Chapter 10 - Nutrients Involved in Energy Metabolism Flashcards

1
Q

How are vitamins different from the macronutrients?

A
  • Individual molecules i.e. not linked together
  • Not a source of energy
  • Co-activity in metabolic enzyme function
  • µg or mg
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2
Q

What are the fat-soluble vitamins?

A

A, D, E, and K

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3
Q

What are the water-soluble vitamins?

A

C, and Bs (thiamin, niacin, riboflavin, B6, folate, B12, pantothenic acid, biotin)

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4
Q

What are the major minerals?

A
  • Sodium
  • Chloride
  • Potassium
  • Phosphorus
  • Calcium
  • Magnesium
  • Sulphur
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5
Q

What are the trace minerals?

A
  • Iodide
  • Manganese
  • Chromium
  • Selenium
  • Fluoride
  • Iron
  • Zinc
  • Copper
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6
Q

What is the difference between vitamins and minerals?

A

Vitamins are organic, while minerals are inorganic

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7
Q

What is the role of micronutrients in energy metabolism?

A

Working with enzymes or hormones to extract the energy found within the bonds of macronutrients

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8
Q

What is the main function of Thiamin?

A

It is the vitamin portion of coenzyme TPP (Thiamin pyrophosphate); it is involved in both glycolysis and TCA

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9
Q

What are some minor functions of thiamin? (2)

A
  • Membrane function of neuronal cells
  • Biosynthesis of lipid and acetyl-CoA
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10
Q

Where is thiamin absorbed?

A

In the SI, directly to the bloodstream

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11
Q

How is thiamin absorbed?

A
  • At low concentrations (<1.5 uM): carrier-mediated transport (ThTr-1 and ThTr-2)
  • At high concentrations (>5mg) : passive diffusion
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12
Q

Thiamin RDA

A
  • Men: 1.2 mg/day
  • Women: 1.1 mg/day
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13
Q

What are significant food sources of Thiamin?

A
  • Whole grain, fortified, or enriched grains
  • Moderate amounts in all nutritious foods (vegetables, milk, soy)
  • Pork
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14
Q

What commonly causes thiamin deficiency?

A
  • Malnutrition/empty kcal foods
  • Consuming milled, non-enriches grains
  • raw fish
  • alcoholism
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15
Q

What does thiamin deficiency result in?

A

Beriberi

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16
Q

What are the clinical symptoms of thiamin deficiency?

A
  • Englarged heart, cardiac failure
  • Muscular weakness
  • Paralysis of motor nerves of eye
  • Apathy, poor short-term memory, confusion, irritability
  • Anorexica, weight loss
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17
Q

What is the difference between wet and dry beriberi?

A
  • Wet involves the cardiovascular and lymphatic systems; results from physical exertion with high CHO intake. Results in edema
  • Dry involves the neural system; results from chronic caloric restriction. Results in neural, muscle wasting and neural effects
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18
Q

What is Wernicke-Korsakoff syndrome?

A
  • A form of dry beriberi
  • Comes from alcoholism or impaired/absorption or excretion of B1
  • Results in neural deficiencies (disorientation, staggering gait, short-term memory loss, jerky eye movements)
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19
Q

What is the toxicity risk of Thiamin?

A

There are none (no TUL) as it’s a water-soluble vitamin

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20
Q

What is the main function of riboflavin?

A

Coenzyme for FMN and FAD; involved in TCA (accept/donate), delivery of H+ and e- to ETC, and fatty acid oxidation

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21
Q

Where is riboflavin absored?

A

In the SI, directly into the bloodstream

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22
Q

How is riboflavin absorbed?

A
  • First it is digested in the SI through proteolysis or hydrolysis via pyrorphosphatase
  • Enterocyte absorbption is done through carrier mediated transport (RCP)
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23
Q

Riboflavin RDA

A
  • Men: 1.3 mg/day
  • Women: 1.1 mg/day
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24
Q

What are significant food source for riboflavin?

A
  • Milk products
  • Enriched/whole grains
  • Liver
  • Dark leafy greens
  • Yeast
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25
Q

What commonly causes riboflavin deficiency?

A
  • Often accompanies other nutrient deficiencies
  • Low micronutrient diet
  • Absorprtion disorder
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26
Q

What is riboflavin deficiency?

A

Ariboflavinosis

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27
Q

What are the clinical symptoms of ariboflavinosis?

