Vitamin B 1 Thiamin Vitamin B complex Vitamin

Vitamin B 1 Thiamin

Vitamin B complex

Thiamin (anti – beri) • Thiamin was first realized in the 1800 s by Eijkman, when it was discovered that fowl fed a diet of cooked, polished (devoid of the outer layers) rice developed neurologic problems (now called beri). • The substance initially called thiamine that corrected the problems was first isolated from rice bran in 1912 by Casmir Funk. • The vitamin’s structure discovered by R. Williams from the United States in 1930 s.

structure • Thiamin (vitamin B 1) consists of a pyrimidine ring and a thiazole moiety (meaning one of two parts) linked by a methylene (CH 2) bridge.

Sources • Thiamin is widely distributed in foods, including meat, legumes, and whole, fortified, or enriched grain products, cereals, and breads. • Yeast, wheat germ, and soy milk also contain significant amounts of the vitamin. • In supplements, thiamin is found mainly as thiamin hydrochloride or as thiamin mononitrate salt.

Sources

Stability • Thiamin is destroyed by prolonged heat. • Food should be cooked in small amounts of water so that thiamin and other water- soluble vitamins don’t leach out. • Baking soda should not be added to vegetable as it breaks thiamin. • Avoid sulfite preservatives as it breaks thiamin. • Drinking tea with meal will decrease the amount of thiamin that absorbed by the body. • Vitamin B 1 is stable in acid, unstable in aqueous solutions of p. H more than 5.

Digestion, absorption & transport • In plants, thiamin exists in a free (nonphosphorylated) form. • In animal products, 95% of thiamin occurs in a phosphorylated form, primarily thiamin diphosphate (TDP), also called thiamin pyrophosphate (TPP). • Intestinal phosphatases hydrolyze the phosphates from the thiamin diphosphate prior to absorption.

Absorption • Absorption of thiamin from foods is thought to be high. • Antithiamin factors may be present in the diet. For example: • Thiaminases present in raw fish catalyze the cleavage of thiamin, destroying the vitamin. • These thiaminases are thermolabile, so cooking fish renders the enzymes inactive. • Polyhydroxyphenols such as tannic and caffeic acids, which are thermostable, are found in coffee, tea, betel nuts, and certain fruits and vegetables such as blueberries, black currants, Brussels sprouts, and red cabbage. • These inactivate thiamin have an oxyreductive effect to inactivate thiamine; this process facilitated by divalent minerals such as calcium and magnesium. • Thiamin destruction may be prevented, by presence of reducing compounds such as vitamin C and citric acid.

Absorption • Absorption of thiamin occurs primarily in the jejunum, with lesser amounts absorbed in the duodenum and ileum. • Free thiamin, not phosphorylated thiamin, is absorbed into the intestinal mucosal cells. • Yet, within the mucosal cells, thiamin may be phosphorylated. • Absorption of thiamin can be both active and passive, depending on the amount of the vitamin presented in the intestine for absorption.

Absorption • When intakes of thiamin are high, absorption is predominantly by passive diffusion. • At low physiological concentrations, thiamin absorption is active and is sodium-dependent. • Two thiamin transporters from the SLC 19 gene family have been characterized; the protein carriers are called Th. Tr 1 and Th. Tr 2. Both of these carriers are found in a variety of tissues including the intestine and kidneys. • Defects in the gene SLC 19 A 2, which codes for Th. Tr 1, have been shown to cause thiamin deficiency

Transport • Thiamin transport across the basolateral membrane occurs by a thiamin/H 1 antiport system. • Ethanol ingestion, interferes with active transport of thiamin from the mucosal cell across the basolateral membrane, but not the brush border membrane. • Thiamin in the blood is typically either in its free form, bound to albumin, or found as thiamin monophosphate (TMP). Most of thiamine exists as TDP. • Most (~90%) of the thiamin in the blood is present within • the blood cells.

Transport • Another form of thiamin, thiamin triphosphate (TTP), represents about 10% of total body thiamin. • TTP is synthesized by action of a TDP-ATP phosphoryl transferase that phosphorylates TDP. • The terminal phosphate on the TTP may be hydrolyzed by thiamin triphosphatase to yield TDP. • TDP can be converted to TMP by thiamin diphosphatase. • TMP can be then converted to free thiamin by thiamin monophosphatase.

