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Vitamin B > Vitamin B > Flashcards

Vitamin B Flashcards

1
Q

Name the B vitamins

A

Thiamin (B1)
Riboflavin (B2)
Niacin (B3)
Pantothenic Acid (B5)
Pyridoxine (B6)
Biotin (B7)
Folic Acid (B9)
Cobalamin (B12)

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2
Q

B vitamins are important in

A

Carbohydrate metabolism
Lipid metabolism
Protein Metabolism

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3
Q

B vitamins act as

A

a “coenzyme” in one/more of the chemical reactions necessary to generate energy from carbohydrate, fat, and protein.
Acts as carriers of electrons or atoms in metabolic reactions

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4
Q

Coenzyme form for Thiamin (B1)

A

Thiamine pyrophosphate (TPP)

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5
Q

Coenzyme form for Niacin (B3)

A

nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP)

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6
Q

Coenzyme form for Riboflavin (B2)

A

Flavin adenine dinucleotide (FAD), Flavin mononucleotide (FMN)

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7
Q

Coenzyme form for Panthothenic acid (B5)

A

Coenzyme Acetylation (CoA)

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8
Q

Explain the role of B vitamins in Pyruvate Dehydrogenase Reaction

A
  1. Vitamins B, specifically thiamin (B1), niacin (B3), riboflavin (B2), and pantothenic acid (B5), play crucial roles in the pyruvate dehydrogenase reaction as they are involved in the formation and function of coenzymes essential for this metabolic process.
  2. The pyruvate dehydrogenase complex requires these coenzymes to catalyze the conversion of pyruvate to acetyl-CoA.
  3. Thiamin is converted into thiamine pyrophosphate (TPP). TPP serves as a coenzyme in the decarboxylation step of pyruvate. In this step, TPP removes a carbon dioxide molecule from pyruvate, forming a temporary bond with the remaining two-carbon unit.
  4. Niacin, in the form of nicotinic acid or nicotinamide, is adenylated to form nicotinamide mononucleotide (NMN). NMN is adenylylated to form nicotinamide adenine dinucleotide (NAD). NAD serves as a coenzyme, accepting electrons during the oxidation step of the pyruvate dehydrogenase reaction. This oxidation step results in the conversion of the two-carbon unit in pyruvate to CO2 and the production of NADH.
  5. Riboflavin is converted into two coenzyme forms: Flavin Adenine Dinucleotide (FAD) and Flavin Mononucleotide (FMN). FAD and FMN serve as coenzymes in the pyruvate dehydrogenase complex. They participate in redox reactions, accepting and donating electrons during the conversion of pyruvate to acetyl-CoA.
  6. Pantothenic acid is phosphorylated and then converted into 4’-phosphopantetheine.
    4’-phosphopantetheine is adenylated to form dephospho-CoA. Dephospho-CoA is phosphorylated to form coenzyme A (CoA), the active coenzyme form. CoA combines with the oxidized two-carbon unit (acetyl group) to form acetyl-CoA, involving the formation of a thioester bond.
  7. Acetyl-CoA enters the TCA cycle, NADH is utilized within the TCA cycle for electron transport, and CO2 is released as a byproduct of the pyruvate dehydrogenase reaction.
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9
Q

Source of Thiamin (B1)

A

Abundant in germinating seeds and un-milled cereals
- Growing area of roots, leaves, and shoots

Animal products rich in thiamin
- Egg yolk, liver, kidney, lean meat

Also rich in whole grain foods, enriched cereal and soy milk

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10
Q

Thiamine pyrophosphate (TPP) acts as a coenzyme. What are the important reactions?

A
  1. Pyruvate dehydrogenase
    -Conversion of Pyruvate to Acetyl CoA (enters TCA cycle)
  2. Alpha-ketoglutarate dehydrogenase
    - Within the TCA cycle
    - Conversion of intermediate alpha-ketoglutarate to Succinyl CoA
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11
Q

Explain the role of Thiamine pyrophosphate (TPP) in Alpha-ketoglutarate dehydrogenase

A

The overall reaction catalyzed by the alpha-ketoglutarate dehydrogenase complex is:

Alpha-ketoglutarate + Coenzyme A + NAD → Succinyl CoA + NADH + CO2

Thiamine pyrophosphate (TPP), derived from thiamin (Vitamin B1), acts as a crucial coenzyme in the alpha-ketoglutarate dehydrogenase complex.

TPP facilitates the decarboxylation of alpha-ketoglutarate. During the reaction, TPP undergoes a series of changes in its redox state, enabling the removal of a carbon dioxide molecule from alpha-ketoglutarate.

