependent active uptake of glucose against a concentration gradient

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13
Q

What is the rate-limiting step and associated enzyme in glycolysis?

A

Fructose-6-phosphate –> Fructose-1,6-bisphosphate

Enzyme: Phosphofructokinase-1 (PFK-1)

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14
Q

What is glycolysis for?

A

Major pathway for glucose metabolism that converts glucose into 3 carbon compounds to provide energy

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15
Q

Where does glycolysis occur?

A

In the cytosol of all mammalian cells

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16
Q

What is the substrate of glycolysis?

A

Glucose

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17
Q

What are the end-products of glycolysis?

A

2 molecules of either pyruvate or lactate

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18
Q

Fates of Pyruvate (3 carbons)

Process, Enzyme, Product

A
  1. Gluconeogenesis, Pyruvate carboxylase (4 carbons), Oxaloacetate
  2. Citric acid cycle, Pyruvate dehydrogenase complex (2 carbons), Acetyl CoA
  3. Fermentation, Pyruvate decarboxylase, Ethanol
  4. Anaerobic glycolysis, Lactate dehydrogenase, Lactate
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19
Q

Coenzymes (essential co-factors) in Pyruvate –> AcetylCoA

A 
Thiamine phosphate (Vitamin B1)
FAD (Vitamin B2)
NAD+ (Vitamin B3)
Coenzyme A (contains pantothenic acid, Vitamin B5)
Lipoic acid (Arsenic binds to this)
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20
Q

Glycolysis clinical correlates:

Deficiency of which enzyme causes hemolytic anemia?

A

Aldolase A

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21
Q

Glycolysis clinical correlates:

Most common enzyme defect in glycolysis, causes Congenital hemolytic anemia

A

Pyruvate kinase

Step 10: Phosphoenolpyruvate –> Pyruvate

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22
Q

Glycolysis clinical correlates:

Low exercise capacity, especially on high carbohydrate diets, Step 3

A

(Fructose 6 phosphate –> Fructose 1,6 bisphosphate + ADP)

(Muscle) phosphofructokinase 1

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23
Q

Glycolysis clinical correlates:

Pyruvate dehydrogenase deficiency causes ___, treat with

A

Congenital lactic acidosis

Ketogenic diet, since increase in lactate plus decreased AcetylCoA leads to psychomotor retardation and death

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24
Q

Glycolysis clinical correlates:

Requires treatment during pregnancy and is caused by mutations that decrease activity of glucokinase

A

Maturity Onset Diabetes in the Young Type 2 (MODY 2)

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25
Q

Glycolysis clinical correlates:

Competes with inorganic phosphate as a substrate for glyceraldehyde 3P dehydrogenase, no NADH and no ATP is produced

A

Arsenic poisoning

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26
Q

Glycolysis clinical correlates:

Causes potentially fatal pyruvic and lactic acidosis, inhibits thiamine absorption

A

Chronic alcoholism

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27
Q

Classic amphibolic pathway

Final common pathway for the metabolism of carbohydrates, lipids and proteins

A

Citric acid cycle/ Tricarboxylic acid cycle/ Krebs cycle

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28
Q

What is the citric acid cycle for?

A

Major pathway for ATP formation

Provides the substrates for gluconeogenesis, amino acid and fatty acid synthesis

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29
Q

Where does the citric acid cycle occur?

A

In all cells with mitochondria
All ingredients needed are in the mitochondrial matrix, except for succinate dehydrogenase which is in the inner mitochondrial membrane

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30
Q

What is the substrate of the citric acid cycle?

A

Acetyl CoA

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31
Q

What are the end-products of the citric acid cycle?

A

1 - FADH2
1 - GTP
2 - CO2
3 - NADH

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32
Q

What is the rate-limiting step and associated enzyme in the citric acid cycle?

A

Isocitrate –> alpha ketoglutarate

Enzyme: Isocitrate dehydrogenase

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33
Q

What is the rate-limiting step and associated enzyme in the citric acid cycle?

A

Isocitrate –> alpha ketoglutarate

Enzyme: Isocitrate dehydrogenase

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34
Q

Enzymes that produce NADH/FADH

A

All are dehydrogenases!