Transport • TTP, as well as TDP and TMP, can be found in small • amounts in several tissues, including the brain, heart, liver, muscles, and kidney. • TMP is thought to be derived from the catabolism of the terminal phosphate on TDP and is believed to be inactive. • Enzymes responsible for thiamin phosphorylation and dephosphorylation are found in a variety of organs and tissues, including the brain.

FUNCTIONS AND MECHANISMS OF ACTION • Thiamin plays essential coenzyme and noncoenzyme roles in the body, including these: • Energy transformation (a coenzyme role in crabs metabolism, kreb’s cycle). • Synthesis of pentoses and nicotinamide adenine dinucleotide phosphate (NADPH) (also as a coenzyme role). • Membrane and nerve conduction (in a noncoenzyme capacity).

Co- enzyme roles • As TDP, thiamin functions in energy transformation as a coenzyme of the pyruvate dehydrogenase complex, the α-ketoglutarate dehydrogenase complex, and the branchedchain α-keto acid dehydrogenase complex. • In addition, TDP serves as a coenzyme for transketolase needed for the synthesis of NADPH and pentoses.

Energy Transformation • Thiamin as TDP functions as a coenzyme necessary for the oxidative decarboxylation of pyruvate, α-ketoglutarate, and the three branched-chain amino acids isoleucine, and valine. • These reactions are instrumental in generating energy (ATP). • Inhibition of the decarboxylation reactions: • pyruvate and α-ketoglutarate prevents synthesis of ATP and of the acetyl Co. A needed for the synthesis of, fatty acids, cholesterol, and other important compounds. • The inhibition also results in the accumulation of pyruvate, lactate, and α-ketoglutarate in the blood.

Noncoenzyme Roles • Membrane and Nerve Conduction • Thiamin, as TTP, is thought to function in a manner other than as a coenzyme. • In nerve membranes, TTP is thought to activate ion (specifically chloride) transport. • Thiamin also may be involved in nerve impulse transmission by regulation of sodium channels and acetylcholine receptors.

METABOLISM AND EXCRETION • Excess of thiamin of tissue needs and storage capacity is excreted intact, as well as catabolized for urinary excretion. • Degradation of thiamin begins when the molecule is cleaved into its pyrimidine and thiazole moieties. • The two rings are then further catabolized, generating 20 or more metabolites. • TDP and TMP are also excreted intact.

RECOMMENDED DIETARY ALLOWANCE • The 1989 RDA for thiamin, the basis on studies examining urinary excretion of thiamin, changes in erythrocyte transketolase activity, and thiamin intake data. • For adult men 1. 2 mg/d • For adult women 1. 1 mg/d • For pregnancy 1. 4 mg/d • For lactation 1. 5 mg/d • The daily requirement increase with high carbohydrate intake and for hard worker or athletes.

DEFICIENCY: BERI • Beriberi (beri means “weakness”). • One of the first symptoms of thiamin deficiency is a loss of appetite (anorexia) and thus weight loss. • As the deficiency worsens, cardiovascular system involvement (such as hypertrophy and altered heart rate) and neurological symptoms (such as apathy, confusion, decreased shortterm memory, and irritability) appear.

DEFICIENCY: BERI • Three types of beri have been identified: 1. Dry beri found predominantly in older adults, is thought to result from a chronic low thiamin intake with a high carbohydrate intake. Characterized by muscle weakness and wasting. 2. Wet beri cardiomegaly (enlarged heart), rapid heart beat (tachycardia), rightside heart failure and peripheral edema. 3. Acute beri seen mostly in infants, has been documented in countries including Japan. Acute beri is associated with anorexia, vomiting, lactic acidosis. • Use of parenteral nutrition devoid of thiamin cause acute thiamin deficiency within a few weeks.

DEFICIENCY: BERI

TOXICITY • There appears to be little danger of thiamin toxicity associated with oral intake of large amounts (500 mg daily for 1 month) of thiamin. • Excessive thiamin (100 X RDA) administered intravenously or intramuscularly, associated with headache, convulsions, cardiac arrhythmia, and anaphylactic shock, among other signs. • No tolerable upper intake level has been established.