A
  • Inflamed eyelids
  • Reddening of cornea
  • Light sensitivity
  • Sore throat
  • Cheilosis
  • Glottitis
  • Skin lesions with greasy scales
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28
Q

What is the toxicity risk of riboflavin?

A

There is none as its water soluble

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29
Q

What is the main function of niacin?

A

Part of coenzymes NAD and NADP used in energy metabolism (glycolysis, TCA, ETC, biosynthesis, fatty acid oxidation)

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30
Q

Where is niacin absorbed?

A

In the SI, directly to the blood stream

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31
Q

How is niacin absorbed?

A
  • First it is digested in the SI through proteolysis or hydrolysis via pyrorphosphatase
  • Enterocyte absorbption is done through carrier mediated transport (SMCT1, SMTC2, and MCT1) or passive diffusion
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32
Q

Niacin RDA

A
  • Men: 16 mg NE/day
  • Women: 14 mg NE/day
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33
Q

How is niacin formed in the body?

A
  • Endogenous synthesis from dietary trptophan
  • 60 mg tyrptophan to make 1 mg B3
34
Q

What are significant food sources of niacin?

A
  • Milk, eggs, meat, poultry, fish
  • Whole grains, enriched breads and cereals, nuts
  • All protein-containing foods
35
Q

What is a NE equivalent to?

A

1mg niacin or 60mg tryptophan

36
Q

What causes niacin deficiency?

A
  • Corn or sorghum diet, which is low protein and low available niacin
  • Inability to use niacin (genetic/malabsorption disorders, alcoholism, medications)
37
Q

What does a niacin deficiency cause?

A

Pellagra

38
Q

What are the clinical symptoms of niacin deficiency?

A
  • Diarrhea
  • Vomiting
  • Glossitis
  • Depression, apathy, fatigue, dementia
  • Bilateral symmetrical dermatitis on areas exposed to sunlight
39
Q

What is the toxicity risk of niacin?

A

TUL: 35 mg/day

40
Q

What is niacin flush?

A

When oversupplementation (3-4x DRI) of niacin occurs; causes painful flush, excessive sweating, blurred vision, and gastro sensitivity

41
Q

Why do individuals take pharmacological doses of niacin?

A

High doses of niacin (~2000mg) can decrease total cholesterol, VLDL, and LDL; increases HDL

42
Q

What is the main function of biotin?

A

A coenzyme to carboxylases
* TCA: recycling of oxaloacetate
* Gluconeogenesis
* Fatty acid synthesis
* Breakdown of some fatty acids and amino acids

43
Q

Where is biotin absorbed?

A

In the SI, directly into the bloodstream

44
Q

How is biotin absorbed?

A
  • First it is digested through proteolysis (a large fraction of biotin is covalently bonded to lysine)
  • Absorbed throught the SMVT in SI
45
Q

Biotin RDA

A

No RDA; AI for adults in 30 mcg/day

46
Q

What are significant food sources for biotin?

A

Widespread in foods
* Liver
* Egg yolds
* Soy beans
* Fish
* Whole grains
* Produced by GI bacteria

47
Q

What is biotin deficiency caused by?

A
  • Raw egg whites; they contain avidin which binds to biotin, preventing absorption
  • Protein-energy malnutrition
48
Q

What are the symptoms of biotin deficiency?

A
  • Skin rash
  • Hair loss
  • Neurological impairment
49
Q

What is the toxicity risk of biotin?

A

There is no toxicity risk with biotin

50
Q

What is biotinidase deficiency?

A

Inherited disorder where there is a deficiency of biotinidase, an enzyme that helps recycle biotin to be reused by the body

51
Q

What are the symptoms of bioinidase deficiency?

A
  • Depression, lethargy, hallucinations
  • Numb or tingling sensation in limbs
  • Red, scaly rash around the eyes, nose, and mouth
  • Hair loss
52
Q

How can biotinidase deficiency be corrected?

A

Supplementing dietary, free biotin

53
Q

What is the main function of panthothenic acid (B5)?

A

Substrate for Coenzyme A synthesis
* CoA is used in energy metabolism
* Needed for synthesis of acyl carrier protein which is involved in fatty acid synthesis

54
Q

How is CoA turned into free pantothenic acid during digestion?

A

Action of alkaline phosphatase in the SI

55
Q

How is pantotheic acid digested?

