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Thiamine

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Thiamine
Names
IUPAC name
2-[3-[(4-amino- 2-methyl- pyrimidin- 5-yl) methyl]- 4-methyl- thiazol- 5-yl] ethanol
Other names
Aneurine hydrochloride
Identifiers
3D model (JSmol)
ChemSpider
MeSH Thiamine
  • [Cl-].Cc1c(CCO)sc[n+]1Cc2cncnc2N
Properties
C12H17N4OS+
Molar mass 265.35 g/mol
Melting point 248-260 °C (hydrochloride salt)
Hazards
Occupational safety and health (OHS/OSH):
Main hazards
 Allergies
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).

Thiamine, also called thiamin or vitamin B1, is best known for the cofactor role of thiamine diphosphate (ThDP) in many enzymes and multienzyme complexes.[1] The mechanism by which the thiamine moiety of ThDP exerts its coenzyme function by proton substitution on position 2 of the thiazolium ring was elucidated by Ronald Breslow in 1958.[2]

Thiamine is a colorless compound with a chemical formula C12H17N4OS. Its structure contains a pyrimidine ring and a thiazole ring. Thiamine is soluble in water, methanol, and glycerol and practically insoluble in acetone, ether, chloroform, and benzene. It is stable at acidic pH, but is unstable in alkaline solutions.[3] Thiamine is unstable to heat, but stable during frozen storage.[4] It is unstable when exposed to ultraviolet light[3] and gamma irradiation.[5][6] Thiamine reacts strongly in Maillard-type reactions.[4]

Thiamine phosphate derivatives have essential metabolic roles in carbohydrate and protein metabolism and in neural function.[4] As for other vitamins, animals are unable to synthesize thiamine and its deficiency leads to severe symptoms, involving the nervous system and the heart. In less severe deficiency, nonspecific signs include malaise, weight loss, irritability and confusion.[7]

History: the discovery of vitamine and the biochemical lesion

Thiamine was the first water-soluble vitamins to be described,[4] leading to the discovery of more such trace compounds essential for survival and to the notion of vitamin. Chinese medical texts referred to beriberi (a thiamine deficiency disease) as early as 2700 BC.[8]The history of the discovery of thiamine has been remarkably reviewed by Kenneth J. Carpenter in his book "Beriberi, white rice, and vitamine B1".[9] It was not until AD 1884 that Kanehiro Takaki (1849-1920), a surgeon general in the Japanese navy, rejected the previous germ theory and attributed the disease to insufficient nitrogen intake (protein deficiency). In 1897 Christiaan Eijkman (1858-1930), a military doctor in the Dutch Indies, discovered that fowl fed on a diet of cooked, polished rice developed paralysis, which could be reversed by discontinuing rice polishing. He attributed that to a nerve poison in the endosperm of rice, from which the outer layers of the grain gave protection to the body. Eijkman was awarded the Nobel Prize in Physiology and Medicine in 1929, because his observations led to the discovery of vitamins. An associate, Gerrit Grijns, correctly interpreted the connection between excessive consumption of polished rice and beriberi in 1901: he concluded that rice contained an essential nutrient in the outer layers of the grain that was removed by polishing.[8] In 1911 Casimir Funk isolated an antineuritic substance from rice bran that he called a “vitamine” (on account of its containing an amino group). Dutch chemists, Barend Coenrad Petrus Jansen (1884-1962) and W.P. Donath, went on to isolate and crystallize the active agent in 1926, whose structure was determined by Robert Runnels Williams (1886-1965), a US chemist, in 1934. Thiamine (“sulfur-containing vitamin”) was synthesized in 1936[10] by the same group. It was first named “aneurin” (for anti-neuritic vitamin).[11]

Biosynthesis

Complex thiamine biosynthetic occurs in bacteria, some protozoan, plants and fungi.[12][13] The thiazole and pyrimidine moieties are synthesized separately and then assembled to form ThMP by thiamine-phosphate synthase (EC 2.5.1.3). The exact biosynthetic pathways may differ among organisms. In E. coli and other enterobacteriaceae ThMP may be phosphorylated to the cofactor ThDP by a thiamine-phosphate kinase (ThMP + ATP → ThDP +ADP, EC 2.7.4.16). In most bacteria and in eukaryotes, ThMP is hydrolyzed to thiamine, that may then be pyrophosphorylated to ThDP by thiamine diphosphokinase (thiamine + ATP → ThDP + AMP, EC 2.7.6.2).