  1. Isocitrate dehydrogenase (isocitrate to alpha ketoglutarate)
  2. Alpha ketoglutarate dehydrogenase (alpha ketoglutarate to succinyl CoA)
  3. Succinate dehydrogenase (succinate to fumarate) –> the only FADH producing
  4. Malate dehydrogenase (malate to oxaloactetate)
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35
Q

Products in the steps of the citric acid cycle

A

Cindy Is Kind So She Forgives More Often

Citrate
Isocitrate
(alpha) Ketoglutarate
Succinyl CoA
Succinate
Fumarate
Malate
Oxaloacetate
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36
Q

What is gluconeogenesis for?

A

Process of synthesizing glucose from non-carbohydrate precursors, in order to prevent hypoglycemia during a fast

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37
Q

Where does gluconeogenesis occur?

A

Mitochondria and cytosol
90% in the liver
10% in the kidney

*40% in kidney if prolonged fast, hence hypoglycemia in renal failure patients

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38
Q

What are the substrates of gluconeogenesis?

A

Intermediates of glycolysis and the TCA, except for Acetyl CoA
Glycerol and propionyl CoA from triacylglycerols
Lactate through the Cori cycle
Carbon skeletons of glucogenic amino acids

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39
Q

What is the product of gluconeogenesis?

A

Glucose

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40
Q

What is the rate-limiting step and its enzyme in gluconeogenesis?

A

Fructose 1,6 bisphosphate –> Fructose 6 phosphate

Enzyme: Fructose 1,6 bisphosphatase

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41
Q

What do steps 1 and 2 of gluconeogenesis reverse in glycolysis?

A

Step 1: Pyruvate –> Oxaloacetate
Enzyme: Pyruvate carboxylase

Step 2: Oxaloacetate –> Phosphoenol pyruvate
Enzyme: Phosphoenolpyruvate carboxykinase

Reverses Step 10: pyruvate kinase which converts phosphoenolpyruvate to pyruvate

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42
Q

What do carboxylases do and what is the required co-factor?

A

Attach a carbon atom using CO2 as a substrate, require biotin as a co-factor

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43
Q

What does step 9 of gluconeogenesis reverse in glycolysis?

A

Fructose 1,6 bisphosphate –> Fructose 6 phosphate
Enzyme: Fructose 1,6 bisphosphatase

Reverses step 3: Phosphorylation of Fructose 6 phosphate to Fructose 1,6 bisphosphate by PFK 1

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44
Q

What does step 11 of gluconeogenesis reverse in glycolysis?

A

Glucose 6 phosphate –> Glucose
Enzyme: Glucose 6 phosphatase
Step shared with glycogenolysis, so glucose may exit the cell and enter bloodstream

Reverses step 1: Glucose to glucose 6 phosphate by enzyme hexokinase

45
Q

What is the Cori cycle?

A

Occurs in the liver, lactate from skeletal muscle is converted back to glucose through gluconeogenesis

46
Q

What is the significance of the Cori cycle?

A

Prevent lactic acidosis in the muscles

47
Q

What regulates gluconeogenesis?

A
  1. Circulating levels of glucagon
  2. Availability of glucogenic substrates
  3. Allosteric activation of hepatic pyruvate carboxylase by acetyl CoA
  4. Allosteric inhibition of fructose 1,6 bisphosphatase by AMP
48
Q

Where does the energy used in gluconeogenesis come from?

A

Fatty acid oxidation a.k.a. beta oxidation

49
Q

What is the energy requirement of gluconeogenesis?

