Vitamin B1 (thiamin).
Vitamin B1 metabolism.
Thiamine in food is biologically inactive.
In the liver, under the action of the enzyme thiaminkinase, it is phosphorylated, turning into thiamine diphosphate, thiamine monophosphate, thiamine triphosphate.
The biological role of thiamine is associated with its participation in the construction of coenzymes of a number of enzymes:.
• pyruvate dehydrogenase, which catalyzes the oxidation of pyruvic acid to acetyl-Co-A;
• a-ketoglutarate dehydrogenase, which participates in the Krebs cycle, converting a-ketoglutaric acid to succinyl-Co-A;
• transketolase, which is involved in the pentose phosphate cycle.
These three enzymes provide the metabolism of various nutrients, but primarily carbohydrates, and therefore energy metabolism (carbohydrates are the main supplier of energy). With an excess of carbohydrates in the diet, the need for thiamine increases, and a relative deficiency of vitamin B1 may develop. With avitaminosis B1, there is a decrease in the respiratory coefficient, the accumulation of pyruvate undeoxidation products, which are toxic to the central nervous system.
The resulting metabolic acidosis and energy deficit impairs the work of gradient pumps of cells, including those of the nerve, cardiac and muscle.. In conditions of impaired oxidation of carbohydrates, the body is forced to use proteins and fats, which leads to muscle atrophy, delayed physical development in children. The conversion of carbohydrates into fats and the synthesis of fatty acids are impaired.
Thiamine is essential for the biosynthesis of the most important neurotransmitter, acetylcholine. With a deficiency of thiamine, the formation of acetyl-Co-A from pyruvate and acetylation of choline are hampered, which leads to a violation of the synthesis of acetylcholine and the corresponding clinical symptoms (atonic constipation, decreased gastric secretion, neurological disorders).
Vitamin B1 deficiency.
With avitaminosis B1, beriberi disease develops, which is characterized by the following symptoms:.
• headache, irritability, memory impairment, peripheral polyneuritis, in severe cases, paralysis;
• tachycardia, pain in the heart, expansion of the boundaries of the heart, muffled tones, shortness of breath, edema;
• decreased appetite, abdominal pain, nausea, decreased bowel tone, constipation.
The name "
B1 hypovitaminosis occurs quite often in civilized countries due to the excessive use of refined carbohydrate foods and sweets. Thiamine deficiency is present in every fourth alcoholic. Vitamin B1 deficiency can develop as a result of the consumption of food containing a significant amount of thiaminase (an enzyme that breaks down thiamine) and other anti-vitamin factors, which are rich in raw fish (carp, herring, etc.. ) and marine animals.
The combination of seafood with polished rice gave rise to beriberi among the Japanese sailors of Admiral K.. Takaki. The admiral reduced the incidence of beriberi, enriching the diet of sailors with vegetables, milk and meat.
Thiamine is destroyed during prolonged cooking, especially in an alkaline environment, is lost during the refining of grain products (muesli, instant cereals, etc.. ) The absorption of vitamin B1 is impaired by tobacco, alcohol, coffee and foods containing carbonate and citric acid.
Vitamin B1 requirements and sources.
The daily requirement for thiamine is 0.4 mg for every 1000 kcal, or 1.1-2.1 mg (hereinafter, the daily requirement is indicated according to the " Thiamine stores are found in skeletal muscle (50%), heart, liver, kidney, brain.
Food sources of thiamine (mg / 100g): pork tenderloin (1.45), piglet meat (1.40), split peas (0.9), bacon pork (0.60), yeast (0.60), oatmeal (. Vegetables and fruits, as well as milk are poor in vitamin B1.
Vitamin B2 (riboflavin).
Vitamin B2 metabolism.
The biological role of riboflavin is determined by its participation in the construction of two most important coenzymes - flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD), which are part of redox enzyme systems, the so-called flavoproteins. FAD is involved in the construction of flavoproteins that catalyze succinic acid (a metabolite of the Krebs cycle) and fatty acids.
In addition, flavin adenine dinucleotide is a part of monoamine oxidase (MAO) - the main enzyme for the destruction of catecholamines, a-glycerophosphate dehydrogenase (provides glycerol metabolism and phosphotriosis), xanthine oxidase (catalyzes the oxidation of purines to uric acid) and a number of other enzymes. Thus, riboflavin is involved in biological oxidation and energy metabolism.. Along with this, it is necessary for the construction of visual purpura, which protects the retina from excessive exposure to ultraviolet radiation.. Vitamin B2 is needed for erythrocyte glutathione reductase, which protects red blood cells from autooxidation.
Vitamin B2 deficiency.
