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Biochemistry (MPAS) > Lecture 5: Nutrition, metabolism and energy balance > Flashcards

Lecture 5: Nutrition, metabolism and energy balance Flashcards

1
Q

The main dietary nutrients, carbohydrates, proteins, and lipids are metabolized for?

A
  1. Generation of energy in the form of ATP (catabolism).
  2. Biosynthetic activity of molecules (anabolism) that depends on ATP, linking these two processes, and the synthesis of other useful metabolites
  3. Synthesis of reduced and oxidized coenzymes, such as NADPH/NADP and NADH/NAD.
  4. The transfer of hydrogen from the reduced coenzymes to enter the electron transport chain in mitochondrial for the synthesis of water and energy/ATP in a process known as oxidative phosphorylation.
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2
Q

In which pathway is carbon dioxide produced?

A

TCA cycle

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3
Q

Where does initiation of metabolism pathways occur?

A

In the cytoplasm

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4
Q

Where do the end stages of most biological pathways occur?

A

Mitochondria

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5
Q

What is glycolysis?

A

Glucose breakdown in the absence of oxygen

glucose is eventually processed to PYRUVATE

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6
Q

Enzymes involved in carbohydrate metabolism

A

Glycolysis Hexokinase

Glucose-6-phosphate dehydrogenase

Pyruvate kinase

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7
Q

What is produced during glycolysis?

A

ATP, reduced coenzymes (NADH) and lactic acid

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8
Q

Hexokinase

A

Converts glucose to glucose-6-P

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9
Q

Which enzyme diverts glucose into the pentose phosphate pathway?

A

Glucose 6-phosphate dehydrogenase

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10
Q

Deficiency in Glucose-6-P DH causes?

A

drug-induced anemia

If you have this deficiency and take a drug that creates an oxidizing environment, free radicals are formed. Erythrocytes cannot overcome the oxidative stress and lyse.

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11
Q

What does Glucose-6-P need to be converted to before being acted upon by pyruvate kinase?

A

Phosphoenolpyruvate

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12
Q

Pyruvate kinase reaction

A

Converts Phosphoenolpyruvate to pyruvate

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13
Q

How is ATP generated by pyruvate kinase?

A

A phosphate is transferred directly from pyruvate to ADP.

This is called substrate level phosphorylation

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14
Q

How can a deficiency of enzymes in the glycolytic pathway can lead to hemolytic anemia?

A

Red blood cells depend on glucose entirely to survive

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15
Q

What reaction is catalyzed by lactate DH?

A

Pyruvate -> lactic acid (reversible reaction)

NADH is used as coenzyme

Anaerobic conditions

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16
Q

What is the Cori cycle?

A

Lactic acid is converted into glucose via gluconeogenesis in the liver (Cori cycle)

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17
Q

What would inhibition of oxidative phosphorylation cause to levels of pyruvate?

A

Pyruvate would accumulate

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18
Q

What happens if the conversion of pyruvate to acetyl CoA is inhibited?

A

Accumulation of pyruvate

build up of pyruvate will lead to more lactic acid and eventually acidosis will cause problems for tissues.

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19
Q

How would you treat patients with deficiency in the glycolytic enzymes?

A

Since RBCs are most affected, should first give blood transfusion

Could also try to introduce enzymes, but this is not well researched

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20
Q

Pyruvate dehydrogenase

A

Pyruvate is oxidatively decarboxylated to acetyl coA

Irreversible reaction

Large complex enzyme

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21
Q

Where does the TCA cycle occur?

A

Mitochondria

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22
Q

What does pyruvate dehydrogenase require to function?

A

Vitamins

Thiamine (thiamine pyrophosphate)

Niacin (to produce NAD)

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23
Q

Is acetyl coA a precursor for gluconeogenesis?

A

No

The reaction of pyruvate -> acetyl coA is irreversible

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24
Q

What happens to the hydrogen ions produced in the TCA cycle in mitochondria

A

taken up by the oxidized coenzymes (NAD AND FAD)

NAD and FAD become reduced and then oxidized in the respiratory chain

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25
Q

What happens if there is a deficiency pyruvate dehydrogenase?

A

Accumulation of pyruvate, which leads to:

Lactic acidosis (production of lactate)

hypotonia (weakness)

vomiting

neurological disorders (due to build up of alanine which is converted into ammonia)

poor development (ammonia)

seizures

ataxia (lack of voluntary control of muscles)

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26
Q

How would you treat patients with pyruvate dehydrogenase deficiency?

A

Activate enzyme using vitamin supplements (niacine, thiamine etc)

Nutritional limitations (not too much carbohydrates)

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27
Q

TCA cycle and interactions between pyruvate, fatty acids and acetyl CoA

A

See figure

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28
Q

Acetyl CoA as a central molecule diagram

A

See figure

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29
Q

Intermediates of TCA cycle and their links

A

Pyruvate (from carbohydrates and amino acids)

Acetyl-CoA (central metabolite).