Thiamine phosphate derivatives and function

Thiamine is mainly the transport form of the vitamin, while the active forms are phosphorylated thiamine derivatives. There are four known natural thiamine phosphate derivatives: thiamine monophosphate (ThMP), thiamine diphosphate (ThDP), also sometimes called thiamine pyrophosphate (TPP), thiamine triphosphate (ThTP), and the recently discovered adenosine thiamine triphosphate (AThTP).

Thiamine monophosphate

There is no known physiological role of ThMP.

Thiamine diphosphate

The synthesis of thiamine diphosphate (ThDP), also known as thiamine pyrophosphate (TPP) or cocarboxylase, is catalyzed by an enzyme called thiamine diphosphokinase according to the reaction thiamine + ATP → ThDP + AMP (EC 2.7.6.2). ThDP is a coenzyme for several enzymes that catalyze the transfer of two-carbon units and in particular the dehydrogenation (decarboxylation and subsequent conjugation with coenzyme A) of 2-oxoacids (alpha-keto acids). Examples include:

The enzymes transketolase, pyruvate dehydrogenase (PDH) and oxoglutarate dehydrogenase (OGDH) are all important in carbohydrate metabolism. The cytosolic enzyme transketolase is a key player in the pentose phosphate pathway required for the biosynthesis of NADPH and the pentose sugars deoxyribose and ribose. The mitochondrial PDH and OGDH are part of biochemical pathways that result in the generation of adenosine triphosphate (ATP), which is a major form of energy for the cell. PDH links glycolysis to the citric acid cycle, while the reaction catalyzed by OGDH is a rate-limting step in the citric acid cycle. In the nervous system, PDHC is also involved in the production of acetylcholine, a neurotransmitter, and for myelin synthesis.[10]

Thiamine triphosphate

Thiamine triphosphate (ThTP) was long considered a specific neuroactive form of thiamine. However, recently it was shown that ThTP exists in bacteria, fungi, plants and animals suggesting a much more general cellular role.[14] In particular in E. coli it seems to play a role in response to amino acid starvation.[15]

Adenosine thiamine triphosphate

Adenosine thiamine triphosphate (AThTP) or thiaminylated adenosine triphosphate has recently been discovered in Escherichia coli where it accumulates as a result of carbon starvation.[16] In E. coli, AThTP may account for up to 20 % of total thiamine. It also exists in lesser amounts in yeast, roots of higher plants and animal tissue.

Nutrition

Sources

Thiamine is found in a wide variety of foods at low concentrations. Yeast and pork meat are the most highly concentrated sources of thiamine. Cereal grains, however, are the most important dietary sources of thiamine in the diet as these foods are consumed readily in most diets. Of the cereal grains, whole grains contain more thiamine than refined grains, as thiamine is found mostly in the outer layers of the grain and in the germ. During the refining process these segments of the grain are removed therefore decreasing the thiamine content in products such as white rice and white bread. For example, 100 g of whole wheat flour contains 0.55 mg of thiamine while 100 g of white flour only contains 0.06 mg of thiamine. In addition to cereal grains some vegetables and meats are also good sources of thiamine. Listed below are foods rich in thiamine.[7]

Reference Daily Intake and high doses

The RDA in most countries is set at about 1.4 mg. However, tests on volunteers at daily doses of about 50 mg have claimed an increase in mental acuity.[17] There are no reports available of adverse effects from consumption of excess thiamine by ingestion of food and supplements. Because the data are inadequate for a quantitative risk assessment, no Tolerable Upper Intake Level (UL) can be derived for thiamine.

Antagonists

Thiamine in foods can be degraded in a variety of ways. Sulfites, which are added to foods usually as a preservative,[18] will attack thiamine at the methylene bridge in the structure, cleaving the pyrimidine ring from the thiazole ring.[7] The rate of this reaction is increased under acidic conditions. Thiamine is degraded by thermolabile thiaminases (present in raw fish and shellfish.[4]) Some thiaminases are produced by bacteria. Bacterial thiaminases are cell surface enzymes that must dissociate from the membrane before being activated. The dissociation can occur in ruminants under acidotic conditions. Rumen bacteria also reduce sulfate to sulfite, therefore high dietary intakes of sulfate can have thiamin-antagonistic activities.