With hypo- and avitaminosis B2, the highly aerobic epithelium of the skin and oral cavity is affected. There are lesions of the mucous membrane of the lips with vertical cracks and desquamation epithelium (cheilosis), angular stomatitis (seizures), glossitis (tongue swollen, "
There is corneal vascularization (interstitial keratitis), blepharitis and conjunctivitis, dark adaptation is impaired and color vision is impaired. The detoxification potential of hepatic oxidases decreases during the metabolism of a number of drugs. Ariboflavinosis can be accompanied, especially often in children, by normochromic hyporegenerative anemia and leukopenia. The manifestations of vitamin deficiency are aggravated by fat and carbohydrate load.
The main causes of B2 hypovitaminosis are a sharp decrease in the consumption of dairy products, chronic diseases of the gastrointestinal tract, taking medications that are riboflavin antagonists (acriquine and its derivatives). Tobacco and alcohol reduce the absorption of riboflavin, which is destroyed when combined with baking soda and exposed to light.
Riboflavin needs and sources.
The daily requirement for vitamin B2 is 1.3-2.4 mg.
Food Sources of Riboflavin (mg / 100 g): liver (2.60), kidney (1.8), heart (0.75) yeast (0.68), almonds (0.65), cheeses (0.32-. Vitamin Resistant to Heat Treatment.
Vitamin PP (niacin).
The main representatives of niacin are nicotinic acid and nicotinamide. The biological activity of these compounds is the same, but nicotinic acid has a more pronounced vasodilator effect.. Niacin is found in animal tissues mainly as nicotinamide.
Niacin metabolism.
Niacin is a coenzyme in NAD-dependent dehydrogenases (providing tissue respiration, metabolism of carbohydrates and amino acids), NADP-dependent enzymes of the pentose cycle and lipid synthesis, LMH-dependent enzymes (alcohol dehydrogenase, malicenzyme). The function of dehydrogenases is the primary dehydrogenation (removal of hydrogen ions and electrons) of various nutrients and their metabolites and the supply of hydrogen ions and electrons to the biological oxidation chain associated with phosphorylation.
Niacin deficiency.
With vitamin deficiency, pellagra develops - a disease that affects the gastrointestinal tract, skin, central nervous system (three " The name of the disease comes from the Italian pelle agra - rough skin. The poor rural population of those countries where corn played an important role in nutrition was sick with pellagra. Corn leucine inhibits the conversion of tryptophan to niacin.
The main clinical manifestations of niacin deficiency:.
• dry and pale lips. Tongue coated, swollen, furrowed or dry, bright red. Possible aphthous stomatitis, with hypersalivation, esophagitis, erosion and ulceration of the gastrointestinal tract. Erythema on the back of the hands and feet (" Dermatitis in the neck (" Urethritis, vaginitis, proctitis may develop;
• neurasthenic syndrome (irritability, insomnia, depression, lethargy, neuromuscular and headaches, paresthesias), psychosis, in severe cases - dementia;
• diarrhea without mucus and blood, caused by atrophy of the intestinal and gastric mucosa, decreased gastric secretion. Dehydration due to malabsorption in acute pellagra can lead to death in 2-3 weeks;
• anemia, myasthenia gravis, myocardial dystrophy.
Nicotinamide, as an acceptor of methyl groups, is involved in the regulation of the synthesis of very low density lipoproteins (VLDL) in the liver. Taking niacin reduces the synthesis of VLDL and decreases the rate of degradation of high density lipoprotein (HDL), which is used in the treatment and prevention of hyperlipoproteinemia. But large doses of vitamin PP with long-term use contribute to reversible hepatic steatosis.. Methyl donors (choline, methionine, betaine) when combined with niacin interfere with this process.
Nicotinic acid can release histamine from mast cells nonspecifically, as an allergoid reaction. In this case, urticaria, itching, skin hyperemia, fever, increased gastric secretion, and sometimes collapse occur.
Niacin Needs and Sources.
As mentioned above, the development of pellagra can be associated with a one-sided diet of corn, in which niacin is in a bound form and is almost not absorbed.. In addition, corn is low in tryptophan, which the body converts to niacin (60 mg of tryptophan makes 1 mg of niacin). In this regard, there is the concept of " The adult requirement for niacin is 6.6 niacin equivalents per 1000 kcal per day (14-28 mg / day). Adequate level of consumption for dietary nutrition for vitamin PP - 20 mg, safety - 60 mg.
Niacin deficiency can result from: malabsorption, alcoholism, protein starvation, long-term therapy with anti-tuberculosis drugs (ftivazid, cycloserine, isoniazid), which are antagonists of pyridoxine, which is necessary for the conversion of tryptophan to niacin. Niacin-dependent enzymes often contain zinc, magnesium, manganese, molybdenum and cobalt, the deficiency of which contributes to the manifestation of PP hypovitaminosis. Secondary pellagra occurs in Hartnup's disease (niacin is poorly absorbed from the intestines) and carcinoid syndrome due to impaired niacin metabolism.