A
  1. Cleavage of 6 high energy phosphate bonds

2. Oxidation of 2 NADH

50
Q

Clinical correlates of gluconeogenesis:

Excessive gluconeogenesis in response to injury and infection

A

Hyperglycemia in critically ill patients (stress hyperglycemia)

51
Q

Clinical correlates of gluconeogenesis:

Another state of excessive gluconeogenesis, glucose spills out in another fluid other than plasma

A

Glucosuria

52
Q

Clinical correlates of gluconeogenesis:

Hypoglycemic states and their description

A

Hypoglycemia during pregnancy - high fetal glucose consumption
Hypoglycemia in neonates - premature and LBW infants (little adipose tissue, undeveloped enzymes for gluconeogenesis)
Hypoglycemia in alcoholics - high amounts of cytoplasmic NADH from alcohol metabolim, intermediates of gluconeogenesis are diverted into alternate pathways, less glucose synthesis

53
Q

Branched polymer of alpha-D-glucose

A

Glycogen

Branched for more efficient breakdown
Primary glycosidic bond: horizontal bond = alpha 1-4
Secondary bond: vertical bond = alpha 1-6

54
Q

What is glycogenesis for?

A

Synthesis of glycogen during the well-fed state

55
Q

Where does glycogenesis occur?

A

Cytosol of liver and muscle

56
Q

What is the substrate of glycogenesis?

A

alpha-D-glucose

57
Q

What is the product of glycogenesis?

A

Glycogen

58
Q

What is the rate-limiting step in glycogenesis

A

Elongation of glycogen chains (creation of alpha 1-4 glycosidic bonds)
Enzyme: Glycogen synthase

59
Q

Protein that serves as a primer for glycogen synthesis when glycogen is completely depletes

A

Glycogenin

Without this, residual glycogen fragments can accept glucose residues

60
Q

What is the role of UDP glucose in glycogenesis?

A

Source of glucosyl residues that are added to the glycogen molecule (“Yaya”, ihahatid si glucose para humaba si glycogen)
Enzymes: phosphoglucomutase, UDP-glucose pyrophosphorylase

61
Q

Component and function of branching enzymes in glycogenesis

A

Amylo alpha 1-4 –> alpha 1-6 transglucosidase

Forms new alpha 1-6 bonds by transferring 5 to 8 glucosyl residues

62
Q

What is glycogenolysis for?

A

Mobilization of stored glycogen during fasting state

63
Q

Where does glycogenolysis occur?

A

Cytosol of liver and muscle

64
Q

What is the substrate in glycogenolysis?

A

Glycogen

65
Q

What are the products in glycogenolysis?

A

Glucose in liver

Glucose 6 phosphate in muscle

66
Q

What is the rate-limiting step in glycogenolysis?

A

Shortening of glycogen chains

Enzyme: Glycogen phosphorylase

67
Q

What is the coenzyme for shortening of glycogen chains? What is the enzyme?

A

Co-enzyme: Pyridoxal phosphate

Enzyme: Glycogen phosphorylase

68
Q

What is “limit dextrin”?

A

Last 4 glucosyl units remain in the shortening of glycogen chains, stop signal for glycogenolysis

69
Q

Component and function of debranching enzymes in glycogenolysis

A

alpha 1-4 –> alpha 1-4 glucantransferase, amylo alpha 1-4 glucosidase

Cleavage of alpha 1-4 and alpha 1-6 bonds, yields free glucose from the cleavage of the alpha 1-6 bond

70
Q

Glycogenolysis end products and enzymes for their conversion

A

Enzymes: phosphoglucomutase, and when present, glucose 6 phosphatase

End products:
Liver: glucose
Muscle: glucose 6 phosphate

71
Q

Function of alpha 1-4 glucosidase or acid maltase

A

Lysosomal degradation of glycogen (1-3% of glycogen)

Enzyme deficiency leads to Pompe disease

72
Q

Presentation of glycogen storage diseases

A

Abnormal glycogen metabolism
Accumulation of glycogen in cells

12 types, due to enzyme deficiencies

73
Q

Deficiency in glucose 6 phosphatase
Disease
Clinical features

A

Von Gierke Disease (GSD Ia)

Increased glycogen in renal tubule cells and liver
Hepatomegaly
Hypoglycemia (severe)
Lactic acidosis
Ketosis
Hyperlipidemia
74
Q

Deficiency in lysosomal acid maltase
Disease
Clinical features

A

Pompe Disease (GSD II)

Increased glycogen in lysosomes
Juvenile onset: hypotonia, death from heart failure by age 2
Adult onset: muscle dystrophy

