Consequences of Mineral and
Deficiencies
Part II
Se
Selenium
Se
Overview: Selenium is one of the major mineral antioxidants in animal
systems. Therefore, all functions that are related to selenium deficiency
have to do with an impairment in the system’s role to curb the damaging
effects of oxidants
Selenium Levels in Soil
Se
Se
White Muscle Disease (WMD)
• WMD: Selenoprotein W deficient degenerative
muscle disease found in all large animals
(especially sheep and goats)
– most commonly found in newborns or fast growing
animals
Se
Se
Deficiency
– Keshan Disease
Se
Se
• Causes congestive cardiomyopathy (disease of the
myocardium with deterioration in function)
• First observed in the Keshan province of China.
• It was due to low amounts of selenium in the soil.
•Left ventricle of heart has a thickened, dilated left ventricle with
subendocardial fibrosis apparent with amplified whiteness of endocardium.
Deficiency Continued
• Kashin-Beck Disease
– Degeneration of articular
cartilage between joints
(osteoarthritis)
– Associated with poor selenium
status in areas of northern
China, North Korea, and
eastern Siberia.
– Affects children between 5
and 13 years of age.
– Severe forms may result in
joint deformities and dwarfism.
– There is little evidence that
improving selenium nutritional
status prevents Kashin-Beck.
– Other causative factors have
been suggested: fungal toxins
in grain, iodine deficiency, and
contaminated drinking water.
Se
Goiter
• Since Selenium is
required to convert
T4 (inactive) into T3
(active).
• A deficiency in
Selenium could
cause an enlarged
thyroid gland in the
neck.
Se
Manganese
Manganese serves as a cofactor for metalloenzymes, the three most
prominent are:
1. Arginase (urea cycle)
2 Pyruvate carboxylase (gluconeogenesis)
3. Mitochondria superoxide dismutase (antioxidant)
HUMAN STUDIES
Deficiencies of Mn rarely occur in humans
Doisy (1972): Human subjects fed a diet containing 0.34 mg/day Mn
1.
2.
3.
4.
Slight reddening of the hair
Scaly transient dermatitis
Hypocholesterolemia
Moderate weight loss
Friedman et al (1987): Human subjects fed 0.11 mg/day Mn
1. Transient dermatitis in 5 or 7 subjects
2. Hypocholesterolemia
ANIMAL STUDIES
Multiple species
1.
2.
3.
4.
Disorder in lipid and carbohydrate metabolism
Impaired growth
Impaired skeletal development (neonates)
Impaired reproductive function (disturbance in estrous cycle,
testicular degeneration)
5. Low viability of young at birth, ataxia in viable young
6. Decrease in egg production, shell quality, hatchability in poultry
7. Impaired embryonic development
1. Shortening of the limbs
2. Enlargement of joints
3. Twisting of limbs
-Mn
Manganese
deficiency in
24 day-old chicks
+Mn
Swollen joints
(After Leach and Harris,
1999)
Chromium
Deficiency
Typical Symptoms
1. A diabetic-like state (hyperglycemia, insulin resistance)
2. Growth impairment
3. Elevated blood lipids
4. Increased aortic plaque formation
5. Decreased fertility and longevity
Deficiency (cont.)
• Situations
– Infants and children malnutrition:
diabeticlike disorder of metabolism
– Impaired glucose tolerance
– Disturbances in lipid and protein
metabolism
– TPN patients (weight loss)
Glucose Tolerance
-Cr
Blood
glucose
+Cr
0
1
2
3
4
Post Absorption (hr)
Chromium in Human and Animal Nutrition: A Status Report
The essentiality of chromium (Cr) in animal and human nutrition is now
well accepted. Its well established that Cr potentiates insulin sensitivity. Cr
deficiency is known to occur in patients on total parenteral nutrition without
added Cr. Such patients show impaired glucose tolerance, hyperglycemia,
relative insulin resistance, peripheral neuropathy, and a metabolic
encephalopathy. These symptoms are reversed by Cr repletion. Cr deficiency is
also seen in diabetes mellitus, pregnant and parous (having given birth) women,
and the aged population. Cr supplementation improves glucose metabolism in
glucose intolerant individuals and decreases total/HDL cholesterol ratio.
Whether Cr supplementation has long-term health benefits is unknown. It is still
unclear whether Cr deficiency, latent or overt, is a common occurrence in
humans on normal diets without added Cr. Cr contamination of food by the use
of stainless steel processing equipment and eating utensils, and the lack of a
clinically feasible test for Cr deficiency continue to impede progress in Cr
research. Nevertheless, there is considerably clarity as to plasma and urine Cr
levels, food and tissue Cr content, and metabolic pathways of Cr metabolism.
Critical questions still remain regarding the role of Cr in human nutrition.