Plant thiamine antagonists are heat stable and occur as both the ortho and para hydroxyphenols. Some examples of these antagonists are caffeic acid, chlorogenic acid and tannic acid. These compounds interact with the thiamine to oxidize the thiazole ring, thus rendering it unable to be absorbed. Two flavonoids, quercetin and rutin, have also been implicated as thiamine antagonists.[7]

Absorption and transport

Absorption

Thiamine is released by the action of phosphatase and pyrophosphatase in the upper small intestine. At low concentrations the process is carrier mediated and at higher concentrations, absorption occurs via passive diffusion. Active transport is greatest in the jejunum and ileum (it is inhibited by alcohol consuption and by folate deficiency.[4] Decline in thiamine absorption occurs at intakes above 5 mg.[19] The cells of the intestinal mucosa have thiamine pyrophosphokinase activity, but it is unclear whether the enzyme is linked to active absorption. The majority of thiamine present in the intestine is in the pyrophosphorylated form ThDP, but when thiamine arrives on the serosal side of the intestine it is often in the free form. The uptake of thiamien by the mucosal cell is likely coupled in some way to its phosphorylation/dephosphorylation. On the serosal side of the intestine, evidence has shown that discharge of the vitamin by those cells is dependent on Na+-dependent ATPase.[7]

Bound to serum proteins

The majority of thiamine in serum is bound to proteins, mainly albumin. Approximately 90% of total thiamine in blood is in erythrocytes. A specific binding protein called thiamine-binding protein (TBP) has been identified in rat serum and is believed to be a hormonally regulated carrier protein that is important for tissue distribution of thiamine.[7]

Cellular uptake

Uptake of thiamine by cells of the blood and other tissues occurs via active transport and passive diffusion.[4] About 80% of intracellular thiamine is phosphorylated and most is bound to proteins. In some tissues, thiamine uptake and secretion appears to be mediated by a soluble thiamine transporter that is dependent on Na+ and a transcellular proton gradient.[7]

Tissue distribution

Human storage of thiamine is about 25 to 30 mg with the greatest concentrations in skeletal muscle, heart, brain, liver, and kidneys. ThMP and free (umphosphorylated) thiamine is present in plasma, milk, cerebrospinal fluid, and likely all extracellular fluids. Unlike the highly phosphorylated forms of thiamine, ThMP and free thiamine are capable of crossing cell membranes. Thiamine contents in human tissues are less than those of other species.[7][20]

Excretion

Thiamine and its acid metabolites (2-methyl-4-amino-5-pyrimidine carboxylic acid, 4-methyl-thiazole-5-acetic acid and thiamine acetic acid) are excreted principally in the urine.[3]

Deficiency

Thiamine derivatives and thiamine-dependent enzymes are present in all cells of the body, thus, a thiamine deficiency would seem to adversely affect all of the organ systems. However, the nervous system (and heart) shows particular sensitivity to the effects of a thiamine deficiency at the cellular level.

Thiamine deficiency can lead to myriad problems including neurodegeneration, wasting and death. A lack of thiamine can be caused by malnutrition, a diet high in thiaminase-rich foods (raw freshwater fish, raw shellfish, ferns) and/or foods high in anti-thiamine factors (tea, coffee, betel nuts)[21] and by grossly impaired nutritional status associated with chronic diseases, such as alcoholism, gastrointestinal diseases, HIV-AIDS, and persistent vomiting.[10] It is thought that many people with diabetes have a deficiency of thiamine and that this may be linked to some of the complications that can occur.[22][23]

Well-known syndromes caused by thiamine deficiency include beriberi and Wernicke-Korsakoff syndrome, diseases also common with chronic alcoholism.

Beriberi

Beriberi is a neurological and cardiovascular disease. The three major forms of the disorder are dry beriberi, wet beriberi, and infantile beriberi.[3]

  • Dry beriberi is characterized principally by peripheral neuropathy consisting of symmetric impairment of sensory, motor, and reflex functions affecting distal more than proximal limb segments and causing calf muscle tenderness.[10]
  • Wet beriberi is associated with mental confusion, muscular wasting, edema, tachycardia, cardiomegaly, and congestive heart failure in addition to peripheral neuropathy.[4]
  • Infantile beriberi occurs in infants breast-fed by thiamin-deficient mothers (who may show no sign of thiamine deficiency). Infants may manifest cardiac, aphonic, or pseudomeningitic forms of the disorder. Infants with cardiac beriberi frequently exhibit a loud piercing cry, vomiting, and tachycardia.[3] Convulsions are not uncommon, and death may ensue if thiamine is not administered promptly.[10]