75
Q

Deficiency in debranching enzyme
Disease
Clinical features

A

Cori Disease (GSD IIIa)

Fasting hypoglycemia
Hepatomegaly in infancy
Muscle weakness
Increased limit dextrin

76
Q

Deficiency in branching enzyme
Disease
Clinical features

A

Andersen Disease (GSD IV)

Hepatosplenomegaly
Increased polysaccharide with few branch points
Death from heart or liver failure by age 5

77
Q

Deficiency in muscle phosphorylase
Disease
Clinical features

A

McArdle Syndrome (GSD V)

Poor exercise tolerance
Muscle cramps and myoglobinuria but no lactic acidosis
Increased muscle glycogen (unable to use)

78
Q

Deficiency in liver phosphorylase
Disease
Clinical features

A

Hers Disease (GSD VI)

Hepatomegaly
Hypoglycemia (Mild)

79
Q

Phosphorylation of galactose
Step
Enzyme
Clinical manifestation

A

Galactose –> Glucose 1 phosphate (becomes glucose 6 phosphate to enter glycolysis)

Galactokinase

Galactokinase deficiency

80
Q

Formation of UDP galactose
Step
Enzyme
Clinical manifestation

A

Galactose 1 phosphate + UDP glucose –> UDP galactose + Glucose 1 phosphate

Galactose 1 phosphate uridyl transferase (GALT)

Classic galactosemia

81
Q

Use of galactose as a carbon source
Step
Enzyme

A

UDP-galactose –> UDP glucose

UPD hexase 4 epimerase

82
Q

Galactokinase deficiency
Clinical presentation
Treatment

A

Benign
Galactosemia and glactosuria
Cataracts in early childhood

Eliminate sources of galactose from diet

83
Q

Classic galactosemia
(galactose 1 phosphate uridyl transferase deficiency)
Clinical presentation
Treatment

A 
Toxic 
Galactosemia and galactosuria
Diarrhea, vomiting, jaundice
Poor growth, severe mental retardation and liver damage in children
Premature ovarian failure in females

Eliminate sources of galactose from the diet
Prenatal diagnosis is possible
Newborn screening is available

84
Q 
Phosphorylation of fructose
Step
Enzyme
Clinical presentation
Treatment
A

Fructose –> Fructose 1 phosphate

Fructokinase or hexokinase

Essential fructosuria: Benign and asymptomatic

85
Q 
Formation of DHAP and Glyceraldehyde
Step
Enzyme
Clinical presentation
Treatment
A

Fructose 1 phosphate –> DHAP + Glyceraldehyde

Aldolase B 
(Aldolase A is in Glycolysis: reversible conversion of fructose-1,6-bisphosphate to glyceraldehyde 3-phosphate and dihydroxyacetone phosphate)

Hereditary fructose intolerance (fructose only requires facilitated diffusion):
Profound hypoglycemia and vomiting after consumption of fructose or sucrose
Jaundice, hemorrhage, hepatomegaly, liver failure, renal dysfunction, hyperuricemia, lactic acidosis, death

Symptoms appear after weaning from milk
Eliminate sources of fructose, sucrose and sorbitol from diet

86
Q

Conversion of glucose to sorbitol
Step
Enzyme
Location

A

Glucose –> Sorbitol (reduction reaction, lose H)

Aldose reductase

Lens, retina, Schwann cells, liver, kidney, placenta, RBC, ovaries, seminal vesicles

87
Q

Conversion of sorbitol to fructose
Step
Enzyme
Location

A

Sorbitol –> Fructose

Sorbitol dehydrogenase

Liver, ovaries, seminal vesicles

88
Q

Lactose intolerance
Enzyme deficiency
Clinical presentation
Treatment

A

Lactase deficiency

Flatulence and diarrhea after ingestion of dairy products
(osmotic laxative)
90% of Asians and Africans

Reduce consumption of milk but may eat yogurt, cheese, brocolli for adequate calcium intake
Lactase-treated or containing products

89
Q

Sucrase-isomaltase complex deficiency
Clinical presentation
Treatment

A

Intolerance of ingested sucrose
10% of Inuits in Greenland and Canada

Dietary sucrose restriction
Enzyme replacement therapy

90
Q

Why can guinea pigs and primates not produce ascorbic acid?