Ketones (from fatty acid oxidation, and amino acids).

Ketoglutarate (from Acetyl–CoA and transamination of amino acids)

See figure

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30
Q

How are lipids and triglycerides degraded?

A

by hormone sensitive lipase into Fatty acids and glycerol

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31
Q

Metabolism of glycerol

A

converted to glucose via gluconeogenesis in the liver.

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32
Q

Metabolism of fatty acids

A

generally converted to ketones in liver mitochondria via beta-oxidation of fatty acids.

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33
Q

Where does beta oxidation of fatty acids occur?

A

Liver mitochondria

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34
Q

What does carnitine palmitoyl transferase require?

A

Carnitine as a cofactor

35
Q

Examples of ketone bodies

A

beta-hydroxybutyrate, acetone, and acetoacetate

36
Q

When is fatty oxidation inhibited?

A

When fatty acid synthesis is active

Ex: during well fed state

37
Q

Fatty acid oxidation during starvation

A

Important!!

38
Q

Why don’t red blood cells and neurons (brain) oxidize fatty acids?

A

RBCs do not have mitochondria

Neurons don’t have enzymes to oxidize fatty acids

39
Q

Why don’t red blood cells and neurons (brain) oxidize fatty acids?

A

RBCs do not have mitochondria

Neurons don’t have enzymes to oxidize fatty acids. Fatty acids do not cross blood brain barrier

40
Q

Where does beta oxidation of FAs occur?

A

In mitochondria of most cells

41
Q

Acyl-CoA dehydrogenase

A

Involved in beta oxidation of fatty acids

Dehydrogenates acyl-CoA in the presence of FAD and NAD

42
Q

What happens to NADHH and FADHH that are generated in the liver mitochondria during fatty acid oxidation?

A

They are oxidized, leading to generation of ATP.

This energy generated is used up during gluconeogenesis.

43
Q

Where does the energy for gluconeogenesis come from?

A

ATP

mainly generated by the oxidation of fatty acids.

44
Q

Why is a lack of FA oxidation deleterious during fasting?

A

gluconeogenesis is important to occur in the absence of glucose (fasting)

45
Q

The beta-oxidation of fatty acids results in the production of:

A

Ketone bodies

Acetyl CoA (converted to fatty acids)

Reduced coenzymes that enter into mitochondria

Energy/ATP (for gluconeogenesis)

46
Q

What is the cause of defects in Beta oxidation of fatty acids?

A

deficiencies in:

carnitine

carnitine-palmitoyl transferase I/II

acyl-CoA dehydrogenase

47
Q

How would you treat a patient with deficiency in oxidation of fatty acids?

A

Feed regular meals of carbohydrates?

48
Q

When can deficiency in oxidation of fatty acids lead to hypoglycemia?

A

If you are not eating?

49
Q

What is one of the most critical physiological function of liver cell?

A

removal and excretion of nitrogen from proteins

This nitrogen is converted to ammonia in most cells

Ammonia is converted to urea that is excreted by the kidneys

50
Q

How is nitrogen removed from proteins?

A

Removed as an amino group in transamination reactions

51
Q

What enzymes are responsible for transamination reactions?

A

transaminases (AST/ALT)

convert amino acid into a keto acid.

For example, alanine is converted to pyruvate.

52
Q

What happens to the amino group during transamination?

A

amino group must be received or accepted by another molecule.

The acceptor in this case is invariable ketoglutarate, which combines with the amino group to form glutamate (glutamate can combine with amino groups to form glutamine in a reversible reaction).

53
Q

What do transaminases require to be functional?

A

vitamin B6 also known as pyridoxal phosphate/pyridoxine as a cofactor.

54
Q

What happens to glutamate produced during transamination reactions?

A

enzyme: glutamate dehydrogenase

glutamate is oxidatively deaminated to form ammonia

ammonia generated is then converted into urea in the liver. The urea is released into the blood and excreted by the kidneys

55
Q

What happens to remaining carbon skeleton after amino acid metabolism reactions?

A

used up in gluconeogenesis, and other pathways.

Generation of metabolic energy

See figure

56
Q

Why does ammonia need to be removed from body?

A

hazardous waste that is neurotoxic

removed from the body in a soluble and harmless form, urea, by the kidneys.

57
Q

Where is urea made?

A

Liver

58
Q

Urea cycle

A

in mitochondria, ammonia/ammonium ion combines with water + ATP + Carbon dioxide to form carbamoyl phosphate

catalyzed by carbamoyl phosphate synthase

carbamoyl phosphate is converted to citrulline, and citrulline is eventually converted to arginine.

Arginine is degraded to urea and ornithine, in the presence of the enzyme, arginase.

The ornithine interacts with carbamoyl phosphate to form citrulline to repeat the cycle.

