Assignment for 2nd Semester Hons (FNT) 2020 Soft copy to be mailed at [email protected] by 6th April, 2020 Marks-10 Write a note on the following topics: Vitamin D: Biochemical and Physiological Role Bioavailability Requirements Roll No. 1-15 Sources Deficiency Excess (Toxicity) Vitamin E: Biochemical and Physiological Role Bioavailability Requirements Roll No. 16-30 Sources Deficiency Excess (Toxicity) Vitamin K: Biochemical and Physiological Role Bioavailability Requirements Roll No. 31- 45 Sources Deficiency Excess (Toxicity) Water: Functions Roll No. 46-60 Daily requirements Water balance VITAMIN D FOR 2ND SEM (H) BY SAJIDA KHATOON ASSISTANT PROFESSOR FNT DEPARTMENT MKC THE SUNSHINE VITAMIN Vitamin D is a unique vitamin and its availability in the body largely depends on its synthesis in the skin when exposed to sunlight. Hence, its dietary requirement is usually very small especially in the Indian context. VITAMIN D is widespread in nature and photosynthesized in most plants and animals exposed to sunlight Its major role in vertebrate animals and humans is to increase the absorption of calcium and phosphate for the mineralization of the skeleton. In the case of vitamin D deficiency in children, the cartilage is not calcified, causing rickets. In adults, the newly formed bone matrix (the osteoid) is not mineralized, causing osteomalacia. Vitamin D exists in 2 forms: Vitamin D3 (cholecalciferol) of animal origin Vitamin D2 (ergocalciferol) of plant origin The precursors of vitamin D are: 7-dehydro-cholesterol in animals Ergosterol in plants Vitamin D3, or cholecalciferol, is synthesized in the skin. Its precursor, 7-dehydrocholesterol (provitamin D3), is converted by the UV light of the sun (UVB 290–315 nm) into previtamin D3, which is slowly isomerized to vitamin D3. Vitamin D3 is photosynthesized in the skin of vertebrates by the action of solar ultraviolet (UV) B radiation on 7-dehydrocholesterol. Vitamin D2 is produced by UV irradiation of ergosterol, which occurs in molds, yeast, and higher-order plants. Dietary vitamin D3 is absorbed from jejunum with the aid of bile salts and is incorporated within chylomicrons, which take it through the lymph and then into the blood. On release from lymph into the blood the vitamin D is removed from the chylomicrons and becomes bound to a specific vitamin D-binding protein (DBP), called alpha globulin and gets transported to the liver. Vitamin D from the skin or diet is only short-lived in circulation (with a half-life of 1–2 days), as it is either stored in fat cells or metabolized in the liver. Vitamin D produced in the skin may last at least twice as long in the blood compared with ingested vitamin D. In circulation, vitamin D is bound to vitamin D- binding protein and transported to the liver, where it is converted to 25-hydroxyvitamin D3 (calcidiol). To be biologically activated at physiologic concentrations, 25(OH)D3 must be converted in the kidneys to 1,25-dihydroxyvitamin D3 (calcitriol) which is thought to be responsible for most, if not all, of the biologic functions of vitamin D3. The production of calcidiol in the liver and of calcitriol in the kidney is tightly regulated. In the liver, vitamin D-25-hydroxylase is down- regulated by vitamin D and its metabolites, thereby limiting any increase in the circulating concentration of calcidiol following intakes or following production of vitamin D after exposure to sunlight. In the kidney, in response to serum calcium and phosphorus concentrations, the production of calcitriol is regulated through the action of parathyroid hormone (PTH). Active vitamin D functions as a hormone, and its main biologic function is to maintain serum calcium and phosphorus concentrations within the normal range by enhancing the efficiency of the small intestine to absorb these minerals from the diet. When dietary calcium intake is inadequate to satisfy the body’s calcium requirement, calcitriol, along with PTH, mobilizes calcium stores from the bone. In the kidney, calcitriol together with PTH, increases calcium reabsorption by the distal renal tubules. Calcitriol and PTH hormone together regulate the concentration of calcium in blood plasma. This is important not only for bone formation and maintenance, but also for maintaining blood calcium levels to facilitate the proper interaction between nerves and muscles. REQUIREMENTS Under situations of minimal exposure to sunlight, a specific recommendation of a daily supplement of 400 IU is recommended. 