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ZINC IN NUTRITION
1509, recognized as element Essentiality demonstrated
Plants: 1869 Animals: 1934
Deficiency Considered unlikely until 1955
conditioned human deficiency demonstrated in 1956
1961, hypogonadal dwarfism suggested to be zinc deficiency
sources
Relatively abundant mineral Good sources: shellfish, beef and other red meats Slightly less good: Whole-grains
most in bran and germ portions 80% lost to milling phytates, hexa & penta phosphates depress
absorption P/Zn ratios of 10 or more
Relatively good sources: nuts and legumes Eggs, milk, poultry & fish diets lower than
pork, beef, lamb diets High meat diets enhance absorption
280g or 10 oz fits right into food pyramid guide cys & met form stable chelate complexes
Zinc absorption is greater from a diet high in animal protein than a diet rich in plant proteins . Phytates, which are found in whole grain breads, cereals, legumes and other products, can decrease zinc absorption .
Distribution
Whole body: 1.5g (female)-2.5g (male) Skeletal Muscle 57% Bone 29% Skin 6% Liver 5% Brain 1.5% Kidneys 0.7% Heart 0.4% Hair ~0.1% Blood Plasma ~0.1
sources
Foods contain element zinc, much of it bound to protein or DNA.
Oysters (> 70 mg per
serving).
Meats (2-3 mg/100g).
Shellfish (2.7 mg/100g)
Other good food sources include: beans, nuts, certain seafood,
whole grains, fortified breakfast cereals, and dairy products .
Role of Zinc
Required for growth in children and infants.
absorption
GIT modulates the quantity of exogenous dietary zinc absorbed and the quantity of endogenous zinc excreted
More than 70% of a small zinc dose (less than 3 mg) is absorbed from the small intestine.
Maximum absorption occurs in duodenum
There is sustained release from enterocytes into portal circulation for ~ 9h
Zinc absorption mainly achieved by 2 families of zinc transporters;
1. ZIP Family2. ZnT Family
Excretion
Routes: intestine, kidneys, integument, and semen
After a meal, maximum zinc secretion occurs through pancreatobiliary secretions
Maximum reabsorption occurs from mid-jejunum and ileum
Total amount excreted = Amount secreted – Amount reabsorbed
Excretion of endogenous zinc by the intestine depends on the ‘zinc status’ of the body.
Zinc deficiency
Causes; Malnutrition Alcoholism Malabsorption Burns Chronic renal disease Acrodermatitis enteropathica
Signs Growth retardation Delayed sexual maturation & impotence
Impaired testicular development Hypogonadism & hypospermia Alopecia Acroorifical skin lesions
Other, glossitis, alopecia & nail dystrophy Immune deficiencies Behavioral changes
Night blindness Impaired taste (hypoguesia) Delayed healing of wounds, burns, decubitus
ulcers Impaired appetite & food intake Eye lesions including photophobia & lack of
dark adaptation
Zinc deficiency
1. Severe dermatitis, alopecia, diarrhea, emotional disorder,
weight loss, infections, hypogonadism in males2. Moderate
growth retardation and delayed puberty in adolescents, hypogonadism in males, rough skin, poor appetite, mental lethargy, delayed wound healing, taste abnormalities and abnormal dark adaptation
3. Mild oligospermia, slight weight loss and
hyperammonaemia
Deficiency during pregancy
Zn deficient rats failed to conceive Abnormalities of blastocyst development Offspring had high incidence of
abnormalities Deformities of brain, skull, limbs, eyes, heart,
lungs Low Zn intake during the third trimester
may not have such profound effects Main stages of differentiation are already
complete Can result in low birth weight, and prolonged
and difficult parturition
(Left) This boy has a zinc deficiency, and his hair is very thin and sparse; (right) after treatment his hair is
growing more strongly)
Zinc toxicity
Excess accumulation within cells may disrupt functions of biological molecules Protein, enzymes, DNA
Leads to toxic consequences Anemia
Impaired copper availability Acute excessive intakes
Local irritant to tissues and membranes GI distress, nausea, vomiting, abdominal cramps,
diarrhea Relatively non-toxic
Sources of exposure – drinking water, feed, polluted air
Acrodermatitis enteropathica
Genetic disorder of zinc absorption. Presents during infancy. Characterized mainly by a triad
consisting of1. Acral dermatitis2. Alopecia3. diarrhea
Age
In infants bottle fed with bovine milk, days to week, breast fed infants soon after feeding
In older children its acquired zinc deficiency.
Etiology
Acrodermatitis enteropathica; autosomal recessive trait resulting in failure to absorb zinc.
Acquired zinc deficiency; secondary to reduced dietary intake , malabsorption, increased urinary loss, etc.
Clinical evaluation
Skin mucous membrane and hair are involved.
Lesions are pink and later become brightly erythematous.
Impaired wound healing. Irritable with depressed mood Growth failure
Other symptoms
Loss of weight Sensitivity to light Diarrhea Conjuctivitis Red glossy tongue and mouth ulcers
Investigations
Complete blood count Serum/ plasma zinc levels Urine; zinc excretion is reduced Dermatopathology; intraepidermal clefts
and blisters
treatment
1mg/kg body weight of oral zinc supplementation per day of life.
Zinc gluconate better tolerated than sulfate.
Dietary or iv supplementation with zinc salts with two or three times , the RDA restores normal zinc status in days or week.
5 days of zinc replacement
Treatment of diarrhea
All children above 6months should receive a uniform dose of 20mg elemental zinc as soon as diarrhoea starts and continue for 14 days.
2 to 6mnths- 10mg/day for 14 days.