The decarboxylation step results in the formation of a high-energy thiamin-bound intermediate, which then transfers the two-carbon unit to Coenzyme A, forming Succinyl CoA.
Succinyl CoA is a downstream intermediate in the TCA cycle and is further metabolized to produce ATP. As part of the reaction, NAD+ is reduced to NADH.

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12
Q

What is the name of Thiamin (B1) deficiency?

A

Beri beri

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13
Q

What does beri beri affect?

A

nervous and cardiovascular systems

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14
Q

What are the two main forms of beri beri?

A

dry beri beri and wet beri beri.

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15
Q

What are the symptoms of dry beri beri?

A

[mostly nervous system]

Fatigue and loss of appetite

Muscle weakness, cramps and loss of reflexes

Dysfunction of nervous system (paralysis of motor nerves)

Tacychardia (abnormally fast heart rate), heart failure (severe cases)

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16
Q

Explain the symptoms of dry beri beri

A

The neurological symptoms are due to thiamin’s role in maintaining the health of nerve tissues and its involvement in the synthesis of neurotransmitters.

Thiamin is involved in glucose metabolism, maintains the functions of the nerve membrane and supports the synthesis of myelin and several neurotransmitters, e.g., acetylcholine, serotonin, and amino acids (aspartate and glutamate)

Muscle weakness and cramps result from impaired energy metabolism, as thiamin is crucial for the conversion of pyruvate to acetyl-CoA in processes like the pyruvate dehydrogenase complex.

The heart is one of the most energy-demanding organs in the body, and thiamin is essential for the production of energy needed for the heart’s function

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17
Q

What are the symptoms of wet beri beri?

A

[Mostly cardiovasular system]

Severe edema in arms and legs

Enlargement of the heart (cardiomegaly)

Respiratory problems

Symptoms may last for years and then cardiac complications may develop and death occur quickly

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18
Q

Explain the symptoms of wet beri beri

A

The edema is a result of weakened heart function, leading to fluid retention in the extremities.

Enlargement of the heart and respiratory problems are indicative of severe cardiovascular involvement.

Wet beri beri often has a more acute and severe course, with potentially rapid progression to cardiac failure and life-threatening complications.

19
Q

What is infantile beri beri?

A

A severe form of thiamin (Vitamin B1) deficiency that primarily affects infants. It is particularly prevalent in regions with a high prevalence of maternal thiamin deficiency.

Important cause of child mortality in south-east Asia
The condition arises when the mother has insufficient thiamin levels, resulting in thiamin deficient breast milk

Thiamin is crucial for the infant’s metabolic processes, growth, and the proper functioning of the cardiovascular and nervous systems.

Infantile Beri-Beri starts in first few months of life

20
Q

What are the initial symptoms of infantile beri beri?

A

Anorexia (lack of appetite)
Vomiting
Abdominal distension (swelling or bloating of the abdomen)
Progression to edema

21
Q

What are the signs of infantile beri beri as the deficiency worsens?

A
  1. Cardiovascular signs - become more prominent, these may include tachycardia and signs of heart failure
  2. Neurological signs
    - may include irritability, difficulty sleeping, and changes in behaviour
  3. Without intervention, infantile beri beri can lead to a critical stage.
    - The infant may eventually experience coma due to severe neurological impairment
    If left untreated, it can lead to death
22
Q

What is the cause of Thiamin (B1) deficiency?

A
  1. Polished rice
    - In many countries, especially in Asia, polished rice is the major staple.
  • Brown rice has its bran and germ layer removed to produce white rice, a process known as polishing.
  • Polished rice is lower in thiamin compared to its unpolished counterpart
  1. Alcoholism
  • Alcoholism can contribute to thiamin deficiency due to several factors
  • Impaired absorption: chronic alcohol consumption can lead to damage in the gastrointestinal tract, impairing the absorption of essential nutrients, including thiamin.
  • Diminished utilization: alcohol can interfere with the body’s ability to use thiamin effectively in metabolic processes
  • Alcohol-Induced Thiamin Excretion: Alcohol consumption can increase the excretion of thiamin by the kidneys, further contributing to thiamin deficiency.
  • Diuretic effect: Alcohol is diuretic, leading to increased urine production and potential loss of water-soluble vitamins, including thiamin.
23
Q

Which B vitamin functions as two conezymes: Flavin monoclueotide (FMN) and
Flavin adenine dinucleotide (FAD)?

A

Riboflavin (B2)

24
Q

Coenzymes Flavin monoclueotide (FMN) and
Flavin adenine dinucleotide (FAD) are involved in oxidation reduction reactions including

A
  1. Electron transport
  2. Fatty acid synthesis and oxidation
25
Q

Explain the role of Riboflavin (B2) in the Electron Transport Chain

A

The first step in the transfer of electrons through the electron transport chain is the oxidation of NADH and FADH2 by the enzyme NADH dehydrogenase (Complex I) and succinate dehydrogenase (Complex II), respectively.

