Vitamin B1, also known as thiamine or antineuritisin, is synthesized by fungi, microorganisms and plants, but animals and humans can only obtain it from food. Vitamin B1 is mainly found in the seed skin and germ, such as rice bran and bran content is very rich, in yeast content is also very rich. Thiamine is a combination of pyrimidine and thiazole rings and is involved in sugar metabolism in the body. [2]
Physical and chemical properties
Thiamine is often found in the form of its hydrochloride [3], molecular formula C12H17ClN4OS·HCl, molecular weight 337.29. Also known as thiamine hydrochloride. White crystalline powder. Has a weak special odor, bitter taste, deliquescent. Melting point 248ºC, soluble in water, slightly soluble in ethanol, insoluble in ether and benzene. Vitamin B1 has the function of maintaining normal glucose metabolism and nerve conduction. Vitamin B1 content in yeast is the highest in nature. It can be synthesized byand vinylnitrile, or by β-ethoxypropionate and
Relevant history
thiamine deficiency (TD) was prevalent in the 18th and 19th centuries, when hundreds of thousands of people died of beriberi caused by vitamin B1 deficiency every year in China, Japan, especially in Southeast Asia. At the end of the 19th century, Dutch physician Christiaan Eijk-man studied beriberi in the of the Dutch East Indies and proposed the nutritional hypothesis of beriberi. In later studies, it was found that the real cause of beriberi is nutritional deficiency, and brown rice can prevent and treat beriberi in humans. Polish chemist Casimir Funk claimed to purify this substance in 1912, because this substance contains amino, so it is named Vitamine, which is the Latin life (Vita) and abbreviation of the word created, in Chinese is translated as vitamin or vitamin. However, the true anti-beriberi factor was extracted from bran in 1926 by two Dutch chemists, Barend. C. P. Jansen and Willem. P. Donath, and named Thiamin. In 1936, the American Robert R. Williams determined its chemical structure and synthesized thiamine by chemical methods. With the development of modern medicine and nutrition science, as well as the wide distribution of vitamin B1, epidemic vitamin B1 deficiency has been difficult to recur. Outbreaks of vitamin B1 deficiency caused by improper food processing and cooking methods are often reported [2]. For example, in 2004, a formula milk powder was forcibly recalled in Israel, which caused the death of 3 infants and the illness of 10 infants, because vitamin B1 was not added in the milk powder, resulting in brain damage of infants. [5]
Physiological function
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EDITOR
Clinically used vitamin B1 is a product of chemical synthesis. In the cell [6], the bioactive form of vitamin B1 is thiamine pyrophosphate (TPP), which is the pyruvate dehydrogenase complex (pyruvate dehydrogenase complex). Important cofactors in PDHC, α-ketoglutarate dehydrogenase complex (KGDHC), and tran-sketolase (TK) reactions of phosphopentose pathways. PDHC and KGDHC are important components of ATP production pathway by glucose. TK is the key enzyme of gluconeogenesis. As a coenzyme of two key catalases in glycolysis, thiamine plays an important role in glucose metabolism. In addition, reduced nicotinamide adenine dinucleotide, a major component of the REDOX reaction in vivo, NADH, reduced nicotinamide adeninedinucleotide phosphate (NADPH), and glutathione are all produced in enzymatic reactions with thiamine pyrophosphate as a cofactor. Thiamine plays an important role in maintaining oxidative metabolic balance in the brain, such as lipid peroxidation product levels and glutathione reductase activity. In addition, enzymes that use thiamine pyrophosphate as a coenzyme are also involved in the synthesis of amino acids and other organic compounds in cell metabolism. Recent studies have shown that vitamin B1 derivatives can participate in important physiological processes such as gene expression regulation, cellular stress response, signal transduction pathways, and nervous system signal transduction, and these effects of vitamin B1 derivatives are independent of their coenzyme actions. [2] Vitamin B1 is a cofactor of key enzymes in glucose metabolism and plays an important role in maintaining oxidative metabolic balance in the brain. Vitamin B1 is an important bioactive substance to maintain the normal function of the nervous system, heart and digestive system. [7]
Deficiency pathology
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EDITOR
Alcohol-related vitamin B1 deficiency is one of the most common causes of vitamin B1 deficiency in clinic, which is called Wernicke-Korsakoff's Syndrome (WKS). In addition to obvious cognitive loss and memory loss, the brain lesions of patients are selective neuronal death. The activity of KGDHC is significantly reduced with neuronal tangles similar to those seen in Alzheimer's disease. Pathological changes in the brain of mice induced by TD first appear in the submedial thamalic nucleus (SmTN), showing selective neuronal death, microglial hypertrophy and hyperplasia. heme oxyge-nase-1 (HO-1), a marker of oxidative stress, and intercellular adhesion molecule-1 (ICAM-1) were expressed in vascular endothelial cells, and astrocyte hyperplasia occurred in the late stage. There were bleeding foci and amyloid accumulation in the diseased brain area. When vitamin B1 is deficient, tricarboxylic acid circulation is hindered, pyruvate and lactic acid are accumulated, and ATP production is hindered, which first affects nervous tissues that mainly rely on glucose metabolism for energy. TD can cause oxidative stress both in vivo and in vitro, and is a classic model for studying brain metabolic disorders leading to selective neuronal death. Further studies showed that mitochondrial dysfunction, endoplasmic reticulum stress, inflammation and immune factors were involved in the process of TD-induced neuronal death. [2]
Subclinical vitamin B1 deficiency is common in patients with digestive tract diseases and in older adults over 65 years of age. In people over 65, blood levels of vitamin B1 are reduced by about one-third. Thiamine deficiency is detected in approximately one-third of patients with congestive heart failure; In patients with type 1 and type 2 diabetes, the plasma thiamine is reduced by about 75% and 49%, respectively. Vitamins are closely related to diabetes, especially vitamin B1 [8]. [2]
Deficiency performance
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beriberi
When VB1 is deficient, sugar metabolism is obstructed and sugar oxidation is blocked to form pyruvate lactic acid accumulation, which affects the body's energy supply, and clinical symptoms of digestion and circulatory system occur. Beriberi was discovered around 1630. In 1882, a Japanese general observed that many sailors had poor appetite, constipation, slow bowel movement, abdominal distention and other symptoms, and noticed that it was related to food, and later he added rice, meat, and vegetables to the drink, and found that there were many fewer people with these symptoms. It has been confirmed that these symptoms are caused by a lack of VB1. Deficiency of VB1 often presents with digestive symptoms such as poor stomach, constipation, slowed bowel movement, and abdominal distension. The cardiovascular system showed tachycardia, edema, cardiac hypertrophy and dilatation. The nervous system is characterized by fatigue, memory loss, insomnia, and central and peripheral inflammation or confusion in severe cases. Some patients can also appear symmetrical toe sensation abnormalities: foot burning pain, gastrocnemius spasm, foot pain and other symptoms. The treatment of beriberi should first correct the cause, [9] can be treated by supplementing vitamin B1, diuretic deswelling, regulating gastrointestinal tract and other symptomatic treatment. [10]
Lactic acid accumulation
VB1 plays an important role in the metabolism of sugar and maintaining the normal function of the nervous system. The lack of VB1 during lactation will cause metabolic disorders of carbohydrate substances, the accumulation of lactic acid and other metabolites, and harmful substances will also accumulate in breast milk, which is easy to cause toxic reactions in infants. [9]
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