59
Q

What does a deficiency in carbamoyl phosphate synthase cause?

A

can lead to accumulation of ammonia

hyperammonaemia

60
Q

What can be done with excess ammonia?

A

can be diverted into glutamate.

excess glutamate in the presence of excess ammonia can also give rise to excess glutamine.

61
Q

What is glutamine used for?

A

used in the synthesis of purines

(the nitrogen in DNA molecules are derived from glutamine).

62
Q

How would you treatpatient with deficiency in carbamoyl phosphate synthase?

A

Would cause hyperammonaemia and accumulation of metabolic intermediates

Dialize blood

Then take blood samples to figure out which enzyme is affected

63
Q

Hemolytic anemia

A

due to enzyme deficiencies in the glycolytic pathway

Happens because red blood cells produce energy only from the glycolytic pathway.

64
Q

Hepatomegaly

A

enlargement of the liver causing distention of the abdomen, due to accumulation of glycogen

Happens due to deficiency in the enzyme glycogen phosphorylase (converts glycogen to glucose) and glucose-6 phosphatase in the liver.

65
Q

What happens if there is a deficiency of glycogen phosphorylase in muscle?

A

McArdle’s syndrome

Leads to muscle weakness during exertion

66
Q

Glucose 6- phosphatase deficiency

A

This enzyme converts G6P to Glucose in the last reaction of gluconeogenesis

Deficiency = Von Gierke’s syndrome

results in deficiency in gluconeogenesis from lactate, amino acids, and glycerol

Leads to hepatomegaly

67
Q

What would happen if oxidative phosphorylation of glucose is inhibited?

A

Lactic acidosis

68
Q

What would happen if glucose metabolism in cells or uptake is affected?

A

Ketosis

69
Q

What would happen If gluconeogenesis is prevented?

A

Hypoglycemia

Hypertriglyceridemia

70
Q

What is the treatment for people with carbohydrate metabolism disorders?

A

Patients with these disorders are advised to eat regularly (i.e. to avoid fasting), and monitor their carbohydrate intake.

Fasting for more than 8 hours is fatal in the case of Von Gierke’s.

71
Q

Hypoketosis in lipid metabolism disorders during fasting

A

If there is deficiency in beta-oxidation of fatty acids, relatively small levels of ketones will be produced than normal.

This is critical during fasting, because the brain uses ketones for energy.

72
Q

Hypoglycemia in lipid metabolism deficiencies

A

Will occur during fasting, if there is deficiency in beta-oxidation of fatty acids, because there will be no source of energy for gluconeogenesis.

73
Q

What occurs during lipid metabolism disorders during fasting

A

Hypoketosis

Hypoglycemia

Coma

Muscle weakness

Muscle cramping

Fat infiltration (droplets) of the liver because Acyl CoA can be converted to triglycerides.

Fatty degeneration of the liver

Fat droplets in the muscles

74
Q

Treatment for patients with lipid metabolism disorders

A

patients should avoid fasting

control their dietary intake because carbohydrates can be converted to fatty acids and eventually to triglycerides.

75
Q

Causes of disorders in amino acid metabolism

A

Inherited deficiencies

Aggravated by dietary protein

76
Q

Clinical features of disorders in amino acid metabolism

A

Encephalopathy causing poor intellectual development and delay

Neurotoxicity

Feeding difficulties

Vomiting

Ataxia (involuntary muscle movements)

Lethargy

Coma

77
Q

How to treat deficiencies in amino acid metabolism?

A

hemodialysis to lower the ammonia concentration and to stabilize the patient.

Longer-term treatment includes low protein diet, and use of benzoic acid and phenylacetic acid.

These acids can combine with glutamine and other amino acids to be eliminated as an alternative to urea.

78
Q

Requirement for vitamins and minerals

A

required in small quantities in our diets for normal growth, development and for the maintenance of health.

required in small quantities in our diets for normal growth, development and for the maintenance of health.

79
Q

Reasons for vitamin deficiencies

A

Inadequate intake (with normal requirements)

Impaired absorption

Impaired metabolism (If metabolism is necessary for function)

Increased requirement

Increased losses

80
Q

What is the most common deficiency worldwide?

A

Iron deficiency

81
Q

Cause of iron deficiency

A

Acute massive haemorrhage

chronic haemorrhage

growth in children

pregnancy and lactation

82
Q

What does iron deficiency lead to?

A

Microcytic hypochronic anemia

83
Q

What does accumulation of iron cause?

A

aka hemochromatosis

can induce organ damages, including liver, heart (cardiomyopathy), joint pain (arthralgia) , skin (hyperpigmentation) and pancreas (diabetes mellitus) resulting from pancreatic involvement.

84
Q

What can deficiencies in carbohydrate metabolism cause?

A

hemolytic anemia

hypertriglyceridemia

ketosis

could be fatal if fasting is prolonged.

Biochemistry (MPAS) (10 decks)

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