A

Lack of L-gulonolactone oxidase

91
Q

Alternative pathway for glucose oxidation in the liver
Does not produce ATP
Produce glucoronic and iduronic acid

A

Uronic Acid Pathway

92
Q

Essential component of GAGs

Required in the detoxification of insoluble compounds such as bilirubin, steroids, morphine and other drugs

A

Glucuronic acid

93
Q

Essential pentosuria
Enzyme deficiency
Clinical presentation
Treatment

A

Xylulose reductase deficiency

Increased urinary xylulose
Benign with no clinical consequence

94
Q

A.k.a. Hexose monophosphate shunt

A

Pentose phosphate pathway

95
Q

What is the pentose phosphate pathway for?

A

NADPH production - it is a cofactor for many enzymes
Produces ribose 5 phosphate needed for nucleotide biosynthesis
Metabolic use of 5-carbon sugars
Does not consume nor produce ATP

96
Q

Where does the pentose phosphate pathway occur?

A

Cytosol of RBCs and tissues that produce lipids (liver, adipose tissue, adrenals, thyroid, testes, lactating mammaries)

97
Q

What is the substrate in the pentose phosphate pathway?

A

Glucose 6 phosphate

98
Q

What are the products of the pentose phosphate pathway?

A

NADPH

Ribose 5 phosphate

99
Q

What is the rate limiting step in the pentose phosphate pathway?

A

Glucose 6 phosphate –> 6 phosphogluconate

Enzyme: Glucose 6 phosphate dehydrogenase

100
Q

First phase of the pentose phosphate pathway
Oxidative? Reversible?
Key enzyme
Products

A

Oxidative, Irreversible

Glucose 6 phosphate dehydrogenase

2 NADPH, Ribulose 5 phosphate

101
Q

First phase of the pentose phosphate pathway
Oxidative? Reversible?
Key enzyme
Products

A

Non-oxidative, Reversible

Transketolases, Co-factor: Vit B1

Ribose 5 phosphate
Fructose 6 phosphate
Glyceraldehyde 3 phosphate
Other carbohydrates

102
Q

5 functions of NADPH

A
  1. Reductive biosynthesis of fatty acids and steroids
  2. Glutathione reduction in RBCs
  3. Cytochrome P450 monooxygenase system
  4. Oxygen-dependent bactericidal mechanism of WBCs
  5. Synthesis of nitric oxide
103
Q

Glutathione precursors

A

Glycine
Cysteine
Glutamate

104
Q

What does glutathione peroxidase do?

A

Catalyzes removal of H2O2 by reduced glutathione

105
Q

What is the enzyme for reduction of gluatathione?

A

Glutathione reductase, requires NADPH

106
Q

Most common disease-producing enzyme deficiency in humans

Clinical presentation?

A

G6PD Deficiency

Hemolytic anemia after oxidative stress (poor RBC defense against oxidizing agents)

Following a specific trigger, symptoms such as yellowish skin, dark urine, shortness of breath, and feeling tired may develop. Complications can include anemia and newborn jaundice.[2] Some people never have symptoms.

It is an X-linked recessive disorder

107
Q

Precipitating factors of G6PD deficiency disease

A

Infection (most common)
Drugs (sulfonamides, primaquine, chloramphenicol)
Fava beans

108
Q

Pathologic findings in G6PD deficiency

A

Heinz bodies - altered hemoglobin that precipitates in RBCs

Bite cells - abnormally shaped RBCs due to phagocytic removal of Heinz bodies in spleen

109
Q

Chronic Granulomatous Disease
Enzyme deficiency
Clinical presentation

A

NADPH oxidase deficiency - no superoxide formation needed by leucocytes to induce oxidative damage to bacteria

Severe, persistent chronic pyogenic infections caused by catalase-positive bacteria –> Gram (+) bacteria, just walled off in granuloma, not killed

PLE (14 decks)

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