1 mcg of vitamin D = 40 IU of vitamin D DEFICIENCY, why it happens? The major source of vitamin D for children and adults is exposure to natural sunlight. Thus, the major cause of VDD is inadequate exposure to sunlight. Wearing a sunscreen with a sun protection factor (SPF) of 30 reduces vitamin D synthesis in the skin by more than 95%. UVB light cannot pass through glass and clothing; exposure of the skin to sunlight through glass and clothes will not result in vitamin D synthesis. People with a dark skin tone require at least three to five times longer exposure to make the same amount of vitamin D than a person with a white skin tone. Larger amounts of the pigment melanin in the epidermal layer result in darker skin and reduce the skin's ability to produce vitamin D from sunlight. Season of the year (the lower the sun on the horizon in the winter, the greater the time needed) The latitude (within 1 or – 35 degrees from the equator, the most vitamin D can be produced when skin is exposed to UVB rays) A person should be exposed to sunlight 2 to 3 times per week from March through October in northern climates to accumulate enough vitamin D to get through the winter with adequate vitamin D. The time of day (more vitamin D is synthesized by the skin when the sun is directly overhead between 11:00 am and 3:00 pm.) Older adults are at high risk of developing vitamin D insufficiency because of aging. Their skin cannot synthesize vitamin D as efficiently, they are likely to spend more time indoors, and they may have inadequate intakes of the vitamin. Patients with one of the fat malabsorption syndromes and bariatric patients are often unable to absorb the fat-soluble vitamin D, and patients with nephritic syndrome lose 25(OH)D bound to the vitamin D-binding protein in the urine. Vitamin D is fat soluble, therefore it requires some dietary fat in the gut for absorption. Individuals with reduced ability to absorb dietary fat might require vitamin D supplements. Fat malabsorption is associated with a variety of medical conditions including some forms of liver disease, cystic fibrosis, and Crohn's disease. CONSEQUENCES OF DEFICIENCY Vitamin D deficiency is characterized by inadequate mineralization or by demineralization of the skeleton. Among children, vitamin D deficiency is a common cause of bone deformities known as rickets. Vitamin D deficiency in adults leads to a mineralization defect in the skeleton, causing osteomalacia, and induces secondary hyperparathyroidism with consequent bone loss and osteoporosis. One of the most serious disorders associated with vitamin D deficiency is the convulsive state of hypocalcemic tetany, which is caused by insufficient supplies of calcium to nerves and muscles. Potential roles for vitamin D beyond bone health, such as effects on muscle strength, the risk for cancer and for type 2 diabetes, are currently being studied. PRESENT SCENARIO It is pertinent to note that in India, young growing children and adults, particularly in urban areas, are physically less active and are not being exposed outdoors. Outdoor physical activity is a means of achieving adequate vitamin D status. TOXICITY (EXCESS) Excess Vitamin D causes increased calcium absorption from intestine, leading to increased plasma calcium (hypercalcemia) Hypercalcemia is associated with deposition of calcium in many soft tissues such as kidney and arteries. It leads to formation of stones (renal calculi) Some infants are sensitive to intakes of vitamin D as low as 50 g/d, resulting in an elevated plasma concentration of calcium. This can lead to contraction of blood vessels, high blood pressure, and calcinosis—the calcification of soft tissues. Hypercalcemia in adults results in loss of appetite, nausea, weight loss and failure to thrive. The early symptoms disappear if Vitamin D rich foods are withdrawn from the diet. If hypercalcemia persists for a long period, the calcification of soft tissues can eventually cause death. Although excess dietary vitamin D is toxic, excessive exposure to sunlight does not lead to vitamin D poisoning because there is a limited capacity to form the precursor 7-dehydrocholesterol and to take up cholecalciferol from the skin. VITAMIN E BY SAJIDA KHATOON FOR 2ND SEM (H) ASSISTANT PROFESSOR FNT DEPARTMENT MKC Vitamin E is a naturally occurring fat soluble vitamin that exists in eight different forms: . Alpha (α), beta (β), gamma (γ) and delta (δ) tocopherol . Alpha (α), beta (β), gamma (γ) and delta (δ) tocotrienol They have varying levels of biological activity. Alpha (α) tocopherol appears to be the most active form. It is the only form that is recognised to meet human requirements. Serum concentrations of alpha- tocopherol depend on the liver, which takes up the nutrient after absorption of all the forms from the small intestine. The liver then preferentially secretes only alpha-tocopherol and metabolizes and excretes the other vitamin E forms. As a result, blood and cellular concentrations of other forms of vitamin E are lower than those of alpha-tocopherol and thus have been less studied. FUNCTIONS Vitamin E has powerful antioxidant activities which protect cells from the damaging effects of free radicals. Free radicals are produced endogenously when the body metabolises food to energy. Exogenous sources come from exposure to cigarette smoke, air pollution and ultraviolet radiation from the sun.