NADH is an electron carrier and is able to donate electrons.

NADH binds to Complex I and transfers 2 electrons to Flavin mononucleotide (FMN). NADH is then oxidised to NAD+ by NADH dehydrogenase and FMN is reduced to FMNH2. FMNH2 transfers the electrons to a series of Fe-S proteins which then transfers electrons to ubiquinone (Coenzyme Q).

Succinate binds to Complex II and is oxidised to Fumarate by Succinate Dehydrogenase.

Succinate loses two electrons during the reaction. The electrons are then transferred to flavin adenine dinucleotide (FAD), a coenzyme bound to Complex II. This results in the reduction of FAD to FADH2, which is an electron carrier and is able to transfer electrons to Fe-S clusters. The electrons are then transferred to Coenzyme Q from Fe-S clusters.

26
Q

Source of Riboflavin (B2)

A

Dairy products (milk, yogurt, cheese)

Poultry, meat and fish, eggs

Asparagus, broccoli and spinach

27
Q

What is the name of Riboflavin (B2) deficiency?

A

Ariboflavinosis (cracking of the mouth)

28
Q

Explain Ariboflavinosis

A

Ariboflavinosis typically occurs in the context of severe malnutrition and often accompanies deficiencies of other B vitamins, such as niacin (B3), thiamin (B1), and vitamin B6. This is because these nutrients often occur in the same food sources.

29
Q

What are the specific symptoms of Ariboflavinosis?

A

Cracking around corners of mouth

Magenta tongue

Hypersensitivity to light

Reddening of cornea

Skin rash

30
Q

What is the generic term for nicotinic acid and nicotinamide?

A

Niacin (B3)

31
Q

Source of Niacin (B3)

A

Meat, beef, tuna and other fishes

Whole grain, wheat bran

Asparagus

Peanuts

32
Q

Niacin can be synthesized from the amino acid….

A

Tryptophan, which is an essential amino acid obtained from the diet

33
Q

Functions of Niacin (B3)

A

Its primary functional role is associated with its involvement in the formation of coenzymes: nicotinamide adenine dinucleotide (NAD) & nicotinamide adenine dinucleotide phosphate (NADP).

34
Q

NAD and NADP are involved in which reactions?

A
  1. Carbohydrate metabolism
    - Glycolysis
    - TCA Cycle
  2. Lipid metabolism
    - Fatty acid synthesis/oxidation
  3. Protein metabolsim
    - Amino acid synthesis/oxidation
35
Q

NADH and NADPH have similar structure but different functions. Explain

A

NADH is often involved in energy producing reactions

  • Glycolysis, oxidative decarboxylation of pyruvate, oxidation of acetyl Co-A via krebs cycle
  • Transfers electrons through the electron transport chain
  • NADH is oxidised by the respiratory chain to generate ATP

NADPH is often involved in biosynthetic reactions (anabolic)

  • Generated in the pentose phosphate pathway
  • Synthesis of macromolecules (fatty acids, cholesterol, and steroid hormone)
36
Q

What is the name of Niacin (B3) deficiency?

A

Pellagra

37
Q

Explain what is pellagra

A

Pellagra is a condition caused by a deficiency of niacin (Vitamin B3) in the diet. It results from a prolonged inadequate intake of niacin or tryptophan, an amino acid that can be converted into niacin in the body. Pellagra is characterized by a set of symptoms affecting the skin, digestive system, and nervous system.

38
Q

Niacin deficiency will cause:

A

Dermatitis

Diarrhea

Dementia

Death (If left untreated)

39
Q

What are the 3 classes of Pellagra symptoms?

A

Reddening of skin

Lesions of mucous membranes, including mouth, tongue, stomach and intestine

Changes in the nervous system

40
Q

What are the early signs of Pellagra?

A

Inflammation and soreness of mouth

Reddening of skin

Swollen tongue

41
Q

The symptoms of pellagra can progress to

A

Anorexia

Abdominal discomfort

Diarrhoea

42
Q

What are the mental symptoms of pellagra

A

Lassitude (fatigue)

Apprehension

Depression

Loss of memory

Hysteria

Maniacal outbursts

43
Q

What is the cause of Niacin (B3) deficiency?

A

Traditionally associated with populations dependent on corn as a major staple.

Corn contains niacin, but it is bound by a protein called niacytin, which reduces its absorption in the human body.

In corn, niacin is present in a form known as niacytin, which is a complex of niacin and proteins. This bound form of niacin is not readily absorbed during digestion, limiting the availability of niacin for the body to utilize.

Rare in more affluent countries

44
Q
A

Vitamin B (1 decks)

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