Following thiamine treatment, rapid improvement occurs generally within 24 hours.[3] Improvements of peripheral neuropathy may require several months of thiamine treatment.[24]

Alcoholic brain disease

Nerve cells and other supporting cells (such as glial cells) of the nervous system require thiamine. Examples of neurologic disorders that are linked to alcohol abuse include Wernicke’s encephalopathy (WE, Wernicke-Korsakoff syndrome) and Korsakoff’s psychosis (alcohol amnestic disorder) as well as varying degrees of cognitive impairment.[25]

Wernicke’s encephalopathy is the most frequently encountered manifestation of thiamine deficiency in Western society,[26] though it may also occur in patients with impaired nutrition from other causes, such as gastrointestinal disease,[26] those with HIV-AIDS, and with the injudicious administration of parenteral glucose or hyperalimentation without adequate B-vitamin supplementation.[27] This is a striking neuro-psychiatric disorder characterized by paralysis of eye movements, abnormal stance and gait, and markedly deranged mental function.[28]

Alcoholics may have thiamine deficiency because of the following:

  • inadequate nutritional intake: alcoholics tend to intake less than the recommended amount of thiamine.
  • decreased uptake of thiamine from the GI tract: active transport of thiamine into enterocytes is disturbed during acute alcohol exposure.
  • liver thiamine stores are reduced due to hepatic steatosis or fibrosis.[29]
  • impaired thiamine utilization: magnesium, which is required for the binding of thiamine to thiamine-using enzymes within the cell, is also deficient due to chronic alcohol consumption. The inefficient utilization of any thiamine that does reach the cells will further exacerbate the thiamine deficiency.
  • Ethanol per se inhibits thiamine transport in the gastrointestinal system and blocks phosphorylation of thiamine to its cofactor form (ThDP).[30]

Korsakoff Psychosis is generally considered to occur with deterioration of brain function in patients initially diagnosed with WE.[31]. This is an amnestic-confabulatory syndrome characterized by retrograde and anterograde amnesia, impairment of conceptual functions, and decreased spontaneity and initiative.[10]

Following improved nutrition and the removal of alcohol consumption, some impairments linked with thiamine deficiency are reversed; particularly poor brain functionality, although in more severe cases, Wernicke-Korsakoff syndrome leaves permanent damage. (See delirium tremens.)

Thiamine deficiency in poultry

As most feedstuffs used in poultry diets contain enough quantities of vitamins to meet the requirements in this species, deficiencies in this vitamin does not occur with commercial diets. This was, at least, the opinion in the 1960s.[32]

Mature chickens show signs 3 weeks after being fed a deficient diet. In young chicks, it can appear before 2 weeks of age.

Onset is sudden in young chicks. There is anorexia and an unsteady gait. Later on, there are locomotor signs, beginning with an apparent paralysis of the flexor ot the toes. The characteristic position is called "stargazing", meaning a chick "sitting on its hocks and the head in opisthotonos.

Response to administration of the vitamin is rather quick, occurring a few hours later.[33][34]

Differential diagnosis include riboflavin deficiency and avian encephalomyelitis. In riboflavin deficiency, the "curled toes" is a characteristic symptom. Muscle tremor is typical of avian encephalomyelitis. A therapeutic diagnosis can be tried by supplementing Vitamin B1 only in the affected bird. If the animals do not respond in a few hours, Vitamin B1 deficiency can be excluded.

Thiamine deficiency in ruminants

Polioencephalomalacia (PEM), is the most common thiamine deficiency disorder in young ruminant and nonruminant animals. Symptoms of PEM include a profuse, but transient diarrhea, listlessness, circling movements, star gazing or opisthotonus (head drawn back over neck), and muscle tremors.[35] The most common cause is high-carbohydrate feeds, leading to the overgrowth of thiaminase-producing bacteria, but dietary ingestion of thiaminase (e.g. in Bracken fern) or inhibition of thiamine absorption by high sulfur intake are also possible.[36]

Analysis and diagnostic testing

Oxydation of thiamine derivatives to fluorescent thiochromes by potassium ferricyanide in alcaline medium