Food sources of niacin (mg / 100 g): peanuts (14.7), yeast (11.4), liver (7.1-12.0), sunflower seeds (10.1), fresh mushrooms (4.8-.
Vitamin B6.
Representatives of vitamin B6 - pyridoxal, pyridoxine and pyridoxamine. The most common foods are pyridoxal and pyridoxamine.
Vitamin B6 metabolism.
All these forms are interconverted in the course of enzymatic reactions. The biologically active form of vitamin B6 is its phosphorylated derivatives: pyridoxal-5-phosphate and pyridoxamine-5-phosphate. Phosphorylation occurs in the liver.
Vitamin B6 is a coenzyme of amino acid metabolism enzymes that provide transamination, deamination and decarboxylation reactions. As part of aminotransferases catalyzing transamination, it participates in the synthesis of nonessential amino acids; as part of decarboxylases that uncouple carboxyl groups from amino acids, participates in the formation of biogenic amines (serotonin, histamine, tyramine, tryptamine, etc.. With a deficiency of vitamin B6, protein metabolism is primarily disturbed and there is a negative nitrogen balance, hyperaminoacidemia, aminaciduria and oxaluria, caused by a violation of glyoxalic acid metabolism.
When decarboxylation of glutamic acid is formed? -aminobutyric acid, which is a mediator of inhibition in the central nervous system, which is why pyridoxine is the only vitamin deficient in which epileptiform seizures are observed. Glutamate decarboxylase is also required for the utilization of tryptophan and the synthesis of serotonin, when metabolic disorders are formed, metabolites such as xanthurenic acid are formed, which interferes with insulinogenesis, which can cause hyperglycemia.
Pyridoxine-dependent enzymes are involved in the synthesis of niacin and serotonin from tryptophan, as well as the destruction of excess homocysteine.
Along with participation in the exchange of amino acids, pyridoxal phosphate is needed for the construction of phosphorylase, which catalyzes the cleavage of glycogen to glucose-1-phosphate, for the synthesis of the heme precursor? -aminolevulinic acid, as well as for the conversion of linoleic acid into arachidonic. Thus, pyridoxine is essential for carbohydrate and fat metabolism and hemoglobin synthesis..
Vitamin B6 has lipotropic activity, since it is involved in the metabolism of methionine.
Deficiency and hypervitaminosis of vitamin B6.
Since vitamin B6 is widespread in food, a purely dietary deficiency is almost impossible.. Hypovitaminosis can develop due to a number of reasons, in particular, with malabsorption, increased breakdown in alcoholism, stress, fever, hyperthyroidism and other conditions that accelerate protein catabolism. Tobacco impairs the absorption of pyridoxine, so smokers need extra vitamin B6.
B6 hypovitaminosis is expressed by the following symptoms:.
• damage to the skin and mucous membranes - seizures, cheilosis, glossitis, seborrheic dermatitis of the face and scalp. Dermatitis can be edematous;
• CNS damage - irritability, insomnia or drowsiness, epileptimorphic convulsions, depression, peripheral polyneuritis;
• microcytic hypochromic anemia;
• leukopenia, which develops as a result of impaired transamination and, therefore, protein synthesis in rapidly proliferating tissues;
• gastrointestinal disorders.
B6 hypovitaminosis can be caused by hereditary diseases: homocystinuria, cystathioninuria, xanturenuria (Knapp-Comrover syndrome), pyridoxine-dependent convulsive syndrome and pyridoxine-dependent anemia. Deficiency of pyridoxine develops when using drugs that have antagonistic properties to it (isoniazid, ftivazid, tubazid, cycloserine penicillamine, chloramphenicol, ethionamide, immunosuppressants, L-DOPA and estrogens).
With the use of ultrahigh doses of synthetic pyridoxine - from 2 g / day - acute hypervitaminosis B6 develops: sensory neuropathy with skin numbness, especially around the mouth, limbs, impaired coordination and vibration sensitivity.
Vitamin B6 requirements and sources.
The need for vitamin B6 depends on age, gender and is largely determined by protein intake. For adult men, the daily requirement for vitamin B6 is 2.0 mg, for women - 1.8 mg (increases to 2.1-2.2 mg during lactation and pregnancy) In this case, the ratio of 0.
032 mg of vitamin B6 per 1 g of consumed. Adequate dietary intake 1 mg, safety 6 mg.
Dietary sources of vitamin B6: liver (0.50-0.70), skin (0.52), kidneys (0.50), meat (0.42-0.50). Plant products: beans (0.90), soybeans (0.85), horseradish (0.70), garlic (0.60), yeast (0.58), whole wheat flour (0.55), rice (0.
Vitamin B6 is photosensitive, lost during canning, resistant to heat treatment, but in an alkaline environment it can be destroyed by 20-35%.
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