Other Trace Minerals (Chromium, Manganese, Molybdenum) Flashcards

1
Q

Cr supplements

A

2nd largest-selling mineral supplement in
the U.S.
Promises:
Weight loss with increased lean body mass and
decreased fat mass.
Improved control of blood glucose.

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2
Q

most stable form of Cr

A

Cr+3 in foods

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3
Q

Cr absorption

A

Absorption low (0.4-2.5%) – mechanism unclear
Dietary factors/ligands such as amino acids improve absorption by ↑
solubility, prevent olation (reaction of Cr with OH- in small intestine to form
polymers that precipitate out)

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4
Q

Cr supplements contain:

A

Inorganic Cr salt. e.g. Cr chloride, but likely not well absorbed unless with vitamin C
Organic Cr complex: (foods)
Cr-amino acids
Cr picolinate and Cr nicotinic acid are common

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5
Q

Function of Cr

A

Function: major = potentiate action of insulin
via Chromodulin (oligopeptide = GLY-CYS-ASP-GLU)
How:? (Fig. 13.22)
Cr is transported by transferrin
TfR used to get Cr-transferrin into cells
Cr + apochromodulin = chromodulin
which binds the insulin receptor -> amplifies the signal

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6
Q

insulin promotes

A

cellular uptake of glucose, storage of
energy (glucose as glycogen; fatty acids as fat),
muscle protein synthesis

**Cr added will only see change if person is inadequate

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7
Q

insulin inhibits

A

glycogen breakdown, gluconeogenesis,
lipolysis, protein degradation.

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8
Q

Chromium and Obesity?

A

Early evidence for body weight changes, as well as diabetes
control?

Well-controlled studies show:
no effects on strength, accretion of muscle, or fat loss
results on weight loss are minor and conflicting

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9
Q

Cr Sources

A

widespread
note: molasses, brewer’s yeast (beer), dark choc, tea, coffee
stainless steel equipment
lose Cr when processing sugar

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10
Q

Cr DRI

A

AI=
M: 35mch
F: 25mcg
No UL (Cr+6 industrial poison)

intake studies: intake of healthy individuals, balanced diets

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11
Q

Cr Deficiency

A

in humans rare
discovered in Canada, hospital patients showed symptoms of diabetes (wgt loss, neuropathy, impaired glucose tolerance)
Cr was added to feeding solution and now routinely added when intravenous nutrition used as complete food source

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12
Q

Manganese
Functions and mechanisms of action

A

Constituent of metalloenzymes – across many classes.
Bone, cartilage, and connective tissue synthesis
Urea synthesis
Amino acid/carbohydrate metabolism
Antioxidant roles
MnSOD – mitochondrial superoxide dismutase

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13
Q

Mn excretion

A

Mostly in bile
Like Cu, if a patient has problems in secreting bile
from the liver, we are very cautious about adding Mn
to an intravenous feeding.
Little in urine
Small amounts in sweat and skin desquamation

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14
Q

Mn Food sources

A

Whole grain cereals, nuts, and leafy vegetables
i.e. plant > animal sources

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15
Q

Digestion and absorption

A

Females may absorb greater amounts than M
Reasons unclear
Low < 5%; tightly regulated
Absorption poorly understood
Absorption throughout small intestine

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16
Q

Mn DRI

A

AI=
Men: 2.3 mg; women: 1.8 mg

17
Q

Mn Deficiency

A

Very rare
From experimental study, deficiency signs are impaired
growth, skeletal defects, transient skin rash, altered lipid
and carbohydrate metabolism.

18
Q

Mn Assessment of Nutriture

A

Plasma/serum/whole blood concentrations
Enzyme activity
Mn-SOD and arginase, but not good indicators

19
Q

Mn toxicity

A

(of much interest)
Tolerable Upper Intake Level: 11 mg/day
Causes/Sources:
Airborne Mn - welders, battery manufacturers
High well water Mn – some southern US states
Liver failure
Neurotoxicity = current research
Cognitive and motor (Parkinson’s-like symptoms)
Mechanisms of neurotoxicity unknown

20
Q

Molybdenum general functions

A

Mo, as molybdopterin, functions as co-factor in only 4
metalloenzyme functions
all catalyze oxidation-reduction reactions.
Mo is essential for enzyme activity.

21
Q

4 enzymes Mo is in

A
  1. Sulfite oxidase
  2. Xanthine oxidoreductase
  3. Aldehyde oxidase
  4. Amidoxime reductase
22
Q

sulfite oxidase

A

Sulfur metabolism – final step in oxidation of cysteine and methionine

sulfite to sulfate ->
Mo+6 regenerated to Mo+4 ->
2 Fe+3 regenerated to 2 Fe+2 <-
cytochrome C (ox) to cytochrome C (reduced) >

23
Q

Xanthine oxidoreductase

A

Purine degradation
Converts hypoxanthine to xanthine, and converts
xanthine to uric acid.

24
Q

aldehyde oxidase

A

Various roles – aldehyde oxidation
retinal -> retinoic acid
drug metabolism

25
Q

Amidoxime reductase

A

physiological function is unknown
role in lipogenesis
reductive activation of N-hydroxylated prodrugs

26
Q

Mo food sources

A

Legumes, meat, fish, poultry, and grains

27
Q

Mo absorption

A

Poorly understood
~50-85%

28
Q

Mo RDA

A

adults= 45mcg

29
Q

Molybdenum Deficiency

A

No human report of Mo deficiency due to low dietary
intake.
One isolated report from an adult male on long-term
total parenteral nutrition

30
Q

Assessment of Mo nutritional status

A

No validated indicators

31
Q

Molybdenum – Toxicity and UL

A

UL= 2 mg
In cattle and sheep: high Mo intake causes secondary Cu deficiency
In Armenia, high soil Mo exposure in humans associated with aching joints, gout from high uric acid.