A positive diagnosis test for thiamine deficiency can be ascertained by measuring the activity of the enzyme transketolase in erythrocytes (Erythrocyte Transketolase Activation Assay). Thiamine, as well as its phosphate derivatives, can also be detected directly in whole blood, tissues, foods, animal feed and pharmaceutical preparations following the conversion of thiamine to fluorescent thiochrome derivatives (Thiochrome Assay) and separation by high performance liquid chromatography (HPLC).[37][38][39] However, this test may not reveal the deficiency in diabetic patients.[40] In recent reports, a number of Capillary Electrophoresis (CE) techniques and in-capillary enzyme reaction methods have emerged as potential alternative techniques for the determination and monitoring of thiamine in samples.[41]

Genetic diseases

Genetic diseases of thiamine transport are rare but serious. Thiamine Responsive Megaloblastic Anemia with diabetes mellitus and sensorineural deafness (TRMA)[42] is an autosomal recessive disorder caused by mutations in the gene SLC19A2,[43] a high affinity thiamine transporter. TRMA patients do not show signs of systemic thiamine deficiency, suggesting redundancy in the thiamine transport system. This has led to the discovery of a second high affinity thiamine transporter, SLC19A3.[44][45] Leigh Disease (Subacute Necrotising Encephalomyelopathy) is an inherited disorder which affects mostly infants in the first years of life and is invariably fatal. Pathological similarities between Leigh disease and WE led to the hypothesis that the cause was a defect in thiamine metabolism. One of the most consistent findings has been an abnormality of the activation of the pyruvate dehydrogenase complex[46]

Other disorders in which a putative role for thiamine has been implicated include Subacute Necrotizing Encephalomyelopathy, Opsoclonic Cerebellopathy (a paraneoplastic syndrome), and Nigerian Seasonal Ataxia. In addition, several inherited disorders of ThDP-dependent enzymes have been reported,[47] which may respond to thiamine treatment.[10]

Research

Research in the field mainly concerns the mechanisms by which thiamine deficiency leads to neuronal death in relation to Wernicke Korsakoff Psychosis. Another important field concerns the understanding of the molecular mechanisms involved in ThDP catalysis. More recently, research has been devoted to the understanding of the possible non-cofactor roles of otehr derivatives such as ThTP and AThTP.

Understanding the mechanism by which thiamine deficiency leads to selective neuronal death

Experimentally induced beriberi polyneuropathy in chickens may be a good model for studying these forms of neuropathy in view of diagnosis and treatment.[48] From studies using rat models, a link between thiamine deficiency and colon carcinogenesis was suggested.[49] Rat model is used also in research of Wernicke's encephalopathy.[50] Thiamine deprived mice are a classic model of systemic oxidative stress, used in research of Alzheimer’s disease.[51]

Catalytic mechnisms in thiamine diphosphate-dependent enzymes

A lot of work is devoted to the understanding of the interplay between ThDP and ThDP-dependent enzymes in catalysis.[52][53]

Non-cofactor roles of thiamine derivatives

Thiamine compounds other than ThDP exist in most cells from many organisms, including bacteria, fungi, plants and animals. Among those compounds are thiamine triphosphate (ThTP) and adenosine thiamine triphosphate (AThTP )are thought to have non-cofactor roles, though at present it is not known to what extent they participate in the symptoms [54][55]

Other

Autism

A 2002 pilot study administered thiamine tetrahydrofurfuryl disulfide (TTFD) rectally to ten autism spectrum children, and reported beneficial clinical effect in eight.[56] There have been no follow-up trials.

Type II diabetes

Recent research conducted by Warwick Medical School (WMS), University of Warwick suggests that high doses of Vitamin B1 could slow down the onset of early diabetic nephropathies.[57]

Early progression of such diseases is associated with the condition microalbuminuria; elevation of the protein albumin found to be present in the patient's urine. Research conducted by Dr Naila Rabbani and Professor Paul J Thornalley (WMS) and in collaboration with researchers at the University of Punjab, Lahore found high doses of oral thiamine can potentially decrease the excretion of albumin and has shown positive signs in type II diabetes patients.[58]

Thiamine deficiency has already been conclusively proven by the group in an earlier study led by Professor Paul Thornalley at WMS which demonstrated that thiamine deficiency was the key to a number of vascular problems in diabetes sufferers.[59]