A

Through the SMVT in the SI, directly into bloodstream

56
Q

RDA Pantothenic Acid

A

No RDA; AI is 5 mg/day for adults

57
Q

What are significant food sources for pantothenic acid?

A

Widespread in plant and animal foods
* Organ meats
* Mushrooms
* Avocados
* Broccoli
* Whole grains

58
Q

What causes pantothenic acid deficiency?

A

Lack of the pantothenate kinase gene (PANK2); this is the gene that encodes pantothenate kinase which is a regulatory enzyme in the synthesis of CoA

59
Q

What is the result of pantothenic acid deficiency?

A

PKAN (Pantothenate kinase-associated neurodegeneration)

60
Q

What are the symptoms of PKAN?

A
  • Insomnia, fatigue, depression, irritability
  • Hypoglycemia, increased sensitivity to insulin
  • Vomiting, nausea, stomach cramps
61
Q

what is the toxicity risk of pantothenic acid?

A

None; possible upset stomach with supplement doses

62
Q

What is the main function of vitamin B6?

A

Coenzyme; either as PLP (Pyridoxal phosphate) and PNP (Pyridoxamine phosphate)
* Transamination reactions
* Conversion of tryptophan to niacin
* Synthesis of serotonin
* Synthesis of heme, nucleic acids, phosphatidycholine
* Metabolism of homocysteine

63
Q

How is vitamin B6 digested?

A

B6 is found bound to glucoside
* hydrolysis of the glucoside by action of β-
glucosidases PLP/PMP hydrolyzed by a
phosphatase

64
Q

How is Vitamin B6 absorbed?

A

Directly into the bloodstream from the SI through passive diffusion

65
Q

RDA B6

A

1.3 mg/day for adults

66
Q

What are significant food sources for B6?

A
  • Meats
  • Potatoes
  • Legumes
  • Non-citrus fruits
  • Fortified cereals
  • Liver
  • Soy products
67
Q

What causes B6 deficiency?

A

Alcoholism and Isoniazid (medication used for TB)

68
Q

What are symptoms of B6 deficiency?

A
  • Scaly dermatitis
  • Microcytic anemia
  • Depression, confusion
  • Abnormal brain wave pattern, convulsions
  • Elevated homocysteine
69
Q

What is toxicity risk of B6?

A

TUL: 100mg/day
* Depression, fatigue, irritability, headaches
* Sensory neuropathy
* Skin lesions
* neurological damage

70
Q

Why may someone take supplements of B6?

A
  • Reduces plasma homocysteine
  • Possibly beneficial for carpal tunnel syndrome and PMS
71
Q

What is the main function of folate?

A

1 Carbon metabolism.
It is used in:
* DNA synthesis
* Amino acid metabolism
* Vitamin B12 activation to co-enzyme

72
Q

What are the additional benefits of folate in the diet?

A
  • CVD
    * folate assists homocysteine catabolism
  • Cancer
    * sufficient folate reduces risk of cancer but excess folate may exacerbate progession cancer and cause initiation of cancer
  • Prevention of neural tube defects (e.g. spina bifia/anencephaly)
73
Q

What is the bioavailability of differing types of folate?

A
  • Naturally found: 50%
  • Added or synthetic: 100%
74
Q

What are the folate consumption reccommendations for prevention of neural tubes defects?

A
  • Supplements at least 4 weeks prior to conception
  • All women childbearing age 400 mcg/day
75
Q

How do you calculate dietary folate equivalents?

A

DFE = mcg good folate = (1.7 x synthetic folate)

76
Q

What are significant food sources for folate?

A
  • Fortified grains, milk, juice
  • Leafy green vegetables
  • Legumes
  • Seeds
  • Liver

Folate is susceptible to heat loss

77
Q

RDA Folate

A

400 mcg DFE/day for adults, 600 mcg/day if pregnant

78
Q

What is the toxicity risk of folate?

A

1000 mcg DFE/day; only applies to synthetic forms or fortified foods
* Can mask a B12 deficiency and cause neurological damage

79
Q

What causes folate deficiency?

A
  • Typically a lack of dietary folate; diets lacking fresh vegetables
  • Malabsroption
  • Increased metabolic requirement
80
Q

What are the symptoms of folate deficiency?

A
  • Anemia
  • Smooth, red tongue
  • Mental confusion
  • Weakness, fatigue, irritability, headache
  • Increased homocysteine
  • Neural tube defects
81
Q
A