PENGANTAR METABOLISME ZAT GIZI MIKRO PROGRAM STUDI ILMU GIZI-FIKES PERTEMUAN 4 DUDUNG ANGKASA PROGRAM STUDI ILMU GIZI-FIKES

VISI DAN MISI UNIVERSITAS ESA UNGGUL

Materi Sebelum UTS 03. Vitamin D 04. Vitamin E dan K 01. Pengantar metabolisme mikro 02. Vitamin A 03. Vitamin D 04. Vitamin E dan K 05. Vitamin Larut Air- C 06. Vitamin Larut Air-B kompleks 07. Vitamins Interaction

Materi Setelah UTS 10. Mineral-Mn, Cr, Cl 11. Mineral-Co, Mo, Cu, F 08. Mineral-Ca, Mg, Na, K, P, S 09. Mineral-Fe, Zn, I 10. Mineral-Mn, Cr, Cl 11. Mineral-Co, Mo, Cu, F 12. Mineral Interactions 13. Mineral-Vitamins Interactions 14. Review

KEMAMPUAN AKHIR YANG DIHARAPKAN Mahasiswa dapat menjelaskan metabolisme vitamin E dan K yang meliputi pencernaan, penyerapan, distribusi (sirkulasi), utilisasi, dan eksresinya serta tingkat kebutuhan dan resiko keracunannya.

METABOLISM OF VITAMIN E Esa Unggul University

Chemical form of vitamin E

Vitamin E in Food

Benefits of Vitamin E

Absorption and Transport Dependent on ability to absorb fat Absorbed into lymphatic system Component of chylomicrons Alpha-tocopherol is major tocopherol in plasma Positive association between serum lipid and tocopherol levels Normal range is 0.5-1.6 mg/dl The ability of an individual to absorb vitamin E is dependent on the ability to absorb fat. Vitamin E is absorbed into the lymphatic system from the intestines and enters the blood as a component of the chylomicrons. The majority of vitamin E in plasma is in the low-density lipoproteins. Alpha-tocopherol is the major tocopherol in adult plasma and accounts for approximately 87% of the total tocopherol concentration.   There is a positive association between serum lipid levels and tocopherol levels. Vitamin concentrations in body tissues vary considerably. Adipose tissue and adrenal glands have the highest levels. Vitamin E levels in plasma range from 0.5-1.6 mg/dl in normal populations. In general, a 10-fold increase in vitamin E intake will double plasma concentrations.

Absorption and Transport The ability of an individual to absorb vitamin E is dependent on the ability to absorb fat. Vitamin E is absorbed into the lymphatic system from the intestines and enters the blood as a component of the chylomicrons. The majority of vitamin E in plasma is in the low-density lipoproteins. Alpha-tocopherol is the major tocopherol in adult plasma and accounts for approximately 87% of the total tocopherol concentration. There is a positive association between serum lipid levels and tocopherol levels. Vitamin concentrations in body tissues vary considerably. Adipose tissue and adrenal glands have the highest levels. Vitamin E levels in plasma range from 0.5-1.6 mg/dl in normal populations. In general, a 10-fold increase in vitamin E intake will double plasma concentrations.

Co-Work Vit C With Vit E

Human requirement For the 19- to 50-year age group, an EAR of 12 mg of α-tocopherol is derived from studies in men based on the criterion of vitamin E intakes suffi cient to prevent hydrogen peroxide-induced haemolysis. The RDA is 120% of the EAR which, after rounding up, is 15 mg per day of α-tocopherol. There is no increase for pregnancy, but for lactation the RDA is increased to 19 mg per day

Toxicity Vitamin E is regarded to be non-toxic. There is no evidence of adverse effects from the consumption of vitamin E naturally occurring in foods. The question of toxicity arises when vitamin E is used in pharmacological amounts for ‘therapeutic’ purposes. Animal studies have shown that α-tocopherol is not mutagenic, carcinogenic or teratogenic. In human studies with double-blind protocols and in large population studies, oral vitamin E supplementation resulted in few side effects even at doses as high as 3200 IU per day

METABOLISM OF VITAMIN K

Chemical form of Vit K

Source of Vit K There are two major natural sources of vitamin K: phylloquinones (vitamin K1) in plant sources menaquinones (vitamin K2) produced by bacterial flora in animals. Endogenous source of vitamin K. The large intestine of healthy adult humans contains a microflora of bacteria.

Benefits of vitamin K Vitamin K: “coagulation vitamin,” “antihemorrhagic vitamin,” and “prothrombin factor.”

Absorption and Transfer Phylloquinone, the major form of vitamin K in the diet, is absorbed in the jejunum, and less effi ciently in the ileum, in a process that is dependent on the normal fl ow of bile and pancreatic juice Like all fat-soluble vitamins, vitamin K is absorbed in association with dietary fats and requires the presence of bile salts and pancreatic juice for adequate uptake from the alimentary canal. Absorption of vitamin K depends on its incorporation into mixed micelles, and optimal formation of these micellar structures requires the presence of both bile and pancreatic juice.

Absorption and Transfer The lymphatic system is the major route of transport of absorbed phylloquinone from the intestine in mammals Ingested phylloquinone is absorbed by an energy-dependent process from the proximal portion of the small intestine Menaquinone is absorbed from the small intestine by a passive non–carrier- mediated process. Efficiency of vitamin K absorption has been measured at 10 to 70%, depending on the form in which the vitamin is administered.

Storage and Excretion About half of the total body pool of vitamin K is in the liver phylloquinone and menaquinones specifically concentrated and retained in the liver Menadione is found to be widely distributed in all tissues and very rapidly excreted. Some breakdown products of vitamin K are excreted in the urine Some vitamin K is re-excreted into the intestine with bile, part of which is excreted in the feces. In humans, 20% of injected phylloquinone was excreted in the urine, and 40 to 50% was excreted in the feces via the bile.

Deficiency The major clinical sign of vitamin K deficiency in all species is impairment of blood coagulation. Clinical signs include low prothrombin levels, increased clotting time, and hemorrhaging. In its most severe form, vitamin K deficiency will cause subcutaneous and internal hemorrhages, which can be fatal. Deficiency can result from insufficient vitamin K in the diet, lack of microbial synthesis within the gut, inadequate intestinal absorption, or inability of the liver to use the available vitamin K.