References

  1. ^ Frank RA, Leeper FJ & Luisi BF (2007). "Structure, mechanism and catalytic duality of thiamine-dependent enzymes". Cell Mol Life Sci. 64: 892–905. doi:10.1007/s00018-007-6423-5.
  2. ^ Breslow R (1958). "On the mechanism of thiamine action. IV.1 Evidence from studies on model systems". J Am Chem Soc. 80: 3719–3726. doi:10.1021/ja01547a064.
  3. ^ a b c d e f Tanphaichitr V. Thiamin. In: Shils ME, Olsen JA, Shike M et al., editors. Modern Nutrition in Health and Disease. 9th ed. Baltimore: Lippincott Williams & Wilkins; 1999
  4. ^ a b c d e f g h Mahan LK, Escott-Stump S, editors. Krause's food, nutrition, & diet therapy. 10th ed. Philadelphia: W.B. Saunders Company; 2000
  5. ^ Luczak M, Zeszyty Probi PostepoLc Vauh Roln 1968;80,497; Chem Abstr 1969;71,2267g
  6. ^ Syunyakova ZM, Karpova IN, Vop Pitan 1966;25(2),52; Chem Abstr 1966;65,1297b
  7. ^ a b c d e f g h Combs, G. F. Jr. The vitamins: Fundamental Aspects in Nutrition and Health. 3rd Edition. Ithaca, NY: Elsevier Academic Press; 2008
  8. ^ a b McCollum EV. A History of Nutrition. Cambridge, MA: Riverside Press, Houghton Mifflin; 1957.
  9. ^ Carpenter K.J. (2000) Beriberi, white rice, and vitamin B1: a disease, a cause, and a cure, pp 282, University of California Press, Berkeley and Los Angeles, California
  10. ^ a b c d e f g Butterworth RF. Thiamin. In: Shils ME, Shike M, Ross AC, Caballero B, Cousins RJ, editors. Modern Nutrition in Health and Disease, 10th ed. Baltimore: Lippincott Williams & Wilkins; 2006.
  11. ^ Carpenter KJ. Beriberi, white rice, and vitamin B: a disease, a cause, and a cure. Berkeley, CA: University of California Press; 2000
  12. ^ Webb ME, Marquet A, Mendel RR, Rebeille F & Smith AG (2007) Elucidating biosynthetic pathways for vitamins and cofactors. Nat Prod Rep 24, 988-1008.
  13. ^ Begley TP, Chatterjee A, Hanes JW, Hazra A & Ealick SE (2008) Cofactor biosynthesis—still yielding fascinating new biological chemistry. Curr Opin Chem Biol 12, 118-125.
  14. ^ Makarchikov AF, Lakaye B, Gulyai IE, Czerniecki J, Coumans B, Wins P, Grisar T and Bettendorff L (2003). "Thiamine triphosphate and thiamine triphosphatase activities: from bacteria to mammals". Cell. Mol. Life Sci. 60: 1477–1488. doi:10.1007/s00018-003-3098-4.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  15. ^ Lakaye B, Wirtzfeld B, Wins P, Grisar T and Bettendorff L (2004). "Thiamine triphosphate, a new signal required for optimal growth of Escherichia coli during amino acid starvation". J. Biol. Chem. 279: 17142–17147. doi:10.1074/jbc.M313569200. PMID 14769791.{{cite journal}}: CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link)
  16. ^ Bettendorff L, Wirtzfeld B, Makarchikov AF, Mazzucchelli G, Frédérich M, Gigliobianco T, Gangolf M, De Pauw E, Angenot L and Wins P (2007). "Discovery of a natural thiamine adenine nucleotide". Nature Chem. Biol. 3: 211–212. doi:10.1038/nchembio867.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  17. ^ Thiamine's Mood-Mending Qualities, Richard N. Podel, Nutrition Science News, January 1999.
  18. ^ McGuire, M. and K.A. Beerman. Nutritional Sciences: From Fundamentals to Foods. 2007. California: Thomas Wadsworth.
  19. ^ Hayes KC, Hegsted DM. Toxicity of the Vitamins. In: National Research Council (U.S.). Food Protection Committee. Toxicants Occurring Naturally in Foods. 2nd ed. Washington DCL: National Academy Press; 1973.
  20. ^ Bettendorff L., Mastrogiacomo F., Kish S. J., and Grisar T. (1996). "Thiamine, thiamine phosphates and their metabolizing enzymes in human brain". J. Neurochem. 66: 250–258.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  21. ^ "Thiamin", Jane Higdon, Micronutrient Information Center, Linus Pauling Institute
  22. ^ Thornalley PJ (2005). "The potential role of thiamine (vitamin B(1)) in diabetic complications". Curr Diabetes Rev. 1 (3): 287–98. doi:10.2174/157339905774574383. PMID 18220605.
