consequences of mineral and deficiencies part ii

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Consequences of Mineral and Deficiencies Part II

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Page 1: Consequences of Mineral and Deficiencies Part II

Consequences of Mineral and Deficiencies

Part II

Page 2: Consequences of Mineral and Deficiencies Part II

Selenium

SeSe

Page 3: Consequences of Mineral and Deficiencies Part II

SeSe

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

Page 4: Consequences of Mineral and Deficiencies Part II

Selenium Levels in Soil SeSe

Page 5: Consequences of Mineral and Deficiencies Part II

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

SeSe

Page 6: Consequences of Mineral and Deficiencies Part II

Deficiency– Keshan Disease

• 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 Left ventricle of heart has a thickened, dilated left ventricle with subendocardial fibrosis apparent with amplified whiteness of endocardium.subendocardial fibrosis apparent with amplified whiteness of endocardium.

SeSe

Page 7: Consequences of Mineral and Deficiencies Part II

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.

SeSe

Page 8: Consequences of Mineral and Deficiencies Part II

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.

SeSe

Page 9: Consequences of Mineral and Deficiencies Part II

Manganese

Page 10: Consequences of Mineral and Deficiencies Part II

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)

Deficiencies of Mn rarely occur in humans

Doisy (1972): Human subjects fed a diet containing 0.34 mg/day Mn

1. Slight reddening of the hair2. Scaly transient dermatitis3. Hypocholesterolemia4. Moderate weight loss

Friedman et al (1987): Human subjects fed 0.11 mg/day Mn

1. Transient dermatitis in 5 or 7 subjects2. Hypocholesterolemia

HUMAN STUDIES

Page 11: Consequences of Mineral and Deficiencies Part II

ANIMAL STUDIES

Multiple species

1. Disorder in lipid and carbohydrate metabolism2. Impaired growth3. Impaired skeletal development (neonates)4. Impaired reproductive function (disturbance in estrous cycle,

testicular degeneration)5. Low viability of young at birth, ataxia in viable young6. Decrease in egg production, shell quality, hatchability in poultry7. Impaired embryonic development

1. Shortening of the limbs2. Enlargement of joints3. Twisting of limbs

Page 12: Consequences of Mineral and Deficiencies Part II

Manganese deficiency in

24 day-old chicks +Mn

-Mn

Swollen joints

(After Leach and Harris, 1999)

Page 13: Consequences of Mineral and Deficiencies Part II

Chromium

Page 14: Consequences of Mineral and Deficiencies Part II

Typical Symptoms

1. A diabetic-like state (hyperglycemia, insulin resistance)

2. Growth impairment

3. Elevated blood lipids

Deficiency

4. Increased aortic plaque formation

5. Decreased fertility and longevity

Page 15: Consequences of Mineral and Deficiencies Part II

Deficiency (cont.)

• Situations– Infants and children malnutrition:

diabeticlike disorder of metabolism

– Impaired glucose tolerance

– Disturbances in lipid and protein metabolism

– TPN patients (weight loss)

Page 16: Consequences of Mineral and Deficiencies Part II

Post Absorption (hr)

Glucose Tolerance

-Cr

+Cr

Blood glucos

e

0 1 2 3 4

Page 17: Consequences of Mineral and Deficiencies Part II

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.

Chromium in Human and Animal Nutrition: A Status Report