  23. ^ Diabetes problems 'vitamin link', BBC News, Tuesday, 7 August 2007
  24. ^ Maurice V, Adams RD, Collins GH. The Wernicke-Korsakoff Syndrome and Related Neurologic Disorders Due to Alcoholism and Malnutrition. 2nd ed. Philadelphia: FA Davis, 1989.
  25. ^ Martin, PR, Singleton, CK, Hiller-Sturmhofel, S (2003). "The role of thiamine deficiency in alcoholic brain disease". Alcohol Research and Health. 27: 134–142.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  26. ^ a b Kril JJ (1996). "Neuropathology of thiamine deficiency disorders". Metab Brain Dis. 11 (1): 9–17. doi:10.1007/BF02080928.
  27. ^ Butterworth RF, Gaudreau C, Vincelette J; et al. (1991). "Thiamine deficiency and wernicke's encephalopathy in AIDS". Metab Brain Dis. 6: 207–12. doi:10.1007/BF00996920. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  28. ^ Harper C. (1979). "Wernicke's encephalopathy, a more common disease than realised (a neuropathological study of 51 cases)". J Neurol Neurosurg Psychol. 42: 226–231. doi:10.1136/jnnp.42.3.226. PMID 438830.
  29. ^ Butterworth RF (1993). "Pathophysiologic mechanisms responsible for the reversible (thiamine-responsive) and irreversible (thiamine non-responsive) neurological symptoms of Wernicke's encephalopathy". Drug Alcohol Rev. 12: 315–22. doi:10.1080/09595239300185371.
  30. ^ Rindi G, Imarisio L, Patrini C (1986). "Effects of acute and chronic ethanol administration on regional thiamin pyrophosphokinase activity of the rat brain". Biochem Pharmacol. 35: 3903–8. doi:10.1016/0006-2952(86)90002-X.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  31. ^ McCollum EV A History of Nutrition. Cambridge, MA: Riverside Press, Houghton Mifflin; 1957.
  32. ^ Merck Veterinary Manual, ed 1967, pp 1440-1441.
  33. ^ R.E. Austic and M.L. Scott, Nutritional deficiency diseases, in Diseases of poultry, ed. by M.S. Hofstad, Iowa State University Press, Ames, Iowa, USA ISBN 0-8138-0430-2, p. 50.
  34. ^ The disease is described more carefully here: merckvetmanual.com
  35. ^ National Research Council. 1996. Nutrient Requirements of Beef Cattle, Seventh Revised Ed. Washington, D.C.: National Academy Press.
  36. ^ Polioencephalomalacia: Introduction, Merck Veterinary Manual
  37. ^ Bettendorff L, Peeters M., Jouan C., Wins P., and Schoffeniels E. (1991) Determination of thiamin and its phosphate esters in cultured neurons and astrocytes using an ion-pair reversed-phase high-performance liquid chromatographic method. Anal. Biochem. 198: 52-59.
  38. ^ Losa R, Sierra MI, Fernández A, Blanco D, Buesa JM. (2005) Determination of thiamine and its phosphorylated forms in human plasma, erythrocytes and urine by HPLC and fluorescence detection: a preliminary study on cancer patients.J Pharm Biomed Anal. 37:1025-1029.
  39. ^ Lu J, Frank EL. (2008) Rapid HPLC measurement of thiamine and its phosphate esters in whole blood. Clin Chem. 2008 May;54(5):901-906.
  40. ^ Researchers find vitamin B1 deficiency key to vascular problems for diabetic patients, University of Warwick
  41. ^ Shabangi M, Sutton JA. Separation of thiamin and its phosphate esters by capillary zone electrophoresis and its application to the analysis of water-soluble vitamins. Journal of Pharmaceutical and Biomedical Analysis 2005; 38:1:66-71.
  42. ^ "Thiamine Responsive Megaloblastic Anemia with severe diabetes mellitus and sensorineural deafness (TRMA)". PMID 249270. {{cite journal}}: Cite journal requires |journal= (help)
  43. ^ Kopriva, V; Bilkovic, R; Licko, T (1977). "Tumours of the small intestine (author's transl)". Ceskoslovenska gastroenterologie a vyziva. 31 (8): 549–53. ISSN 0009-0565. PMID 603941. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  44. ^ Beissel, J (1977). "The role of right catheterization in valvular prosthesis surveillance (author's transl)". Annales de cardiologie et d'angeiologie. 26 (6): 587–9. ISSN 0003-3928. PMID 606152. {{cite journal}}: Unknown parameter |month= ignored (help)
  45. ^ Online Mendelian Inheritance in Man (OMIM): 249270
  46. ^ Butterworth RF. Pyruvate dehydrogenase deficiency disorders. In: McCandless DW, ed. Cerebral Energy Metabolism and Metabolic Encephalopathy. Plenum Publishing Corp.; 1985.
  47. ^ Blass JP. Inborn errors of pyruvate metabolism. In: Stanbury JB, Wyngaarden JB, Frederckson DS et al., eds. Metabolic Basis of Inherited Disease. 5th ed. New York: McGraw-Hill, 1983.
  48. ^ Djoenaidi W, Notermans SL, Gabreëls-Festen AA, Lilisantoso AH, Sudanawidjaja A (1995). "Experimentally induced beriberi polyneuropathy in chickens". Electromyogr Clin Neurophysiol. 35 (1): 53–60.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  49. ^ Bruce WR, Furrer R, Shangari N, O’Brien PJ, Medline A, Wang Y (2003). "Marginal dietary thiamin deficiency induces the formation of colonic aberrant crypt foci (ACF) in rats". Cancer Lett. 202: 125–129. doi:10.1016/j.canlet.2003.08.005.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  50. ^ Langlais PJ (1995). "Pathogenesis of diencephalic lesions in an experimental model of Wernicke's encephalopathy". Metab Brain Dis. 10 (1): 31–44. doi:10.1007/BF01991781.
  51. ^ Frederikse PH, Zigler SJ Jr, Farnsworth PN, Carper DA (2000). "Prion protein expression in mammalian lenses". Curr Eye Res. 20 (2): 137–43. doi:10.1076/0271-3683(200002)20:2;1-D;FT137.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  52. ^ Kale S, Ulas G, Song J, Brudvig GW, Furey W & Jordan F (2008) Efficient coupling of catalysis and dynamics in the E1 component of Escherichia coli pyruvate dehydrogenase multienzyme complex.Proc Natl Acad Sci U S A. 105, 1158-1163
  53. ^ Kluger R & Tittmann K (2008) Thiamin diphosphate catalysis: enzymic and nonenzymic covalent intermediates. Chem Rev 108, 1797-1833
  54. ^ Makarchikov AF, Lakaye B, Gulyai IE, Czerniecki J, Coumans B, Wins P, Grisar T & Bettendorff L (2003) Thiamine triphosphate and thiamine triphosphatase activities: from bacteria to mammals. Cell Mol Life Sci 60, 1477-1488.
  55. ^ Bettendorff L, Wirtzfeld B, Makarchikov AF, Mazzucchelli G, Frédérich M, Gigliobianco T, Gangolf M, De Pauw E, Angenot L & Wins P (2007) Discovery of a natural thiamine adenine nucleotide. Nat Chem Biol 3, 211-212.
  56. ^ Lonsdale D, Shamberger RJ, Audhya T (2002). "Treatment of autism spectrum children with thiamin tetrahydrofurfuryl disulfide: a pilot study" (PDF). Neuro Endocrinol. Lett. 23 (4): 303–8. PMID 12195231. Retrieved 2007-08-10.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  57. ^ N. Rabbani, S. S. Alam, S. Riaz, J. R. Larkin, M. W. Akhtar, T. Shafi and P. J. Thornalley (2009). "High-dose thiamine therapy for patients with type 2 diabetes and microalbuminuria: a randomised, double-blind placebo-controlled pilot study". Diabetologia. 52: 208. doi:10.1007/s00125-008-1224-4.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  58. ^ Rabbani, N; Alam, Ss; Riaz, S; Larkin, Jr; Akhtar, Mw; Shafi, T; Thornalley, Pj (2009). "High-dose thiamine therapy for patients with type 2 diabetes and microalbuminuria: a randomised, double-blind placebo-controlled pilot study". Diabetologia. 52 (2): 208–12. doi:10.1007/s00125-008-1224-4. PMID 19057893. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  59. ^ Thornalley, Pj; Babaei-Jadidi, R; Al, Ali, H; Rabbani, N; Antonysunil, A; Larkin, J; Ahmed, A; Rayman, G; Bodmer, Cw (2007). "High prevalence of low plasma thiamine concentration in diabetes linked to a marker of vascular disease". Diabetologia. 50 (10): 2164–70. doi:10.1007/s00125-007-0771-4. PMC 1998885. PMID 17676306. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
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